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1
Friedrich, Katrin, Volker Dimmer, Gunter Haroske, Wolfdietrich Meyer, Franz Theissig, and Klaus Dietmar Kunze. "Correlation between p53 Status, DNA Ploidy, Proliferation Rate and Nuclear Morphology in Breast Cancer. An Image Cytometric Study." Analytical Cellular Pathology 15, no. 2 (1997): 85–97. http://dx.doi.org/10.1155/1997/719876.
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The study was designed to detect differences in the nuclear morphology of tumours and tumour cell populations with different p53 expression in correlation with DNA ploidy and proliferation rate. The paraffin sections from routinely processed samples of 88 breast cancers were immunostained with the monoclonal p53‐antibody DO‐1. After localization and evaluation with a scoring system the sections were destained and stained by the Feulgen method. The nuclei were relocated automatically and measured by means of the image cytometry workstation. Significant differences between the tumours and tumour cell populations with different p53 expression were found in the euploid tumours as well as in the aneuploid tumours and in the breast cancers with a high proliferation rate. The breast cancers with a low immunoreactive score (IRS 1–4) differ from the negative cancers as well as from the cancers with a higher immunoreactive score (IRS 5–12). Evaluating the nuclear populations of the p53 positive cancers, there were differences in the features of the chromatin amount and distribution in the groups of the euploid breast cancers and in cancer with a high proliferation rate. In contrast, the nuclear populations of the aneuploid cancers did not show any differences in their nuclear morphology.The results showed the different impacts of the p53 expression, DNA ploidy and the proliferation rate on the nuclear morphology in breast cancer.
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van den Bulk, Jitske, Els ME Verdegaal, and Noel FCC de Miranda. "Cancer immunotherapy: broadening the scope of targetable tumours." Open Biology 8, no. 6 (June 2018): 180037. http://dx.doi.org/10.1098/rsob.180037.
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Cancer immunotherapy has experienced remarkable advances in recent years. Striking clinical responses have been achieved for several types of solid cancers (e.g. melanoma, non-small cell lung cancer, bladder cancer and mismatch repair-deficient cancers) after treatment of patients with T-cell checkpoint blockade therapies. These have been shown to be particularly effective in the treatment of cancers with high mutation burden, which places tumour-mutated antigens (neo-antigens) centre stage as targets of tumour immunity and cancer immunotherapy. With current technologies, neo-antigens can be identified in a short period of time, which may support the development of complementary, personalized approaches that increase the number of tumours amenable to immunotherapeutic intervention. In addition to reviewing the state of the art in cancer immunotherapy, we discuss potential avenues that can bring the immunotherapy revolution to a broader patient group including cancers with low mutation burden.
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Osterheld, Maria‐Chiara, Liette Caron, Mireille Demierre, Ricardo Laurini, and F. T. Bosman. "DNA-Ploidy in Advanced Gastric Carcinoma is Less Heterogeneous than in Early Gastric Cancer." Analytical Cellular Pathology 26, no. 1-2 (January 1, 2004): 21–29. http://dx.doi.org/10.1155/2004/219293.
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This analysis of DNA‐ploidy heterogeneity in advanced gastric carcinomas is consistent with the hypothesis of the emergence of a single aneuploid cell clone as a crucial mechanism in the progression from early gastric carcinoma to advanced gastric cancer. The prognostic value of DNA‐ploidy in gastric cancers has been a matter of controversy. Tumour DNA‐ploidy heterogeneity, the presence within the same tumour of multiple stemlines differing in DNA content, has been described in various tumours including gastric cancers. The occurrence of such heterogeneity has been accepted as an explanation for the divergent DNA‐ploidy results in this type of tumours. A previous study of early gastric cancers suggested that in pure diploid superficial carcinomas, genetic instability might lead to a cell clone which has undergone a ploidy shift and is more aggressive. If so, this would initially result in DNA‐ploidy heterogeneity. Proliferative dominance of the aneuploid clone could eventually evolve to a homogeneous aneuploid tumour. In order to test this hypothesis, we studied DNA‐aneuploidy and DNA‐ploidy heterogeneity in advanced gastric carcinomas. We performed DNA cytophotometry on multiple samples collected from 16 advanced gastric carcinomas and found 15 DNA‐aneuploid tumours (94%) and one diploid tumour. Multiple DNA‐stemlines were found in 4 cases (26%). Analysis of proliferative activity performed on the same samples revealed higher proliferation rate in DNA‐ploidy homogeneous tumours than in aneuploid heterogeneous tumours. Heterogeneous tumours did not overexpress p53. These results confirm that DNA‐aneuploidy is frequent in advanced gastric cancer and demonstrate that a majority of these aneuploid tumours are not DNA‐ploidy heterogeneous. Furthermore, the higher proliferative activity in homogeneous‐aneuploid carcinomas and their more frequent overexpression of p53 support the hypothesis that in gastric cancer tumour progression implies the development of a dominant and more aggressive (higher proliferative activity, p53 overexpression) aneuploid cell clone.
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Sevyan, N. V., V. B. Karakhan, D. R. Naskhletashvili, A. Kh Bekyashev, E. V. Prozorenko, D. M. Belov, A. A. Mitrofanov, A. A. Pogosova, and B. I. Polyakov. "Brain metastases from gynaecological cancers." Voprosy ginekologii, akušerstva i perinatologii 19, no. 4 (2020): 172–77. http://dx.doi.org/10.20953/1726-1678-2020-4-172-177.
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The spread of female genital tract tumours to the brain is a rare and insufficiently studied pathology. The problems of diagnosis and treatment of this group of patients still remain. The article gives a detail account of the clinical picture, radiological and morphological diagnosis, and the principles of treating patients with brain metastases from gynaecological cancers. Conclusion. A probable cause of a rare occurrence of brain metastases from gynaecological malignancies might be a high resistance of nervous tissue to various kinds of tumours. When local control over a brain tumour is achieved, this might improve the patient’s survival and quality of life in some particular cases. Key words: ovarian cancer, endometrial cancer, cervical cancer, brain metastases
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Santos, J., R. Palacios, J. Ruiz, M. González, and M. Márquez. "Unusual malignant tumours in patients with HIV infection." International Journal of STD & AIDS 13, no. 10 (October 1, 2002): 674–76. http://dx.doi.org/10.1258/095646202760326417.
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The clinical charts of 2560 HIV-infected patients seen in our Unit between 01/89 and 08/01 were reviewed. All patients with a neoplasm were analysed to study the prevalence of tumours other than Kaposi's sarcoma (KS), non-Hodgkin's lymphoma (NHL) or cancer of the cervix. There were 43 unusual malignant tumours: 13 lung cancers, six leukaemias, six skin cancers, two carcinomas of the conjunctiva, two cancers of the penis, three of the anus, three of the larynx, one sarcoma of the ureter, one gastric carcinoid, one non-differentiated thyroid carcinoma, one non-differentiated prostate carcinoma, one cancer of the tongue, one cancer of the bladder, one adenocarcinoma of the rectum and one multiple IgM myeloma. Thirteen (43.3%) of the patients died, 10 (76.9%) from causes related to the tumour itself. These results suggest that HIV-infected patients have a higher prevalence of some neoplasms than the general population.
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Park, Kenneth G. M., Steven D. Heys, Karen Blessing, Peter Kelly, Margaret A. McNurlan, Oleg Eremin, and Peter J. Garlick. "Stimulation of human breast cancers by dietary l-arginine." Clinical Science 82, no. 4 (April 1, 1992): 413–17. http://dx.doi.org/10.1042/cs0820413.
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1. The amino acid L-arginine has been shown to enhance immune mechanisms and inhibit tumour growth in experimental animals, but although many of the immunological effects of arginine have been reproduced in man there have been few studies of its effects on human tumours. In this study the effects of arginine on human breast cancers were determined by measuring tumour protein synthesis and comparing this with immunohistochemical assessments of cell proliferation. 2. Patients with breast cancer were randomized to receive either a standard diet or arginine supplementation. At the time of surgery, the rate of tumour protein synthesis was measured by the incorporation of the stable isotope [1-13C]leucine into tumour protein. Tumours were also assessed histologically and by staining for the presence of the activation antigen Ki67. 3. The median rate of tumour protein synthesis was 10%/ day (range 5.5–15.8%/day) in the control patients and 25.6%/day (range 9-37%/day) in the patients receiving arginine supplements (P < 0.005, Wilcoxon rank sum test). The rates of protein synthesis correlated with Ki67 expression within these tumours (r=0.78, P < 0.001). A double-staining technique confirmed that tumour cells, rather than tumour-infiltrating lymphoreticular cells, expressed Ki67. 4. This study demonstrates that, in contrast to animal studies, L-arginine stimulates human tumours in vivo. This represents the first direct evidence that a single amino acid can modulate the behaviour of a human cancer.
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Roche, Sandra, Fiona O’Neill, Jean Murphy, Niall Swan, Justine Meiller, Neil T. Conlon, Justin Geoghegan, et al. "Establishment and Characterisation by Expression Microarray of Patient-Derived Xenograft Panel of Human Pancreatic Adenocarcinoma Patients." International Journal of Molecular Sciences 21, no. 3 (January 31, 2020): 962. http://dx.doi.org/10.3390/ijms21030962.
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Pancreatic cancer remains among the most lethal cancers worldwide, with poor early detection rates and poor survival rates. Patient-derived xenograft (PDX) models have increasingly been used in preclinical and clinical research of solid cancers to fulfil unmet need. Fresh tumour samples from human pancreatic adenocarcinoma patients were implanted in severe combined immunodeficiency (SCID) mice. Samples from 78% of treatment-naïve pancreatic ductal adenocarcinoma patients grew as PDX tumours and were confirmed by histopathology. Frozen samples from F1 PDX tumours could be later successfully passaged in SCID mice to F2 PDX tumours. The human origin of the PDX was confirmed using human-specific antibodies; however, the stromal component was replaced by murine cells. Cell lines were successfully developed from three PDX tumours. RNA was extracted from eight PDX tumours and where possible, corresponding primary tumour (T) and adjacent normal tissues (N). mRNA profiles of tumour vs. F1 PDX and normal vs. tumour were compared by Affymetrix microarray analysis. Differential gene expression showed over 5000 genes changed across the N vs. T and T vs. PDX samples. Gene ontology analysis of a subset of genes demonstrated genes upregulated in normal vs. tumour vs. PDX were linked with cell cycle, cycles cell process and mitotic cell cycle. Amongst the mRNA candidates elevated in the PDX and tumour vs. normal were SERPINB5, FERMT1, AGR2, SLC6A14 and TOP2A. These genes have been associated with growth, proliferation, invasion and metastasis in pancreatic cancer previously. Cumulatively, this demonstrates the applicability of PDX models and transcriptomic array to identify genes associated with growth and proliferation of pancreatic cancer.
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Shrivastava, Vaidik, Ashwini Tangde, Anil Joshi, and Rajan Bindu. "Clinicopathological study of skin tumours." International Journal of Research in Medical Sciences 7, no. 5 (April 26, 2019): 1712. http://dx.doi.org/10.18203/2320-6012.ijrms20191664.
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Background: Skin cancers are relatively uncommon malignancies worldwide, but the incidence of skin cancers has progressively increased over the last few decades. The distinction between benign and malignant neoplasm are more difficult to define when they appear in skin than when found elsewhere and histopathological examination is frequently required to establish a definitive diagnosis. Diagnosis of any skin tumours can be done by correlating clinical features and histological features. The aim and objective were to study age-sex wise distribution, clinical presentation and histopathological spectrum of various skin tumours.Methods: This is a retrospective study of three years conducted in the Department of Pathology, Government Medical College, Aurangabad, India from December 2015 to December 2018. Specimens received from Department of Dermatology were fixed in formalin and after adequately processing the sections were stained routinely with H and E stain and properly evaluated for histopathological examination. This study includes tumors of epidermis along with melanogenic tumors and skin appendageal tumors. The data collected was tabulated, analysed and compared to other similar studies.Results: The study consists of 130 cases. The ratio of male to female was 1.24:1. Head and neck region (48.46%) was the most common site observed where skin lesions were present followed by extremities (37.69%). Most of the malignant tumours were presented with non-healing ulcers (30.76%) and Noduloulcerative lesions (20.33%). Out of 130 cases, 83 (63.84%) were benign whereas 47 (36.15%) were malignant tumour. According to WHO classification, keratinocytic tumour 55 (42.30%) was the most common tumour type in the present study. Skin adnexal tumours and melanocytic tumours were observed in 54 (41.53%) and 21 (16.15%) respectively.Conclusions: The skin is a complex organ. Because of complexity of skin, a wide range of diseases can develop from the skin. The majority of benign neoplasms are from skin adnexal group whereas most common malignant neoplasm were from keratinocytic group. Skin adnexal tumors can occur anywhere in the body, however head and neck region constitute the most common site. Skin adnexal tumours are clinically often misdiagnosed, so histopathological examination remains gold standard for their correct diagnosis and for their differentiation between benign and malignant neoplasm.
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Alvarado-Cruz, Isabel, Rithy Meas, Sesha Lakshmi Arathi Paluri, Kelly Estelle Wheeler Carufe, Mohammed Khan, and Joann Balazs Sweasy. "The double-edged sword of cancer mutations: exploiting neoepitopes for the fight against cancer." Mutagenesis 35, no. 1 (December 27, 2019): 69–78. http://dx.doi.org/10.1093/mutage/gez049.
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Abstract Defects in DNA repair have been linked to the accumulation of somatic mutations in tumours. These mutations can promote oncogenesis; however, recent developments have indicated that they may also lead to a targeted immune response against the tumour. This response is initiated by the development of new antigenic epitopes (neoepitopes) arising from mutations in protein-coding genes that are processed and then presented on the surface of tumour cells. These neoepitopes are unique to the tumour, thus enabling lymphocytes to launch an immune response against the cancer cells. Immunotherapies, such as checkpoint inhibitors (CPIs) and tumour-derived vaccines, have been shown to enhance the immunogenic response to cancers and have led to complete remission in some cancer patients. There are tumours that are not responsive to immunotherapy or conventional tumour therapeutics; therefore, there is a push for new treatments to combat these unresponsive cancers. Recently, combinatorial treatments have been developed to further utilise the immune system in the fight against cancer. These treatments have the potential to exploit the defects in DNA repair by inducing more DNA damage and mutations. This can potentially lead to the expression of high levels of neoepitopes on the surface of tumour cells that will stimulate an immunological response. Overall, exploiting DNA repair defects in tumours may provide an edge in this long fight against cancer.
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Adachi, Y., H. Yamamoto, F. Itoh, Y. Hinoda, Y. Okada, and K. Imai. "Contribution of matrilysin (MMP-7) to the metastatic pathway of human colorectal cancers." Gut 45, no. 2 (August 1, 1999): 252–58. http://dx.doi.org/10.1136/gut.45.2.252.
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BACKGROUND/AIMMatrilysin is one of the matrix metalloproteinases that has a critical role in tumour invasion, and is often expressed in gastrointestinal cancers. The aim of this study was to examine the role of matrilysin in metastasis of human colorectal cancers.PATIENTS (SUBJECTS)/METHODSThe relation between matrilysin expression and Dukes’s type was investigated immunohistochemically in 83 surgically resected colorectal cancers, including five with liver metastasis. Moreover, the effects of matrilysin on the in vivo invasive and metastatic potential of colon cancer cells transfected with matrilysin cDNA were examined after subcutaneous injection into SCID mice.RESULTSIn 46% of primary and all of metastatic liver tumours, over 10% of cancer cells were stained positively for matrilysin. The expression of matrilysin correlated significantly with the presence of nodal or distant metastases (p<0.05). In addition, matrilysin transfectants formed invasive tumours and multiple liver metastases in SCID mice, without producing any significant difference in the subcutaneous tumour growth from mock transfectants. Casein zymography showed that the invading and metastasised tumours showed conspicuous matrilysin activity, which correlated with the number of metastatic lesions (p<0.001).CONCLUSIONSMatrilysin showed a correlation with metastasis in a cohort of 83 colorectal cancer patients and marked metastatic potentiation in human colorectal cancer xenografts, indicating that it may play a critical role in the metastatic pathway of colorectal cancers.
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Umer, Brittany, David Good, Jozef Anné, Wei Duan, and Ming Q. Wei. "Clostridial Spores for Cancer Therapy: Targeting Solid Tumour Microenvironment." Journal of Toxicology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/862764.
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Solid tumour accounts for 90% of all cancers. The current treatment approach for most solid tumours is surgery, however it is limited to early stage tumours. Other treatment options such as chemotherapy and radiotherapy are non-selective, thus causing damage to both healthy and cancerous tissue. Past research has focused on understanding tumour cells themselves, and conventional wisdom has aimed at targeting these cells directly. Recent research has shifted towards understanding the tumour microenvironment and it’s differences from that of healthy cells/tissues in the body and then to exploit these differences for treatmeat of the tumour. One such approach is utilizing anaerobic bacteria. Several strains of bacteria have been shown to selectively colonize in solid tumours, making them valuable tools for selective tumour targeting and destruction. Amongst them, the anaerobicClostridiumhas shown great potential in penetration and colonization of the hypoxic and necrotic areas of the tumour microenvironment, causing significant oncolysis as well as enabling the delivery of therapeutics directly to the tumourin situ. Various strategies utilizingClostridiumare currently being investigated, and represent a novel area of emerging cancer therapy. This review provides an update review of tumour microenvironment as well as summary of the progresses and current status of Clostridial spore-based cancer therapies.
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Wang, Weining, Chin Jin Seo, Grace Hwei Ching Tan, Claramae Shulyn Chia, Khee Chee Soo, and Melissa Ching Ching Teo. "Can sidedness predict for survival in primary locoregional colon cancers?" Journal of Clinical Oncology 36, no. 4_suppl (February 1, 2018): 584. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.584.
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584 Background: Right and left-sided colon cancers are embryonically distinct and present differently. Recently, there has been growing belief that sidedness could be independently associated with survival outcomes. This has important clinical implications regarding the prognostication, management and surveillance of colon cancer patients. Hence, we aim to investigate the impact of sidedness on survival in our patient population in this study. Methods: Patients who had primary treatment naïve colon cancer who underwent curative surgical resection in our institution from September 2002 to December 2010 were included in this study. Demographic and clinicopathological data was collected from electronic records and clinical charts. Tumours arising from the cecum, ascending colon, hepatic flexure and transverse colon were considered right-sided, while those arising from splenic flexure and descending colon were considered left-sided. Cancers of the rectosigmoid junction and rectum were excluded. Kaplan-Meier curves and log-rank test were used to compare overall, locoregional recurrence-free and distant recurrence-free survivals (OS, LRFS, DRFS respectively) between both groups. Multivariate analysis was performed using Cox regression proportional hazards. Results: 389 patients were included in this study. 238 had left-sided tumours while the remaining 151 had right-sided tumours. In our cohort, right-sided tumours were associated with older age and mucinous histology. Kaplan-Meier curves plotted showed improved LRFS in left-sided tumours (p = 0.04, median survival not reached) but no significant difference in OS and DRFS. On multivariate analysis, sidedness was also found to be an independent prognostic factor for LRFS but not OS and DRFS despite factoring in age, size of tumour, pT, pN and histology. Conclusions: Our study suggests that left-sided tumours in primary colon cancer are independently prognostic for improved locoregional survival as compared to the right-sided tumours, even after taking into account other known factors such as age, staging and histology.
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Lee, Shen-Han, and John R. Griffiths. "How and Why Are Cancers Acidic? Carbonic Anhydrase IX and the Homeostatic Control of Tumour Extracellular pH." Cancers 12, no. 6 (June 18, 2020): 1616. http://dx.doi.org/10.3390/cancers12061616.
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The acidic tumour microenvironment is now recognized as a tumour phenotype that drives cancer somatic evolution and disease progression, causing cancer cells to become more invasive and to metastasise. This property of solid tumours reflects a complex interplay between cellular carbon metabolism and acid removal that is mediated by cell membrane carbonic anhydrases and various transport proteins, interstitial fluid buffering, and abnormal tumour-associated vessels. In the past two decades, a convergence of advances in the experimental and mathematical modelling of human cancers, as well as non-invasive pH-imaging techniques, has yielded new insights into the physiological mechanisms that govern tumour extracellular pH (pHe). In this review, we examine the mechanisms by which solid tumours maintain a low pHe, with a focus on carbonic anhydrase IX (CAIX), a cancer-associated cell surface enzyme. We also review the accumulating evidence that suggest a role for CAIX as a biological pH-stat by which solid tumours stabilize their pHe. Finally, we highlight the prospects for the clinical translation of CAIX-targeted therapies in oncology.
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Beckett, S., E. Karreman, and R. Hughes. "P012: Mortality rate of cancer patients by type presenting to the intensive care unit with sepsis." CJEM 21, S1 (May 2019): S67. http://dx.doi.org/10.1017/cem.2019.203.
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Introduction: Sepsis in cancer patients is associated with higher mortality rates than non-cancer patients. As a whole, hematological or solid tumor cancers have not demonstrated a prognostic link to sepsis survival rates in intensive care units (ICU), however poor-prognosis solid tumours (less than 25% 5-year survival) have not been investigated. This study examined ICU mortality rate and its predictive factors of patients with sepsis and poor-prognosis solid tumors in comparison to patients with higher prognosis solid tumours. Methods: A 6-year retrospective chart review of 79 patients with sepsis and solid tumour cancers and/or metastatic cancers admitted to the ICU was conducted. Information regarding mortality rate within 14 days, length of ICU stay, incidence of intubation, and other primary reasons for ICU admission was collected. Data was analysed using logistic regression. Results: Logistic regression results showed intubation as the only significant factor contributing to patient mortality (p < .001), with the odds of mortality being 12.3 times higher for intubated than non-intubated patients. Five-year cancer survival rate was the second best predictor (p = .082), while age, sex, and metastasis were also not significant predictive factors for survival. Intubated patients with poor prognosis cancers had the lowest survival chance as further indicated by the 16 patients who met this criterion, of which 14 died within two weeks of ICU admission. Conclusion: The fact that poor prognosis cancers in sepsis were not significantly predictive of ICU mortality supports current literature regarding solid tumors in general, while intubation being a significant predictor for mortality in patients with sepsis and cancer regardless of type builds on previous research. A limitation of this study is the relative low number of included cases with poor-prognosis cancer types. Further evaluation is needed to understand the implications of our results for end-of-life care and ICU admission for patients with these characteristics.
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Verma, Nidhi, Kriti Grover, S. P. Sharma, Priya Gupta, Preeti Singh, and Anshu Singh. "Clinicopathological study of benign and malignant ovarian tumours and the role of HER2/neu and ER expression in these tumours." International Journal of Research in Medical Sciences 7, no. 6 (May 29, 2019): 2132. http://dx.doi.org/10.18203/2320-6012.ijrms20192486.
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Background: Ovarian cancers represent the 6th most common cancer among females and are the most common cause of death from gynaecological cancers in the world. The aim is to do clinicopathologic study of ovarian tumours along with evaluation of the expression of estrogen receptor (ER) and human epidermal growth factor receptor (HER2/neu).Methods: A total of 85 cases of ovarian tumors were studied and immunohistochemistry was performed with specific antibodies against ER and HER2/neu as per standard protocol.Results: In present study, surface epithelial tumours were the commonest type comprising 64 cases (75.2%), followed by Germ cell tumours, 17cases (20%) and sex cord stromal tumours, 04 cases (4.8%).Among the surface epithelial tumours , ER‑positive cases were higher in malignant (71.4%) tumours as compared to borderline tumours (33.3%) and benign tumours (7.7%) while Her2/neu positive cases were higher in borderline (66.7%) tumours as compared to malignant tumours (42.9%) and benign tumours (15.3%).Among the germ cell tumours, ER expression was positive in 62.5% cases of mature teratoma while HER2/neu expression was positive in only 12.5% cases of mature teratoma. None of the sex cord stromal tumours showed positive expression of ER and HER2/neu.Conclusions: Positive expression of estrogen receptors is seen predominantly in surface epithelial malignancies and in mature teratoma. It proves the mitogenic role of estrogen in ovarian tumours. Her-2 neu was expressed mainly in malignant tumours. This suggests their carcinogenic role. This also helps in differentiating borderline and malignant tumours.
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STADALNYKAITĖ, Sigutė, and Rūta BRIEDIENĖ. "Radiological diagnostics of triple negative breast cancer: a review." Acta medica Lituanica 18, no. 2 (April 1, 2011): 98–106. http://dx.doi.org/10.6001/actamedica.v18i2.1822.
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Background. Triple negative breast cancer has a poor prognosis. Therefore, it is vital to detect this subtype of breast cancer in its early stage. The imaging features of this clinically important subtype of breast cancer are not well known. There have been no published reports about radiological diagnostics of triple negative breast tumour in Lithuania. The purpose of this study was to review the imaging characteristics of triple receptor negative cancers in mammography, ultrasonography and magnetic resonance imaging (MRI). Materials and methods. The published data for the period 2006–2011 concerning the imaging of triple negative breast cancer were analyzed. There were ten retrospective, ten prospective studies and five reviews. Five studies were on mammography imaging, three on both mammography and ultrasonography imaging, and five studies dealt with MR imaging data. Two studies analysed all three diagnostic methods. Results. In mammography, triple negative breast (TRN) cancers often present as a mass and are most frequently round, oval or lobular in shape, less frequently being irregular. TRN tumours aren’t associated with calcifications. Moreover, architectural distortion is not a characteristic feature of triple negative breast cancer. In ultrasonography, TRN cancer appears as a parallel. TRN breast tumours mostly are irregular in shape and have a circumscribed margin. Attenuating posterior echoes and hypervascularity are not their characteristic features. In MR imaging, TRN breast cancer tends to have a lobulated, round or oval mass shape. Rim enhancement is identified in most of TRN tumours. Initially, rapid enhancement with a washout pattern (a sign of malignancy) does not usually apply to triple-negative breast cancers. Conclusions. TRN breast cancer is difficult to diagnose, because usually it has no specific imaging signs typical of breast cancer. In mammography, TRN cancers aren’t associated with microcalcifications. In ultrasonography, attenuating posterior echoes and hypervascularity are not characteristic features of TRN tumours. In MRI, initially rapid enhancement with a washout pattern does not usually apply to triple-negative breast cancers. Keywords: triple negative breast cancer, mammography, ultrasonography, magnetic resonance imaging
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Rayoo, M., M. Yan, E. A. Takano, G. J. Bates, P. J. Brown, A. H. Banham, and S. B. Fox. "Expression of the forkhead box transcription factor FOXP1 is associated with oestrogen receptor alpha, oestrogen receptor beta and improved survival in familial breast cancers." Journal of Clinical Pathology 62, no. 10 (July 20, 2009): 896–902. http://dx.doi.org/10.1136/jcp.2009.065169.
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Background:The role of FOXP1 in sporadic breast cancers has been widely studied but its role in familial breast cancers is yet unexplored.Aims:To investigate FOXP1 expression in different molecular subtypes of familial breast cancers and to correlate its expression with clinicopathological parameters, oestrogen receptors (ER) and survival.Methods:Immunohistochemical staining for FOXP1 was performed in 126 familial breast carcinomas comprising 35 BRCA1, 34 BRCA2 and 57 BRCAX.Results:Nuclear FOXP1 expression ranged from focal weak to widespread strong expression. Expression of FOXP1 was higher in familial breast cancers (54%) compared with sporadic cancers (46%) (p<0.001). There was a significant correlation between FOXP1 with ERα (p = 0.038) and ERβ (p = 0.007) in familial breast cancers. FOXP1 was more highly expressed in familial breast cancers compared with sporadic cancers for luminal (p = 0.021) and basal (p<0.001), but not HER2 and null phenotypes (both p>0.05). The absence of FOXP1 expression was associated with a shorter relapse-free (p = 0.025) and overall survival (p = 0.009) in familial breast cancer. Negativity for FOXP1 was associated with a significantly worse overall survival in BRCA2 cancers (p = 0.021) and there was a non-significant separation of the survival curves for BRCA1 cancers (p = 0.183). No differences in survival were seen for BRCAX cancers (p = 0.762).Conclusion:Results suggest that FOXP1 demonstrates different expression patterns in familial breast cancers than sporadic tumours, even in tumours showing similar phenotypes. They also suggest a different role of FOXP1 as a tumour suppressor in familial tumours, which is unrelated to ER expression and may impact on therapeutic options.
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Knowles, M. A., N. Hornigold, and E. Pitt. "Tuberous sclerosis complex (TSC) gene involvement in sporadic tumours." Biochemical Society Transactions 31, no. 3 (June 1, 2003): 597–602. http://dx.doi.org/10.1042/bst0310597.
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In tuberous sclerosis patients, inactivation of the tuberous sclerosis complex tumour-suppressor genes TSC1 and TSC2 contributes to the development of a wide range of hamartomatous lesions. These patients do not, however, show an increased risk of the common adult solid cancers. Recent evidence that the TSC genes play a role in the phosphoinositide 3-kinase pathway, a pathway whose dysregulation is implicated in a wide range of human malignancies, raises the possibility that their inactivation could contribute to the development of some sporadic cancers. To date the only evidence for this comes from the finding of mutations of TSC1 in bladder cancer. The mutation spectrum of TSC1 in bladder cancer and functional evidence from TSC1-gene-replacement studies in bladder tumour cells will be presented. The literature on genetic changes in several other sporadic epithelial cancers reveals relatively common deletions in the region of the TSC genes. In ovarian and gall bladder carcinoma and non-small-cell carcinoma of the lung, deletions in both 16p13 and 9q34 are found at significant frequency. Mutation analyses in such tumours are now merited.
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Ivanova, Koni, Julian Ananiev, Elina Aleksandrova, Maria Magdalena Ignatova, and Maya Gulubova. "Expression of E-Cadherin/Beta-Catenin in Epithelial Carcinomas of the Thyroid Gland." Open Access Macedonian Journal of Medical Sciences 5, no. 2 (March 22, 2017): 155–59. http://dx.doi.org/10.3889/oamjms.2017.043.
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BACKGROUND: The aberrant activation of Wnt signalling pathway may be a common denominator for the development of thyroid tumorigenesis. It was announced that the loss of E-cadherin rather than β-catenin mutation represents a crucial event in determining the degree of differentiation of thyroid carcinomas.AIM: The aim of the study was to evaluate the expression of E-cadherin and β-catenin in the thyroid cancer tissue and to correlate these data with some histological and clinical parameters of the tumours.MATERIAL AND METHODS: We investigated 112 patients, having thyroid tumours – papillary, follicular, anaplastic and oncocytic carcinomas immunohistochemically with antibodies against E-cadherin and β-catenin. Survival analyses were done.RESULTS: E-cadherin expression was focally retained in the tumour cell membranes and the tumour cell cytoplasm of the papillary, follicular and oncocytic thyroid cancers, weather in anaplastic cancers it was almost lost (p = 0.0042, and р = 0.019, respectively, Fisher's Exact Test). The expression of β-catenin in tumour cytoplasm and membrane in papillary cancers was higher as compared to that in the other tumours (p = 0.111, and р = 0.0104, respectively).CONCLUSION: Not surprisingly, the presence of aberrant expression of E-cadherin and β-catenin in thyroid cancer has been associated with better patients' prognosis and better differentiated tumour histology.
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Jefferies, Matthew T., Christopher S. Pope, Howard G. Kynaston, Alan R. Clarke, Richard M. Martin, and Josephine C. Adams. "Analysis of Fascin-1 in Relation to Gleason Risk Classification and Nuclear ETS-Related Gene Status of Human Prostate Carcinomas: An Immunohistochemical Study of Clinically Annotated Tumours From the Wales Cancer Bank." Biomarkers in Cancer 9 (January 1, 2017): 1179299X1771094. http://dx.doi.org/10.1177/1179299x17710944.
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Although prostate-specific antigen (PSA) testing can identify early-stage prostate cancers, additional biomarkers are needed for risk stratification. In one study, high levels of the actin-bundling protein, fascin-1, were correlated with lethal-phase, hormone-refractory prostate cancer. Analyses of independent samples are needed to establish the value of fascin-1 as a possible biomarker. We examined fascin-1 by immunohistochemistry in tumour specimens from the Wales Cancer Bank in comparison with nuclear-located ETS-related gene (ERG), an emerging marker for aggressive prostate cancer. Fascin-1 was elevated in focal areas of a minority of tumours, yet fascin-1-positivity did not differentiate tumours of low-, intermediate-, or high-risk Gleason scores and did not correlate with PSA status or biochemical relapse after surgery. Stromal fascin-1 correlated with high Gleason score. Nuclear ERG was upregulated in tumours but not in stroma. The complexities of fascin-1 status indicate that fascin-1 is unlikely to provide a suitable biomarker for prediction of aggressive prostate cancers.
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Liebs, Sandra, Anika Nonnenmacher, Frederick Klauschen, Ulrich Keilholz, and Loredana Vecchione. "Liquid biopsy assessment of synchronous malignancies: a case report and review of the literature." ESMO Open 4, no. 4 (August 2019): e000528. http://dx.doi.org/10.1136/esmoopen-2019-000528.
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Assessment of patients with synchronous primary cancers and metastases is challenging, as it can be difficult to assign the metastases to the correct primary due to low differentiation, high similarity on histology or inaccessibility of tumour tissue. Systemic treatment for metastatic disease, however, needs to be directed at the leading histology or cover multiple tumour types with the same regimen. Considering the additional obstacles in cancer management, including tumour heterogeneity and clonal evolution, blood-based genomic profiling (‘liquid biopsy’) is suggested to be a useful tool to provide accessible tumour-derived biomarkers. We herein report a case of a patient with independent primary tumours of the colon and pancreas, as well as liver metastases. All lesions were resected and genotyped revealing KRAS mutations G12C and G12D in the primary tumours, respectively. The G12D mutation detected in the pancreatic tumour was retrieved in the metastasis, thus confirming the pancreatic cancer to be the origin of the liver lesions. The prevalence of the pancreatic tumour was additionally verified by the detection of the G12D variant in circulating cell-free DNA (cfDNA). This case demonstrates the utility of liquid biopsy to identify the predominant tumour burden in patients with multiple primary cancers, based on the detection of the tumour-associated gene mutation in the plasma. Serial monitoring through liquid biopsies might allow disease surveillance to guide cancer management. The review of the literature highlights the importance of liquid biopsies in personalised oncology, even though only one case report refers to the benefit of cfDNA analysis in a patient affected by synchronous primary tumours.
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Aishwarya, Jagan, Ramasamy Sasikala, and Syed Dilshath. "Efficacy of morphological indexing of ovarian tumor: preoperative determination of risk of malignancy." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 8 (July 26, 2017): 3458. http://dx.doi.org/10.18203/2320-1770.ijrcog20173463.
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Background: Ovarian cancers ranks fifth in cancer death worldwide and in India it ranks third among the female genital tract malignancies. Objective of present study was to assess prospectively the efficacy of morphological indexing (MI) as a method to predict malignancy in sonographically confirmed ovarian tumors.Methods: A prospective study conducted in a tertiary care hospital in Tamil Nadu from September 2011 to August 2012. The risk of malignancy is preoperatively assessed in 136 patients with ovarian tumour using a morphological index based on tumour volume and wall structure. Each tumour was assigned a score of 0 to 10 based on increasing volume and morphologic complexity. The efficacy of the index was assessed by histopathological examination of the tumour.Results: The benign tumours had a mean MI score of 4.3 and malignant tumours had a mean of 8.3 which was statistically significant. Of the 54 tumours with MI <5, only 2 (3.7%) were malignant where else out of the remaining 82 tumours with MI >5, 54 (51.2%) were malignant. With MI >5 as a predictor of malignancy the present study had a Sensitivity-95.5%, Specificity-56.5%, Positive predictive value-51.2%, Negative predictive value-94%, and Accuracy-68%.Conclusions: Morphological index is a simple, valuable and inexpensive diagnostic tool to rule out malignancy in pre operative evaluations of ovarian tumors.
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Stryjewska-Makuch, Grażyna, Bogdan Kolebacz, Małgorzata A. Janik, and Agnieszka Wolnik. "Increase in the incidence of parotid gland tumors in the years 2005–2014." Otolaryngologia Polska 71, no. 2 (April 30, 2017): 29–34. http://dx.doi.org/10.5604/01.3001.0009.8412.
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Introduction: Salivary gland tumours account for 3-6% of tumours of the head and neck. About 80% of salivary gland tumors occur in parotid glands, 10-17% of which are malignant The aim of the study was to assess whether there is an upward trend in cancer incidence within the parotid glands, with particular emphasis on cancers. Materials and methods: 322 patients underwent surgery and 328 parotid gland tumours were removed in the years 2005-2014 at the Department of Laryngology and Laryngological Oncology of the Upper Silesian Medical Centre in Katowice-Ochojec. Clinical, histopathological and statistical analyses of the removed parotid gland tumours were performed. Results and discussion: A significant increase in the incidence of benign tumours, especially mixed and Warthin tumours, was demonstrated. There was no significant increase in the number of malignant tumours over the analysed period of time.
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Lepage, C., A. M. Bouvier, and J. Faivre. "Endocrine Tumours: Epidemiology of malignant digestive neuroendocrine tumours." European Journal of Endocrinology 168, no. 4 (April 2013): R77—R83. http://dx.doi.org/10.1530/eje-12-0418.
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Little is known about patients with malignant digestive neuroendocrine tumours (MD-NETs). Although their incidence is increasing, MD-NETs remain a rare cancer, representing 1% of digestive cancers. Most MD-NETs are well-differentiated. MD-NET poorly differentiated carcinomas account for 20% of cases on average. Anatomical localisation of MD-NETs varied according to geographic region. Stage at diagnosis and prognosis for patients with MD-NETs in the general population are considerably worse than often reported from small hospital case series. Prognosis varies with tumour differentiation, anatomic site and histological subtype. There are significant differences in survival from MD-NETs among European countries, independent of other prognostic factors. Early diagnosis is difficult; new therapeutic options appear to represent the best approach to improving prognosis.
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Damjanov, Ivan, and Mileta Golubovic. "Histopathology of urinary bladder carcinoma: Less common variants." Srpski arhiv za celokupno lekarstvo 139, no. 9-10 (2011): 693–99. http://dx.doi.org/10.2298/sarh1110693d.
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Bladder cancer is a common form of neoplasia which most often presents histologically as urothelial (transitional cell) carcinoma. In this article we review recent publications dealing with the less common variants of urothelial carcinoma such as tumours that show unusual forms of differentiation or the well know squamous, glandular, or sarcomatoid differentiation. Urothelial tumours may also show several distinct growth variants characterized by a nested, micropapillary, lymphoepithelioma-like, or plasmacytoid and giant cell growth pattern. The clinical course of bladder cancer varies depending on the histological type of neoplasia, grade and stage of the tumour. High-grade muscle-invasive urothelial cancers and tumours showing variant microscopic morphology have in general high mortality and poor prognosis.
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Maniam, Subashani, and Sandra Maniam. "Small Molecules Targeting Programmed Cell Death in Breast Cancer Cells." International Journal of Molecular Sciences 22, no. 18 (September 8, 2021): 9722. http://dx.doi.org/10.3390/ijms22189722.
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Targeted chemotherapy has become the forefront for cancer treatment in recent years. The selective and specific features allow more effective treatment with reduced side effects. Most targeted therapies, which include small molecules, act on specific molecular targets that are altered in tumour cells, mainly in cancers such as breast, lung, colorectal, lymphoma and leukaemia. With the recent exponential progress in drug development, programmed cell death, which includes apoptosis and autophagy, has become a promising therapeutic target. The research in identifying effective small molecules that target compensatory mechanisms in tumour cells alleviates the emergence of drug resistance. Due to the heterogenous nature of breast cancer, various attempts were made to overcome chemoresistance. Amongst breast cancers, triple negative breast cancer (TNBC) is of particular interest due to its heterogeneous nature in response to chemotherapy. TNBC represents approximately 15% of all breast tumours, however, and still has a poor prognosis. Unlike other breast tumours, signature targets lack for TNBCs, causing high morbidity and mortality. This review highlights several small molecules with promising preclinical data that target autophagy and apoptosis to induce cell death in TNBC cells.
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Kok, Marleen, Myriam Chalabi, and John Haanen. "How I treat MSI cancers with advanced disease." ESMO Open 4, Suppl 2 (May 2019): e000511. http://dx.doi.org/10.1136/esmoopen-2019-000511.
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Mismatch repair deficiency (dMMR) results in microsatellite instability (MSI) and is strongly associated with responsiveness to programmed death-1 receptor (PD-1)-blocking antibodies. Probably the main driver for the observed high efficacy of immune checkpoint inhibitors in dMMR tumours is the remarkably high tumour mutational burden. MSI can be detected using immunohistochemistry and/or PCR. In addition, next-generation sequencing is becoming increasingly available to clinical laboratories as a cost-effective and scalable method to evaluate multiple genetic aberrations including MSI. Efficacy of PD-1-blockade in MSI tumours is similar for patients with colorectal cancer (CRC; objective response rate (ORR) 36%) or a different cancer type (ORR 46% across 14 other cancer types). Based on these results, PD-1-blocking antibody pembrolizumab was the first tumour-agnostic treatment to be granted Food and Drug Administration approval based on the presence of MSI as a biomarker. Currently, there is no approved PD-1-blocking antibody for MSI cancers in Europe. Here, we present our experience with the screening for MSI and the treatment of patients with advanced disease of MSI CRC and non-CRC with immunotherapy.
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Kafita, Doris, Victor Daka, Panji Nkhoma, Mildred Zulu, Ephraim Zulu, Rabecca Tembo, Zifa Ngwira, Florence Mwaba, Musalula Sinkala, and Sody Munsaka. "High ELF4 expression in human cancers is associated with worse disease outcomes and increased resistance to anticancer drugs." PLOS ONE 16, no. 4 (April 9, 2021): e0248984. http://dx.doi.org/10.1371/journal.pone.0248984.
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The malignant phenotype of tumour cells is fuelled by changes in the expression of various transcription factors, including some of the well-studied proteins such as p53 and Myc. Despite significant progress made, little is known about several other transcription factors, including ELF4, and how they help shape the oncogenic processes in cancer cells. To this end, we performed a bioinformatics analysis to facilitate a detailed understanding of how the expression variations of ELF4 in human cancers are related to disease outcomes and the cancer cell drug responses. Here, using ELF4 mRNA expression data of 9,350 samples from the Cancer Genome Atlas pan-cancer project, we identify two groups of patient’s tumours: those that expressed high ELF4 transcripts and those that expressed low ELF4 transcripts across 32 different human cancers. We uncover that patients segregated into these two groups are associated with different clinical outcomes. Further, we find that tumours that express high ELF4 mRNA levels tend to be of a higher-grade, afflict a significantly older patient population and have a significantly higher mutation burden. By analysing dose-response profiles to 397 anti-cancer drugs of 612 well-characterised human cancer cell lines, we discover that cell lines that expressed high ELF4 mRNA transcript are significantly less responsive to 129 anti-cancer drugs, and only significantly more response to three drugs: dasatinib, WH-4-023, and Ponatinib, all of which remarkably target the proto-oncogene tyrosine-protein kinase SRC and tyrosine-protein kinase ABL1. Collectively our analyses have shown that, across the 32 different human cancers, the patients afflicted with tumours that overexpress ELF4 tended to have a more aggressive disease that is also is more likely more refractory to most anti-cancer drugs, a finding upon which we could devise novel categorisation of patient tumours, treatment, and prognostic strategies.
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Schouten, L. J., J. M. de Rijke, J. A. M. Huveneers, and A. L. M. Verbeek. "Rising incidence of breast cancer after completion of the first prevalent round of the breast cancer screening programme." Journal of Medical Screening 9, no. 3 (September 1, 2002): 120–24. http://dx.doi.org/10.1136/jms.9.3.120.
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OBJECTIVES: After completion of the prevalent screening round of the breast cancer screening programme in Limburg, The Netherlands, incidences started rising once again. This increase was contrary to expectations, which had predicted a slightly higher, but stable, incidence after the first screening round. The trends in incidence were studied to find explanations for the observed rise in incidence. SETTING: Breast cancer screening programme in mid-Limburg and southern Limburg, the Netherlands. METHODS: The data files of the breast cancer screening programme and the Maastricht cancer registry were linked to evaluate the effect of breast cancer screening. Only the first primary breast tumour was included in the evaluation. RESULTS: The second peak of incidence after the prevalent screening round was 45% higher than the incidences before the start of the screening. Also, the decrease in incidence of large and node positive tumours was interrupted. Compared with national detection rates, the number of screen detected cancers was lower before 1995 and higher after that year. After 1997, incidence decreased again of all breast cancers, but also of large and node positive tumours. The incidence of node positive tumours showed large fluctuations, probably due to the introduction of the sentinel node procedure and immunohistochemistry. In 1999, incidence of large tumours and node positive tumours was 18% and 28%, respectively, lower than before the start of the screening. CONCLUSIONS: An increase in the background incidences and improved detection in the screening programme most likely explain this trend. The improved detection after 1995, and the lower than desirable decrease in large tumours, indicate that the screening performance was not optimal before 1996. The incidence of node positive tumours cannot be used any more as an indicator of the success of the screening programme because of detection bias.
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Joshi, Amit, Vijai Simha, Kumar Prabhash, Vanita Noronha, Santosh Menon, Vedang Murthy, Ganesh Bakshi, et al. "Clinical presentation and outcomes of patients with testicular tumors in cryptorchid testis." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 428. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.428.
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428 Background: Undescended testis which occurs in 2-4% of all boys confers a natural risk for development of testicular cancer. Cryptorchidism accounts for 10% of all testicular germ cell tumours. The presentation, natural history and outcomes of testicular tumours occurring in cryptorchid testis has not been described in literature so far. Methods: Case records of patients enlisted in the prospectively maintained ‘ testicular cancer database’ at our tertiary cancer care hospital were retrospectively reviewed. Any patient who presented with testicular germ cell tumour with the testis being absent in the scrotum was considered as ‘undescended testis’. Results: From our database of 490 patients with testicular tumours presenting from the year 2014 -2018, 42 patients had testicular cancer in cryptorchid testis. The mean age was 32.9 years (Range:17-56). 24(57.14%) had seminoma and 18(42.86%) had non seminomatous tumors. Orchidopexy was done in 22(52.3%) patients at median age of 30 yrs (Range 2-33). 23 patients had prior undescended testis underwent high inguinal orchidectomy, 13 patients had testis located in pelvis and 6 patient had testis located in the upper abdomen. The average maximum size of tumours presenting with after orchidopexy was 7.34cm (4-10.5cm), in those presenting with pelvic tumours was 9.86cm (7-12.6cm) and in those with intraabdominal tumours was 14.3cm (9-20cm). The median follow-up for these patients was 36 months (3-64 months). There were 6 patients who relapsed after front line therapy whom 3 were salvaged with second line chemotherapy and 2 patients had residual disease at their last follow up. There was one death due to disseminated tumour with brain metastasis. The disease free survival for the whole cohort was 92.85%. Conclusions: The tumours developing in intraabdominal location of testis presented with a larger size and orchiopexy apart from its role in prevention of testicular cancer also helps in surveillance and early detection leading to effective treatment of these highly curable cancers. In the first of its series on testicular tumours in the cryptorchid, we show that they are also as curable as the germ cell tumours developing in the descended testis.
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Kapfhammer, A., T. Winkens, T. Lesser, A. Reissig, M. Steinert, and M. Freesmeyer. "Enhancing 18F-FDG-PET/CT analysis in lung cancer patients." Nuklearmedizin 54, no. 06 (2015): 247–54. http://dx.doi.org/10.3413/nukmed-0763-15-08.
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SummaryAim: To retrospectively evaluate the feasibility and value of CT-CT image fusion to assess the shift of peripheral lung cancers with/-out chest wall infiltration, comparing computed tomography acquisitions in shallow-breathing (SB-CT) and deep-inspiration breath-hold (DIBH-CT) in patients undergoing FDG-PET/ CT for lung cancer staging. Methods: Image fusion of SB-CT and DIBH-CT was performed with a multimodal workstation used for nuclear medicine fusion imaging. The distance of intrathoracic landmarks and the positional shift of tumours were measured using semitransparent overlay of both CT series. Statistical analyses were adjusted for confounders of tumour infiltration. Cutoff levels were calculated for prediction of no-/infiltration. Results: Lateral pleural recessus and diaphragm showed the largest respiratory excursions. Infiltrating lung cancers showed more limited respiratory shifts than non-infiltrating tumours. A large respiratory tumour-motility accurately predicted non-infiltration. However, the tumour shifts were limited and variable, limiting the accuracy of prediction. Conclusion: This pilot fusion study proved feasible and allowed a simple analysis of the respiratory shifts of peripheral lung tumours using CT-CT image fusion in a PET/CT setting. The calculated cutoffs were useful in predicting the exclusion of chest wall infiltration but did not accurately predict tumour infiltration. This method can provide additional qualitative information in patients with lung cancers with contact to the chest wall but unclear CT evidence of infiltration undergoing PET/CT without the need of additional investigations. Considering the small sample size investigated, further studies are necessary to verify the obtained results.
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Nguyen Van Long, Flora, Audrey Lardy-Cleaud, Susan Bray, Sylvie Chabaud, Thierry Dubois, Alexandra Diot, Lee Jordan, et al. "Druggable Nucleolin Identifies Breast Tumours Associated with Poor Prognosis That Exhibit Different Biological Processes." Cancers 10, no. 10 (October 22, 2018): 390. http://dx.doi.org/10.3390/cancers10100390.
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Background: Nucleolin (NCL) is a multifunctional protein with oncogenic properties. Anti-NCL drugs show strong cytotoxic effects, including in triple-negative breast cancer (TNBC) models, and are currently being evaluated in phase II clinical trials. However, few studies have investigated the clinical value of NCL and whether NCL stratified cancer patients. Here, we have investigated for the first time the association of NCL with clinical characteristics in breast cancers independently of the different subtypes. Methods: Using two independent series (n = 216; n = 661), we evaluated the prognostic value of NCL in non-metastatic breast cancers using univariate and/or multivariate Cox-regression analyses. Results: We reported that NCL mRNA expression levels are markers of poor survivals independently of tumour size and lymph node invasion status (n = 216). In addition, an association of NCL expression levels with poor survival was observed in TNBC (n = 40, overall survival (OS) p = 0.0287, disease-free survival (DFS) p = 0.0194). Transcriptomic analyses issued from The Cancer Genome Atlas (TCGA) database (n = 661) revealed that breast tumours expressing either low or high NCL mRNA expression levels exhibit different gene expression profiles. These data suggest that tumours expressing high NCL mRNA levels are different from those expressing low NCL mRNA levels. Conclusions: NCL is an independent marker of prognosis in breast cancers. We anticipated that anti-NCL is a promising therapeutic strategy that could rapidly be evaluated in high NCL-expressing tumours to improve breast cancer management.
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Losa, Gabriele A., and Riccardo Graber. "Apoptotic Cell Death and the Proliferative Capacity of Human Breast Cancers." Analytical Cellular Pathology 16, no. 1 (1998): 1–10. http://dx.doi.org/10.1155/1998/906749.
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The proliferative capacity (%S‐phase fraction), DNA ploidy, apoptosis frequency (DNA fragmentation) and steroid hormone receptor status (estrogen receptor, ER; progesterone receptor, PR) of 110 samples of human breast tissues with ductal invasive carcinoma were measured using biochemical and cytofluorimetric procedures. The DNA fragmentation had a left‐skewed frequency distribution and an overall median value of 1.64%, whilst the median %S‐phase fraction was 8%. The median %DNA fragmentation and %S‐phase fraction were 1.96% and 16% in hyperdiploid tumours (n=29; DNA index >1.1) higher than in hypodiploid tumors (n=10; DNA index 0.96), 0.38% and 7.5%. DNA diploid tumours (n=71) had median %DNA fragmentation and %S‐phase values of 1.68% and 6%, consistently lower than the median values of DNA hyperdiploid tumours. The ER content of hypodiploid tumours was about one half (median: 5.9 fmol/mg) the median values in hyperdiploid (10.6 fmol/mg) and diploid tumours (14.6 fmol/mg). This may correlate with the lowest frequency of apoptosis in hypodiploid tumours, at least when measured by biochemical methods which only detect cells in the late phases of apoptosis. In contrast, the median PR was lowest in hyperdiploid tumours than in hypo and/or diploid tumours. The %S‐phase/%fragmented DNA ratio for the hypodiploid tumours was 19.7, significantly higher than the ratios for hyperdiploid (8.2) and diploid tumours (3.6). These findings indicated that there is an imbalance between proliferative capacity and cell death or growth arrest in human breast tumours. This imbalance may well be linked to a loss of steroid hormone control.
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Naora, Honami. "The heterogeneity of epithelial ovarian cancers: reconciling old and new paradigms." Expert Reviews in Molecular Medicine 9, no. 13 (May 2007): 1–12. http://dx.doi.org/10.1017/s1462399407000324.
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Epithelial ovarian cancer comprises several subtypes of tumours that exhibit diverse histopathological features. The intriguing assumption by many epithelial ovarian cancers of specialised features of nonovarian tissue lineages has promoted considerable debate as to whether these tumours arise from the deceptively simple surface epithelium of the ovary. This review focuses on recent molecular and pathological studies of epithelial ovarian cancers that support and challenge their surface-epithelial derivation, and discusses the findings in the context of current views of the ‘cell-of-origin’ of solid tumours.
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Murray, G. I., M. E. Duncan, E. Arbuckle, W. T. Melvin, and J. E. Fothergill. "Matrix metalloproteinases and their inhibitors in gastric cancer." Gut 43, no. 6 (December 1, 1998): 791–97. http://dx.doi.org/10.1136/gut.43.6.791.
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Background—The matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) are strongly implicated in tumour invasion and metastasis.Aims—To investigate the presence of individual MMPs and TIMPs in gastric cancer.Methods—The presence of MMP-1, MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 was identified in a group of gastric cancers (n=74) by immunohistochemistry using monoclonal antibodies. These antibodies were effective on formalin fixed, paraffin wax embedded sections.Results—A large proportion (94%) of gastric cancers contained MMP-2; MMP-1 and MMP-9 were also detected in 73% and 70% of tumours respectively. MMP-3 was only present in 27% of tumours. MMP-1 and MMP-9 were found predominantly in intestinal type tumours. TIMP-1 and TIMP-2 were identified in 41% and 57% of tumours respectively. Immunoreactivity for individual MMPs or TIMPs was not identified in normal stomach.Conclusions—This study shows the presence of matrix metalloproteinases, particularly MMP-2, and TIMPs in stomach cancer. Antibodies which are effective in formalin fixed, paraffin wax embedded sections are useful for the identification of MMPs and TIMPs in diagnostic specimens.
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Sarker, Sudip, Allan Spigelman, Marjorie Walker, and Dulcie Coleman. "Nuclear DNA Content of Fine Needle Aspirates of Invasive Ductal Carcinomas of the Breast." Analytical Cellular Pathology 13, no. 1 (1997): 1–8. http://dx.doi.org/10.1155/1997/461402.
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Patients with aggressive breast cancers benefit from chemotherapy prior to surgery. If the biology of the breast cancers were better characterised pre‐operatively, more patients at risk could be offered chemotherapy. We have assessed nuclear DNA content of fine needle aspirates (FNA) of 103 invasive ductal breast cancers and compared this to tumour size, node status and histological grade. Median follow‐up was 18 months so no prognostic studies were made. Diploid and non‐diploid tumours were distributed equally in node negative and positive patients. However non‐diploidy status increased in line with known prognostic markers of tumour size and histological grade. This suggests that ploidy might contribute to the pre‐operative assessment of prognosis. We conclude that nuclear DNA of breast cancer FNAs may be of value in the pre‐operative biological assessment of breast cancer patients.
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Naik, Jay D., Jenny Seligmann, and Timothy J. Perren. "Mucinous tumours of the ovary." Journal of Clinical Pathology 65, no. 7 (October 19, 2011): 580–84. http://dx.doi.org/10.1136/jclinpath-2011-200320.
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Mucinous epithelial ovarian cancers (mEOC) are a relatively rare subset of ovarian cancers. Despite a relatively favourable outcome in early disease, the more frequent advanced presentation is associated with poorer response to platinum/taxane chemotherapies, and poorer survival, compared to serous ovarian cancers. We consider some of the fundamental clinico-pathological and molecular features, and existing clinical trial data regarding mEOC. Underlying molecular differences, between mEOC and serous cancers may contribute to the observed clinical differences, including an increased prevalence of K-RAS mutations in mEOC, more in keeping with gastrointestinal tumours. This observation contributes to the rationale for a trial (“mEOC”) investigating the use of “ovarian” versus “gastrointestinal” style chemotherapy. Looking to potential future approaches, we speculate upon the potential impact of emerging technologies on the future investigation and management of mEOC.
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Rakovich, George, and Lise Tremblay. "Tailored Therapy in Lung Cancer." Canadian Respiratory Journal 20, no. 5 (2013): 367–68. http://dx.doi.org/10.1155/2013/506383.
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Historically, all non-small cell lung cancers were essentially grouped together and considered to be a single disease. However, it is now recognized that non-small cell lung cancer actually comprises a genetically diverse group of tumours. This, in turn, affords a new opportunity for the development of effective treatments tailored to individual tumours and patients. Advances in molecular biology have made possible the development of drugs against specific molecular targets on cancer cells, most notably the tyrosine kinase inhibitors. The relevant literature and current practice guidelines are discussed. In addition, other related areas of active investigation, including tumour vaccines and pharmacogenetics, are briefly reviewed.
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Nepal, Bikash, Yogendra Singh, Prakash Sayami, and Gita Sayami. "An institutional review of tumour biology of breast cancer in young Nepalese women." Journal of Society of Surgeons of Nepal 18, no. 2 (November 10, 2017): 16–19. http://dx.doi.org/10.3126/jssn.v18i2.18569.
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Introduction: Breast cancers in less than 40 years of age group usually present with aggressive biology and has poor prognosis. The aim of this study was to see clinic-pathological and hormone receptors of breast cancers in young women and compare with less than 40 year age group.Methods: Prospective analysis of 97 breast cancer in patients less than 40 years out of total 373 patients (26%) over a period of 8 years (2007 Jan to 2014 Dec) was carried out at the Department of Surgery, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.Result: Among the young women diagnosed with breast cancer, the mean age was 34.5±6.2 years. Mean tumour size was larger in younger women (5±2.5 vs 4.5±2.4 cm). Locally advanced disease was higher in younger patients (55% vs 47%). Lymphatic and vascular invasions were higher (63% vs 35% and 40% vs 25%). Grade II and III tumours was higher (56% vs 25%). ER, PR and HER2 positivity was detected in 46.9%, 48.9% and 28.9% respectively. Significant lower ER or PR expression (34.5% vs 54%) was seen in younger women, p=.002.Triple negative tumours (ER -ve, PR -ve and HER2 -ve) was proportionately higher in younger patients (23% vs 13.7%, p=.043).Conclusion: Young Nepali women presents one quarter of all female breast cancers, more frequently locally advanced with aggressive tumour biology like ER/PR negative and triple negative breast cancers. Journal of Society of Surgeons of Nepal, 2015; 18 (2), page: 16-19
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Amato, Francesco, Colin Rae, Maria Giuseppina Prete, and Chiara Braconi. "Cholangiocarcinoma Disease Modelling Through Patients Derived Organoids." Cells 9, no. 4 (March 30, 2020): 832. http://dx.doi.org/10.3390/cells9040832.
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Cancer organoids are 3D phenotypic cultures that can be established from resected or biopsy tumour samples and can be grown as mini tumours in the dish. Flourishing evidence supports the feasibility of patient derived organoids (PDO) from a number of solid tumours. Evidence for cholangiocarcinoma (CCA) PDO is still sparse but growing. CCA PDO lines have been established from resected early stage disease, advanced cancers and highly chemorefractory tumours. Cancer PDO was shown to recapitulate the 3D morphology, genomic landscape and transcriptomic profile of the source counterpart. They proved to be a valued model for drug discovery and sensitivity testing, and they showed to mimic the drug response observed in vivo in the patients. However, PDO lack representation of the intratumour heterogeneity and the tumour-stroma interaction. The efficiency rate of CCA PDO within the three different subtypes, intrahepatic, perihilar and distal, is still to be explored. In this manuscript we will review evidence for CCA PDO highlighting advantages and limitations of this novel disease model.
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McGrath, Sophie, Nicola E. Annels, Thumuluru Kavitha Madhuri, Ben Haagsma, Emmanuel Douglas Larbi, Hardev S. Pandha, and Agnieszka Michael. "Engrailed protein: A cancer-specific marker in epithelial ovarian cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e15517-e15517. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15517.
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e15517 Background: Ovarian cancer is a common malignancy, accounting for 4% of all cancers and 5% of all cancer deaths in women in the Western world. Engrailed-2 (EN2) is a homeodomain–containing transcription factor that is essential during early development. It is dysregulated in a number of cancers and its presence in urine is diagnostic of prostate cancer. We have investigated its role as a cancer-specific marker in epithelial ovarian cancer (EOC). Methods: Ovarian tumours and normal tissue were collected from patients with epithelial ovarian cancer (EOC) and tested by semi-quantitative RT-PCR as well as by immunohistochemistry. EN2 expression relative to B-actin was calculated using the Livak comparative Ct method (2-DDCt). All slides were scored on a 0-3 scale based on intensity, by two independent assessors. Results: We examined 118 EOC specimens, of which 64 were tested by immunohistochemistry and 54 by RT-PCR. 89 (75.42%) were serous, 18 (15.25%) endometroid, 7 (5.93%) mucinous, and 4 (3.39%) clear cell tumours. Normal ovarian tissue was used as a control. 104 (88.14%) tumours expressed EN2 whilst 14 (11.86%) were negative. Of the EN2 positive tumours examined using immunohistochemistry, 28 (51.85%) strongly expressed the antigen (score of 2-3), whereas 26 (48.15%) were weakly positive (score of 1). Normal tissue did not express EN2 and this difference was statistically significant (p<0.05). There was no correlation with tumour type, grade and stage. EN2 expressing mucinous tumours showed improved overall survival (p=0.0253). There was no correlation for survival or PFS for other histological subtypes. Conclusions: EN2 is a cancer-specific marker in epithelial ovarian cancer. Further work is currently ongoing to evaluate its significance in ascites, blood and urine. We plan to further evaluate its role as a diagnostic biomarker by examining blood, urine, and ascites.
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Ní Leathlobhair, Máire, Kelsey Yetsko, Jessica A. Farrell, Carmelo Iaria, Gabriele Marino, David J. Duffy, and Elizabeth P. Murchison. "Genotype data not consistent with clonal transmission of sea turtle fibropapillomatosis or goldfish schwannoma." Wellcome Open Research 6 (September 2, 2021): 219. http://dx.doi.org/10.12688/wellcomeopenres.17073.1.
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Recent discoveries of transmissible cancers in multiple bivalve species suggest that direct transmission of cancer cells within species may be more common than previously thought, particularly in aquatic environments. Fibropapillomatosis occurs with high prevalence in green sea turtles (Chelonia mydas) and the geographic range of disease has increased since fibropapillomatosis was first reported in this species. Widespread incidence of schwannomas, benign tumours of Schwann cell origin, reported in aquarium-bred goldfish (Carassius auratus), suggest an infectious aetiology. We investigated the hypothesis that cancers in these species arise by clonal transmission of cancer cells. Through analysis of polymorphic microsatellite alleles, we demonstrate concordance of host and tumour genotypes in diseased animals. These results imply that the tumours examined arose from independent oncogenic transformation of host tissue and were not clonally transmitted. Further, failure to experimentally transmit goldfish schwannoma via water exposure or inoculation suggest that this disease is unlikely to have an infectious aetiology.
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Sherwood, Matthew, Robert Ewing, Carolini Kaid, Thiago Giove Mitsugi, and Keith Okamoto. "MOMC-1. Employing the Zika Virus to kill paediatric nervous system tumour cells." Neuro-Oncology Advances 3, Supplement_2 (July 1, 2021): ii3. http://dx.doi.org/10.1093/noajnl/vdab070.011.
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Abstract Malignant paediatric nervous system tumours, such as Medulloblastoma, Neuroblastoma and ATRT commonly harbour tumour cells with stem-like features which are highly tumorigenic and resistant to conventional cancer therapies. These tumours can exhibit high lethality and may result in severe sequelae, including cognitive and motor deficits that significantly affect patients’ quality of life. Oncolytic virotherapy is a novel therapy class that exploits viruses that preferentially infect and destroy tumour cells. These viruses present a unique advantage in targeting highly heterogeneous cancers, such as nervous system tumours, as they possess a secondary mechanism of action through which they induce a tumour-specific immune response. Clinical studies employing oncolytic virotherapy have in general reported low toxicity and minimal adverse effects, deeming oncolytic virotherapy as a potentially attractive and safer intervention against paediatric tumours. The Zika virus (ZIKV) is capable of infecting and destroying neural stem-like cancer cells from human embryonal Central Nervous System (CNS) tumours in vitro and in vivo. Infection of CNS tumour cells with ZIKV effectively inhibits tumour metastasis in mice and, in some cases, induces complete tumour remission. Neuroblastoma arises from immature nerve cells and multiple Neuroblastoma cell lines are susceptible to ZIKV infection and oncolysis. These initial findings have demonstrated the potential for a ZIKV-based virotherapy against paediatric nervous system tumours and warrants examination into the molecular mechanisms through which ZIKV executes its oncolytic ability. My research goal is to elucidate the mechanisms which are of paramount importance for ZIKV-induced oncolysis of brain tumour and Neuroblastoma cells. Utilising global expression omics profiling of ZIKV infection and mapping of viral protein-host protein interactions will identify these mechanisms both at the cellular pathway and molecular levels. These collectively will inform our understanding of how we can employ a future ZIKV-based virotherapy against paediatric nervous system tumours.
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Vinayak, Bhandari, Lydia Liu, Shadrielle Espirritu, Emilie Lalonde, Takafumi Yamaguchi, Lawrence Heisler, Julie Livingstone, et al. "The molecular hallmarks and clinical consequences of tumor hypoxia in prostate cancer." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 81. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.81.
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81 Background: Localised prostate cancers are classified into risk-groups using clinical measurements like grade and stage to inform treatment decisions. However, these groupings are imprecise: ~30% of intermediate-risk patients suffer relapse of their disease despite precision image-guided radiotherapy or radical prostatectomy. One reason for this variability in response to treatment is the underlying cellular and molecular heterogeneity of tumours. Prostate tumour cells exist within a microenvironment characterized by gradients of oxygen levels and prostate tumours with low levels of oxygen (hypoxia) have poor clinical outcomes. Methods: Hypoxia was measured using multiple mRNA-based signatures. We examined 548 patients with localised prostate cancer and statistically assessed the association of hypoxia with copy-number alterations (CNAs), single-nucleotide variants (SNVs), genomic rearrangements, focal genomic events ( i.e. kataegis, chromothripsis), telomere length, clinical indices ( i.e. grade, stage) and subclonal architecture. Results: Elevated hypoxia was associated with allelic loss of PTEN, higher rates of chromothripsis and intraductal and cribriform carcinoma (IDC-CA). To translate these findings into a biomarker for prostate cancer precision medicine, we integrated tumour microenvironmental data with genomic and pathological information to stratify patients into distinct prognostic groups. Patients with localized prostate cancer that have polyclonal tumours with elevated hypoxia, allelic loss of PTEN and IDC-CA were at the highest risk of rapid biochemical failure (P = 3.48 x10-3, Logrank test) and metastasis (P = 4.61 x 10-3, Logrank test), even after controlling for T-category, Gleason score and pre-treatment PSA. Conclusions: These data suggest that the aggressiveness of prostate cancers is driven by the interplay of the tumour microenvironment, tumour evolutionary trajectories and its genomic mutational profile.
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Kissová, Viktória, Zuzana Ševčíková, Viera Revajová, Róbert Herich, and Mikuláš Levkut. "Mast cells and eosinophils in rat mammary gland tumours induced by N-Nitroso-N-methylurea." Bulletin of the Veterinary Institute in Pulawy 59, no. 3 (September 1, 2015): 411–16. http://dx.doi.org/10.1515/bvip-2015-0060.
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Abstract The aim of the study was to evaluate the distribution and number of mast cells and eosinophils in rat mammary gland tumours induced by N-Nitroso-N-methylurea. The highest density of mast cells was found in cystic papillary adenocarcinomas of grade II. Eosinophils were detected only in the cystic papillary adenocarcinoma of grades I and II, in non-invasive cribriform adenocarcinoma and comedo-type carcinoma. Mast cell populations were observed perivascularly in the tumour stroma, in the host tumour interface, as well as in necrotic areas of neoplasms. Mast cells were observed to be intact according to their morphological changes, collectively referred to as degranulation. The obtained results indicate that mast cells and eosinophils play an important role in tumour micro-environment formation. The increased density of these cells in experimentally-induced rat mammary gland tumours suggests a poor prognosis in these cancers. Our results also confirmed that rat mammary gland tumours are good models for the study of breast cancers.
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Radulescu, Liliana Maria, Dan Radulescu, Tudor-Eliade Ciuleanu, Dana Crisan, Elena Buzdugan, Dragos-Mihai Romitan, and Anca Dana Buzoianu. "Cardiotoxicity Associated with Chemotherapy Used in Gastrointestinal Tumours." Medicina 57, no. 8 (August 6, 2021): 806. http://dx.doi.org/10.3390/medicina57080806.
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Cardiotoxicity is a well-recognised side effect of cancer-related therapies with a great impact on outcomes and quality of life in the cancer survivor population. The pathogenesis of chemotherapy-induced cardiotoxicity in patients with gastrointestinal cancers involves various molecular mechanisms, and the combined use of various chemotherapies augments the risk of each drug used alone. In terms of cardiotoxicity diagnosis, novel biomarkers, such as troponins, brain natriuretic peptide (BNP), myeloperoxidases and miRNAs have been recently assessed. Echocardiography is a noninvasive imaging method of choice for the primary assessment of chemotherapy-treated patients to generally evaluate the cardiovascular impact of these drugs. Novel echocardiography techniques, like three-dimensional and stress echocardiography, will improve diagnosis efficacy. Cardiac magnetic resonance (CMR) can evaluate cardiac morphology, function and wall structure. Corroborated data have shown the importance of CMR in the early evaluation of patients with gastrointestinal cancers, treated with anticancer drugs, but further studies are required to improve risk stratification in these patients. In this article, we review some important aspects concerning the cardiotoxicity of antineoplastic drugs used in gastrointestinal cancers. We also discuss the mechanism of cardiotoxicity, the role of biomarkers and the imaging methods used in its detection.
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Brook, Naomi, Emily Brook, Crispin R. Dass, Arlene Chan, and Arun Dharmarajan. "Pigment Epithelium-Derived Factor and Sex Hormone-Responsive Cancers." Cancers 12, no. 11 (November 23, 2020): 3483. http://dx.doi.org/10.3390/cancers12113483.
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Oestrogens and androgens play important roles in normal and cancerous tissue and have been shown to negatively regulate pigment epithelium-derived factor (PEDF) expression in sex hormone-responsive tumours. PEDF suppresses tumour growth and its downregulation by oestrogen is implicated in tumorigenesis, metastasis, and progression. PEDF expression is reduced in cancerous tissue of the prostate, breast, ovary, and endometrium compared to their normal tissue counterparts, with a link between PEDF downregulation and sex hormone signalling observed in pre-clinical studies. PEDF reduces growth and metastasis of tumour cells by promoting apoptosis, inhibiting angiogenesis, increasing adhesion, and reducing migration. PEDF may also prevent treatment resistance in some cancers by downregulating oestrogen receptor signalling. By interacting with components of the tumour microenvironment, PEDF counteracts the proliferative and immunosuppressive effects of oestrogens, to ultimately reduce tumorigenesis and metastasis. In this review, we focus on sex hormone regulation of PEDF’s anti-tumour action in sex hormone-responsive tumours.
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Jovanovic, Ivan, Tamara Alempijevic, Tomica Milosavljevic, Dragan Popovic, Milos Bjelovic, Marjan Micev, and Predrag Pesko. "Clinicopathological characteristics of Barrett's carcinoma, cardia carcinoma type II and distal gastric carcinoma: Influence of observed parameters on the five-year postoperative survival of patients." Srpski arhiv za celokupno lekarstvo 137, no. 5-6 (2009): 249–54. http://dx.doi.org/10.2298/sarh0906249j.
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Introduction. In the past two decades, the increased frequency of distal esophageal adenocarcinoma, esophagogastric junction and proximal gastric adenocarcinoma has been observed. The vast majority of these tumours are diagnosed in advanced stages, when the prognosis is poorer than in other gastric cancers. Objective. The aim of our study was to analyze the demographic and clinicopathological characteristics of patients operated on for Barrett's, cardia and distal gastric adenocarcinomas, as well as to study the influence of manifestations of each cancerogenetic indication on the studied clinicopathological parameters and to analyze the 5-year survival rate of patients surgically treated for cardia adenocarcinoma in relation to the patients operated on for distal gastric adenocarcinoma. Methods. We analyzed gender and age, tumour type, depth of tumour invasion, involvement of blood and lymph vessels in 66 patients surgically treated at the Centre for Oesophageal Surgery of the Institute for Digestive Diseases of the Belgrade Clinical Centre. Results. Except for significant differences in the depth of tumour invasion during surgery, there were no other statistically significant differences between the studied groups of patients. In the patients operated on for Barrett's and cardia cancers, the tumours invaded more deeply the wall layers, i.e. they were significantly more invasive than the distal gastric tumour. The lymph node involvement was present in 87.5% of patients with Barrett's cancer, in 80% with cardia cancer and in 87% with distal gastric cancer. The 3-year survival rate of patients operated on for cardia cancer was 47.4% and the 5-year survival rate was 31.6%, while the 3-year survival rate of patients operated on for distal gastric cancer was 46.2% and the 5-year survival rate was 34.6%. These differences were not statistically significant (Wilcoxon 0,036; p=0,85). Singly, the patients' gender, cancer type and the degree of tumour differentiation had no influence on the length of patients' postsurgical survival rate. Conclusion. At the time of diagnosis cardia cancer and cancers developed at the location of the Barrett's oesophagus, developed significant deeper per continuitatem than gastric cancer. There were no other differences in regard to the analyzed clinicopathological parameters among the tumours of these three locations, and there was no difference between the 3-year and 5-year survival rate between the patients operated on for gastric cancer and cardia cancer. Each studied clinicopathological parameter had no influence on the illness course.
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Friedlander, Michael, Katrin Marie Sjoquist, Dirkje Willemien Sommeijer, Lisa Bailey, Julie Martyn, Kim Gillies, Linda R. Mileshkin, et al. "PARAGON: Phase II study of aromatase inhibitors in women with potentially hormone responsive recurrent/metastatic gynecologic neoplasms: ANZGOG 0903." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): TPS5614. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.tps5614.
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TPS5614 Background: Many gynaecological cancers of different pathological type express estrogen and/or progesterone hormone receptors (ER/PR). Reports of tumour response and clinical benefit with hormonal therapies show variable rates of activity. There is a need to prospectively study the role of aromatase inhibitors in women with potentially hormone responsive recurrent gynaecological cancers to establish response rates, clinical benefit, quality of life (QoL) and identify predictors of response. Methods: PARAGON is phase II Gynecologic Cancer InterGroup trial lead by the Australia New Zealand Gynaecological Oncology Group, Cancer Research UK and the Belgian Gynaecological Oncology Group. The study is designed to facilitate research in rare tumours. The protocol allows postmenopausal women with recurrent gynaecological cancers to enrol into one of 7 subgroups; epithelial ovarian cancer (EOC) with only rising CA125 after first line chemotherapy, platinum resistant/refractory EOC, low grade EOC, endometrial carcinomas, endometrial stromal sarcomas, miscellaneous sarcomas and granulosa cell tumours and other sex cord stromal tumours. ER/PR positivity must be confirmed by immunohistochemistry. Each subgroup will enrol 25-50 patients with defined stopping rules based on response and reviewed by independent data monitoring committee (IDMC). Eligible patients receive 1 mg anastrozole daily until disease progression or unacceptable toxicity. Primary objective: clinical benefit (partial or complete response or stable disease). Secondary objectives: progression free survival, response duration, QoL, toxicity. Blood and tumour samples are being collected for translational studies and confirmation of ER/PR positivity. Recruitment commenced in 2011 in Australia, New Zealand and the United Kingdom. One hundred and fourteen of 350 planned patients have been enrolled to January 2013. In November 2012 IDMC recommended continuing recruitment to the EOC with rising Ca125 only and resistant/refractory subgroups based on review of activity outcomes for the first 25 patients. The trial will open in Belgium in April 2013. ACTRN12610000796088 Clinical trial information: 12610000796088.
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Karim, MI, SM Ali, S. Akhter, SMJ Islam, MM Karim, and MR Alam. "A Study on Histomorphological Spectrum of Childhood Malignant Tumour: Evaluation of 60 Cases at Different Center in Dhaka City." Journal of Armed Forces Medical College, Bangladesh 9, no. 1 (April 28, 2014): 57–62. http://dx.doi.org/10.3329/jafmc.v9i1.18727.
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Introduction: About 2% of all malignant tumours occur in infancy and childhood. Malignancy is the second common cause of childhood death in developed world, accounting for 10 - 12.3% of all childhood deaths. Eighty eight percent of worlds children live in developing countries, where access to adequate care is limited. Incidence of childhood cancer is increasing in this region gradually. Objectives: The objective of this study was to find out the histomorphological pattern of childhood cancers in our country and assess the trends of malignancies in different age group. Methods: This prospective study was carried out from January 2008 to January 2012. During this period data was analyzed for the malignancies occurring in the age group 0-14 years. Data was categorized according to incidence of paediatric malignancies in different age groups, sex and types of tumours. All the children below 15 years with confirmed diagnosis of cancer by means of histopathological examinations were included in this study. Results: Total 3120 patients were diagnosed as having malignancies at Armed Forces Institute of Pathology (AFIP), Delta Hospital Ltd & Bangabandhu Sheikh Mujib Medical University (BSMMU) Dhaka, out of which 60 cases were paediatric malignant tumours. Overall incidence of paediatric tumour was 1.92%. Out of which 26 cases (43.33%) were female and 34 (56.66%) cases male. The male - female ratio was 1.3:1. Males were more affected than females. The peak incidence of paediatric tumors (37%) was found in children between the age group 10 to 14 yrs. The pattern of childhood tumours shows wide variation among the age groups. In this study, at 0-4 yrs age group small round cell tumours (Neuroblastoma, Retinoblastoma), 5-9 yrs germ cell tumour, 10-14 yrs bone tumour (Ewing sarcoma, Osteosarcoma) were the commonest tumour. Conclusion: We conclude that there are certain notable differences between tumours of our study and those reported from other parts of the world. In our study small round cell tumor is most frequent childhood tumour. DOI: http://dx.doi.org/10.3329/jafmc.v9i1.18727 Journal of Armed Forces Medical College Bangladesh Vol.9(1) 2013: 57-62