Relevant bibliographies by topics / Tumours; Cancers

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tumours; Cancers'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Tumours; Cancers"

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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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Dissertations / Theses on the topic "Tumours; Cancers"

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Fawcett, Jonathan. "Molecular aspects of angiogenesis and metastasis." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386753.

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Marcu, Loredana Gabriela. "Deterministic modelling of kinetics and radiobiology of radiation-cisplatin interaction in the treatment of head and neck cancers." Title page, contents and abstract only, 2004. http://hdl.handle.net/2440/37961.

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One of the main objectives of combining radiation treatment and chemotherapy is to obtain a therapeutic gain by an improved tumour control with less or no enhancement of normal tissue toxicity. The optimal schedule for the combined treatment of cisplatin-radiation is still under investigation. Neither the optimal time interval, nor the most adequate sequence of administration of cisplatin and radiation are known. The results of the trials are also inconclusive. Some trials showed a supra-additive effect from the administration of cisplatin before radiotherapy, others, on contrary, from the injection of drug after radiotherapy. The present work encompasses the major challenges brought by the combined modality treatment: cisplatin-radiotherapy. The major goal of this work was to investigate the optimal treatment sequencing between cisplatin and radiotherapy and also the optimal schedule for head and neck carcinomas. Therefore, a computer-based tumour model with literature-given biological parameters has been developed which has allowed the simulation of treatment with radiation and chemotherapy. Radiotherapy has been simulated on the virtual tumour and the effects of radiotherapy on tumour regression and regrowth have been analyzed. Also, the mechanisms of cisplatin's action on tumour have been implemented, and the phenomena of drug resistance and tumour repopulation during chemotherapy studied. Finally, the combined modality treatment has been simulated, and the effect of drug-radiation interaction on tumour behaviour evaluated. The current investigation has shown that cisplatin administered immediately before radiation gives similar tumour control to the post-radiation sequencing of the drug. Furthermore, the killing effect of the combined modality treatment on tumour increases with the increase in cell recruitment. The individual cell kill produced by cisplatin and radiation leads to an additive-only tumour response when the treatments are given concurrently, and for a synergistic effect cisplatin must potentiate the effect of radiation. The final conclusion, by which cisplatin administered on a daily basis leads to a better tumour control than cisplatin administered weekly, is in accordance with the latest trial results on head and neck cancers. Therefore, treatment regimens that correlate better with the pharmacokinetics and the radiobiological properties of the therapeutic agents result in better outcomes.
Thesis (Ph.D.)--School of Chemistry and Physics, 2004.
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Pitter, Mark C. "Imaging through and analysis of multiply scattering media." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342072.

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Arora, Ramandeep. "A study of the aetiology and epidemiology of cancers in teenagers and young adults." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/a-study-of-the-aetiology-and-epidemiology-of-cancers-in-teenagers-and-young-adults(effc3dd6-6655-47cd-af95-6eb26cb055c8).html.

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Introduction: Little is known about the aetiology of cancer in teenagers and young adults (TYA) aged 15-24 years, although in England, cancer is the most common cause of disease-related mortality in this age group. The most common cancers at this age are lymphomas, central nervous system (CNS) tumours and germ cell tumours (GCT). The commonest carcinomas seen at older ages including lung, breast, large bowel and prostate account for only 3-4% of TYA cancers. In this thesis I describe the incidence patterns of selected cancers in TYA and the variation seen with geography, time and in population subgroups. The focus is on CNS tumours, GCT and bone tumours as they either peak in incidence in TYA and/or contribute disproportionately to cancer related mortality in TYA. This will allow formulation of hypotheses regarding aetiology of cancer in this age group which can then be tested by further research. Methods: For the majority of the analysis, anonymised national cancer registration data from England on individual patients of all ages with newly diagnosed cancer between 1979 and 2003 were used. To contrast the incidence patterns in England with that of India, data from five Indian urban population based cancer registries were used for part of the analysis. Age, sex, site and histology specific incidence rates were calculated and expressed per million person years. All rates, where appropriate, were adjusted to the world standard population using direct methods. To explore the link of growth with development of osteosarcoma and Ewing sarcoma, a random-effects meta-analysis was undertaken on studies which investigated an association of these tumours with height at diagnosis. Results: The incidence of cancer in TYA overall in England exceeded that of India. This was also true for most individual sites including epithelial cancers of lung, colon/rectum, breast, ovary and cervix, and non-epithelial cancers including melanoma, Hodgkin lymphoma and testicular cancer. Notable exceptions to this pattern were cancers of the mouth, gall bladder and stomach (females only) where incidence was higher in India. In England, CNS tumours in TYA were a composite of pilocytic astrocytomas and embryonal tumours (representing tail end of childhood CNS tumours), pituitary tumours, nerve sheath tumours, high grade astrocytomas and meningiomas (representing early-onset of CNS tumours that peak in incidence in the 6th and 7th decade of life), and of CNS GCTs, pleomorphic xanthoastrocytomas and neurocytomas which show a peak incidence in TYA. Irrespective of site or histology, GCT in England showed a peak in incidence between ages of 10 to 39 years which was more marked in males. This however varied by site and the peak incidence was seen at 10 to 14 years in the CNS, 15 to 19 years in ovary, 25 to 29 in mediastinum & thorax and abdomen & pelvis, and 30 to 34 years in testicular tumours. Osteosarcoma and Ewing sarcoma were the predominant bone tumours in TYA in England and showed a distinct peak of incidence at 10 to 14 years age in females and a larger peak at 15 to 19 years age in males. The peak incidence of osteosarcoma of long bones of the lower limb was six times more than that at any other site while the peak incidence of Ewing sarcomas located in the bones of the central axis exceeded those in long bones of the lower limb. The average height of patients with osteosarcoma at diagnosis was found to be significantly above the average height of the reference population, at the 95% level. The association of greater height at diagnosis with Ewing sarcoma was also significant at the 95% level but much weaker. Conclusion: In this thesis I have explored the epidemiology of cancer in TYA using some of the established methodologies which have previously been used in advancing our knowledge of childhood and older adult cancers. These studies provide some clues to aetiology. Variation in environmental exposures and lifestyle factors between England and India can explain the majority of the differences in incidence patterns observed. Genetic predisposition to cancer along with carcinogen exposure could lead to early onset of some cancers generally seen in older adults. Regardless of site, the similarity in age-incidence patterns of GCT, suggests a common initiation of these tumours in embryonic/foetal life with variable rates of tumour progression as a result of local factors or events during postnatal and pubertal period. The incidence patterns of osteosarcoma along with the strong and consistent association with a greater height at diagnosis indicate that bone growth is important in the development of this tumour while different biological pathways which may be unrelated to growth could also be relevant for Ewing sarcoma.
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McConechy, Melissa. "PPP2R1A mutations in gynaecologic cancers: functional characterization and use in the genomic classification of tumours." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52829.

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Endometrial carcinoma is the most common gynaecological cancer in developed countries. The current endometrial pathologic classification system lacks reproducibility, which has hampered the development of new treatments for these cancers. The PP2A phosphatase complexes are responsible for regulating many cellular pathways, and may play a role in the deregulation of endometrial cancer-associated pathways. In this thesis, the role of PPP2R1A mutations in the subtype-specific classification of gynaecological tumours was investigated. Additionally, mutational profiles will be used to improve the classification of the subtypes of endometrial carcinomas. Lastly, the functional effect of mutant PPP2R1A on PP2A-subunit protein interactions will be determined, in the context of endometrial cancer cell lines. Next-generation and Sanger sequencing was used to determine the presence of mutations in endometrial and ovarian carcinomas. PPP2R1A isogenic endometrial-specific cell lines were generated using somatic cell gene knockout by homologous recombination. Co-immunoprecipitation and mass spectrometry was used to determine effects of the PPP2R1A W257L mutation on its ability to interact with PP2A subunits. Subtype-specific somatic PPP2R1A mutations were identified in endometrial serous carcinomas. Low-grade endometrial endometrioid carcinomas were defined by mutations in the genes: ARID1A, PTEN, PIK3CA, CTNNB1, and KRAS, whereas high-grade endometrioid also harbor TP53 mutations. Endometrial serous carcinomas harbor mutations in PPP2R1A, FBXW7, PIK3CA and TP53. Consequently, the molecular profiles proved useful in assisting classification of tumours with overlapping morphological features that cause irreproducibility in diagnoses. Proteomic analysis of isogenic cell lines determined that the PPP2R1A W257L mutation disrupts interaction with PPP2R5C and PPP2R5D subunits. In addition, PPP2R1A mutated protein caused an increased interaction with the endogenous PP2A inhibitor SET/I2PP2A. The integration of mutational profiles and other genomic features will be used to improve clinical and pathological classification in endometrial tumours that are difficult to diagnose. PPP2R1A mutations are likely playing a role in the transformation of gynaecological carcinoma, by disrupting PP2A subunit interactions with tumour suppressor functions. Increased interaction of mutant PPP2R1A with SET/I2PP2A adds another layer of complexity to the tumour suppressive role of PP2A. In the future, targeting the PP2A complex with novel therapeutics could provide an alternative method for treating gyneacological cancers with poor outcomes.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Kaewkangsadan, Viriya. "Evaluation of immune cell infiltrates and expression of cytokines/biological molecules in the microenvironment of tumours and tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy : crucial contribution to immune-mediated tumour cell death." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/34155/.

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Background: Neoadjuvant chemotherapy (NAC) is being used as first line treatment in women with large and locally advanced breast cancers (LLABCs). However, the response to NAC is difficult to predict. Growing evidence suggests that these patients are immunosuppressed and that circulating immunosuppressive regulatory cells and humoral factors affect the response to NAC. We explored the possible role of the in situ tumour immune milieu in inducing and affecting the responses to NAC, and the contribution of concomitant systemic circulating regulatory cells. Methods: Paraffin-embedded breast cancers and ipsilateral axillary lymph nodes (ALNs) from pre- and post-NAC samples of a cohort of 33 women with LLABCs, 16 of whom had their blood regulatory cells previously investigated. Various immune cell infiltrations and expression of cytokines/biological molecules in the specimens were studied using appropriate monoclonal antibodies and immunohistochemistry. Statistical analysis was carried out using non-parametric tests with SPSS version 21. Results: High levels of pre-NAC tumour-infiltrating lymphocytes (TILs) (p < 0.001) and subsets of CD4⁺T cells (intratumoural, p=0.023; peritumoural, p=0.001), CD8+T cells (intratumoural, p=0.008; peritumoural, p=0.002) and CD56⁺NK cells (intratumoural, p=0.001; peritumoural, p < 0.001) were significantly associated with a pathological complete response (pCR). High levels of CD163⁺macrophages were also significantly associated with a good pathological response (p=0.004) and pCR (p=0.008). There was a positive correlation between the CD8:FOXP3 ratio and grade of pathological response. In multivariate analyses, TILs and peritumoural CD56+NK cells were found to be independent predictive factors for pCR. There was a significantly high expression of IL-10 in post-NAC breast specimens with poor responses to NAC (p < 0.001). NAC significantly reduced infiltrating T regulatory cells (Tregs) (p=0.001) and PD1⁺T cells (p=0.005), as well as expression of IL-4 (p=0.016). There was no significant difference between the percentages (%) of immune cells present in ALNs with or without metastases but there was a T helper-2 cytokine polarisation in metastatic ALNs. Metastatic ALNs with a high % of CD8+T cells (p=0.048) and low % of FOXP3+Tregs (p=0.019) were significantly associated with an ALN pCR. There was a significantly positive correlation between circulating and intratumoural infiltrating Tregs following NAC (p=0.003). Conclusions: The tumour immune microenvironment is a key factor in achieving a good pathological response with NAC. Tumour and blood immune parameters may be clinically useful in identifying women with LLABCs likely to respond to NAC. Our findings also suggest that the beneficial effects of NAC are mediated via modulation of anticancer immunity, in particular by reduction of T regulatory cells and immunosuppressive humoral factors.
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Burns, Alice Sin Ying Wai. "The role of the p53 tumour suppressor pathway in central primitive neuroectodermal tumours." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300357.

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Morel, Daphné. "Identifying Synthetic Lethal and Selective Approaches to Target PBRM1-Deficiency in Clear Cell Renal Cell Carcinoma PBRM1 Deficiency in Cancer is Synthetic Lethal with DNA Repair Inhibitors Exploiting Epigenetic Vulnerabilities in Solid Tumors: Novel Therapeutic Opportunities in the Treatment of SWI/SNF-Defective Cancers Combining Epigenetic Drugs with other Therapies for Solid Tumours — Past Lessons and Future Promise Targeting Chromatin Defects in Selected Solid Tumors Based on Oncogene Addiction, Synthetic Lethality and Epigenetic Antagonism." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL017.

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L’inactivation de polybromo-1 (PBRM1) est un évènement fréquent dans de nombreux cancers. En particulier, les carcinomes rénaux à cellules claires présentent une déficience en PBRM1 dans 40 à 50% des cas. A ce jour, il n’existe pas d’approche de médecine précision connue capable de cibler spécifiquement les cellules tumorales déficientes en PBRM1.Pour identifier des cibles de létalité synthétique associées à la perte de PBRM1, nous avons (i) réalisé un criblage pharmacologique à haut débit évaluant la sensibilité à 167 molécules dans un modèle cellulaire isogénique pour PBRM1, et (ii) étudié l’impact transcriptomique et protéomique de la perte de PBRM1 dans ce même modèle.Nous avons ensuite caractérisé les mécanismes sous-jacents à la relation de létalité synthétique découverte.Nous avons identifié et validé une relation de létalité synthétique existante entre la perte tumorale de PBRM1 et l’inhibition pharmacologique de PARP, pouvant être potentialisée par l’ajout d’un inhibiteur d’ATR.Cette relation de létalité synthétique était caractérisée par un niveau basal élevé de stress cellulaire chez les cellules déficientes en PBRM1, associant anomalies mitotiques, stress transcriptionnel et stress réplicatif – tous ces phénomènes étant exacerbés à l’ajout d’inhibiteurs de PARP, jusqu’à dépasser les capacités cellulaires à maintenir un phénotype compatible avec la survie.Ces observations apportent la preuve de concept préclinique que les inhibiteurs de PARP sont de potentiels candidats thérapeutiques pour cibler spécifiquement les tumeurs déficientes en PBRM1
Polybromo-1 (PBRM1) inactivation occurs in multiple malignancies and is of particular importance in clear cell renal cell carcinomas (ccRCC), as it drives 40 to 50% of cases. Currently, no precision-medicine approach uses PBRM1 deficiency to specifically target tumour cells. To uncover novel synthetic lethal approaches to treat PBRM1-defective cancers, we performed (i) a high-throughput pharmacological screening, evaluating the sensitivity to 167 small molecules in a PBRM1-isogenic cellular model, and the (ii) systematic mapping of the whole transcriptomic and proteomic profiles associated with PBRM1 loss-of-function within this model. We further investigated the mechanism underlying this synthetic lethal relationship.We identified and validated synthetic lethal effects between PBRM1 loss and both PARP and ATR inhibition. Combinatorial use of PARP with ATR inhibitors exerted additive cytotoxic effects in PBRM1-defective tumor cells. These synthetic lethal relationships were characterized by a pre-existing replication stress in PBRM1-deficient cells associated with mitosis and DNA damage repair abnormalities, which were exacerbated upon PARP inhibition selectively in PBRM1-defective cells.These data provide the preclinical basis for evaluating PARP inhibitors as a monotherapy or in combination in patients with PBRM1-deficient ccRCC
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Chambers, George. "A study of the production of the selected cytokines interleukin 1, interleukin 6, and tumour necrosis factor by certain tumours and tumour cell lines." Thesis, University of Glasgow, 1996. http://theses.gla.ac.uk/4041/.

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An investigation was carried out to examine the production of the inflammatory cytokines IL1, IL1, IL6, TNF, and TNF in two tumour cell lines, the MCF-7 breast cell line and the T-24 bladder cell line, and in samples of breast, bladder, lung and ovarian tumours. Two methods were used to investigate cytokine production. These were the polymerase chain reaction method (PCR) to examine cytokine mRNA production and immuno-staining of frozen or paraffin-embedded tissue sections to demonstrate the presence of the cytokine polypeptide directly. In the PCR experiments, the most frequently found cytokine was IL6, followed by IL1. Only a few tumours of any type displayed TNF, and even fewer produced TNF. In the immunostaining experiments performed on frozen sections, IL1 and IL6 proteins were detected in sections of tumours which gave positive results with PCR. Cell phenotyping indicated that the IL1 and IL6 were probably being synthesised by the tumour cells themselves although there was lymphocyte infiltration in every section examined. In the immuno-histology study performed on the paraffin-embedded sections, a new collection of tumours was used. These tumours were not subjected to parallel PCR due to size of tumour samples being too small. The results obtained from these experiments conflicted with the results observed in the PCR study. IL1 was detected in all of the breast tumours used for immuno-histology but in none of the breast tumours in the PCR experiments. While the conflict could not definately be resolved, it was thought that the results of the immuno-histology experiments were more accurate as they detected expression of cytokine protein on a cellular scale. The immuno-histology experiments demonstrated that some tumour cells produced IL1 in breast and bladder carcinomas, and some produced IL6 in breast and lung carcinomas.
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Bundell, Christine Stephanie. "Immune recognition and editing of tumours expressing multiple antigenic epitopes in two murine models." University of Western Australia. School of Medicine and Pharmacology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0067.

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[Truncated abstract] The design of effective immunotherapies, using tumour antigens to stimulate a functional effector cytotoxic T cell (CTL) response in a tumour bearing host, requires an understanding of the 'real time' in vivo relationship between the host immune system and antigens expressed by the developing tumour. However, effector function of endogenous anti-tumour CTLs generated during tumour progression has largely been assessed by indirect ex vivo assays and often focused on a single antigen. Therefore, studies in this thesis evaluated the endogenous in vivo CTL response to multiple tumour antigenic epitopes in murine tumour models using Lewis lung carcinoma cells transfected with ovalbumin (an antigen that contains several intra-molecular MHC class I epitopes with a defined hierarchy) or a polyepitope (that contains a string of immunodominant MHC class I epitopes). Potent effector CTLs were generated to multiple dominant tumour antigenic epioptes early in tumour progression. However, in general, these CTL effectors only transiently retarded tumour growth, and at the later time points of tumour growth they were no longer generated in tumour draining lymph nodes. This coincided with diminished tumour antigen presentation in the same nodes which was found to be due to antigen loss. In both models antigen loss was the result of two processes; immuno-editing of the tumour by the host immune response and genetic instability resulting in antigen loss variants that could evade immune surveillance. A third model was generated that maintained low level tumour antigen expression throughout tumour progression. ... The impact of pre-existing endogenous dominant-epitope specific CTLs on tumour expressing the same epitope was also assessed, and resulted in a reduced tumour incidence and a CTL response restricted to a single antigen of the same MHC allele. Finally, the effects of two different immunotherapy regimens were examined. Intratumoural IL-2 treatment enhanced pre-existing CTL responses to the dominant epitopes leading to tumour regression. In addition, use of a multiple peptide vaccination regimen that avoided T cells competing for peptide-MHC complexes on APC was far more likely to be effective than one that did not. These results demonstrate that immunotherapies targeting tumours that express several dominant neo antigenic epitopes can be effective. The caveat for this approach is that it will only be effective in tumours that have generated an endogenous CTL response and must be used before antigen loss variants emerge.
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Books on the topic "Tumours; Cancers"

1

Liu, Dongyou. Tumors and Cancers. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/b22275.

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Liu, Dongyou. Tumors and Cancers. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120522.

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Liu, Dongyou. Tumors and Cancers. Boca Raton : Taylor & Francis, a CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc, 2018. | Series: Pocket guides to biomedical sciences: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120546.

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Liu, Dongyou. Tumors and Cancers. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120553.

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1939-, Jones E. L., and Young Jennifer A, eds. Tumours: Structure & diagnosis. London, England: Harvey Miller Publishers, 1991.

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Janes-Hodder, Honna. Childhood cancer: A parent's guide to solid tumor cancers. 2nd ed. Beijing: O'Reilly, 2002.

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M.J. van de Vijver. WHO Classification of Tumours of the Breast: IARC WHO Classification of Tumours, No 4. LYON, FRANCE: International Agency for Research on Cancer, 2012.

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Del Regato, Juan A., 1909-, Spjut Harlan J. 1922-, and Cox James D. 1938-, eds. Ackerman and del Regato's Cancer: Diagnosis, treatment, and prognosis. 6th ed. St. Louis: Mosby, 1985.

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J, James Steven L., Sundaram Murali, and SpringerLink (Online service), eds. Imaging of Bone Tumors and Tumor-Like Lesions: Techniques and Applications. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009.

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M, Lukeman John, and Ordóñz Nelson G, eds. Tumors of the lung. Philadelphia: W.B. Saunders, 1991.

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Book chapters on the topic "Tumours; Cancers"

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Pape, James, and Charles Imber. "Benign Liver Tumours." In Liver Cancers, 295–307. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92216-4_22.

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Touboul, E., and F. Huguet. "Tracheal Cancers." In Management of Rare Adult Tumours, 461–67. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-92246-6_52.

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Bahadur, Sudhir. "Residual/Recurrent Tumours." In Management of Oral Cancers, 149–57. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6499-4_11.

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Durdux, C., and O. Mir. "Uncommon bladder cancers." In Management of Rare Adult Tumours, 225–33. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-92246-6_25.

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Gligorov, J., I. Ray-Coquard, P. Pautier, É. Pujade Lauraine, F. Selle, C. Lhommé, J. P. Lotz, P. Morice, and P. Duvillard. "Rare Ovarian Cancers." In Management of Rare Adult Tumours, 271–78. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-92246-6_30.

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Giannandrea, Fabrizio. "Malignant Tumours of the Male Reproductive System." In Occupational Cancers, 455–65. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30766-0_26.

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Mazabraud, André. "Metastases (secondary cancers of bone)." In Pathology of bone tumours, 381–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-95839-7_33.

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Alifrangis, Constantine, and Michael J. Seck. "Malignant Ovarian Germ Cell Tumours: An Overview of Management and Controversies." In Ovarian Cancers, 247–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32110-3_18.

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Reed, Nicholas. "Mucinous Tumours of the Uterine Corpus." In Rare and Uncommon Gynecological Cancers, 181–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13492-0_17.

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Bahadur, Sudhir. "Tumours of the Oral Cavity: Diagnosis, Assessment and Staging." In Management of Oral Cancers, 83–96. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6499-4_7.

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Conference papers on the topic "Tumours; Cancers"

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Satish, Pranav, Alex Freeman, Daniel Kelly, Alex Kirkham, Clement Orczyk, Benjamin Simpson, Francesco Giganti, Hayley Whitaker, Mark Emberton, and Joseph Norris. "Prostate cancer topography and tumour conspicuity on multiparametric magnetic resonance imaging: A systematic review and meta-analysis." In VIRTUAL ACADEMIC SURGERY CONFERENCE 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.04.001.2.

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Introduction The implications of tumour location on mpMRI conspicuity are not fully understood. Identifying topographical correlates that influence conspicuity may improve outcomes. Here, we present the first systematic review and meta-analysis describing the effect of tumour location on prostate cancer conspicuity on mpMRI. Methods Medline, PubMed, EMBASE and Cochrane databases were systematically searched and results were assessed as per the PRISMA statement. Differential tumour conspicuity on mpMRI was compared between cancers in the peripheral zone (PZ), transitional zone (TZ), base, apex, anterior and posterior. Meta-analysis was conducted to compare diagnostic odds ratios (DOR) of mpMRI detection for tumours in the PZ and TZ. PROSPERO registration: CRD42021228087. Results Thematic synthesis showed apical and basal tumours had reduced conspicuity compared to mid-gland tumours. Cancer in the TZ demonstrated increased conspicuity on T2-weighted imaging, whilst PZ cancers had higher conspicuity on diffusion-weighted and dynamic contrast enhancement imaging. mpMRI had better diagnostic accuracy for PZ lesions, albeit higher specificity for TZ lesions. Meta-analysis showed an increased DOR for PZ tumours (OR: 7.206 [95% CI: 4.991;10.403], compared to TZ (OR: 5.310 [95% CI: 3.082; 9.151]). However, the test for subgroup differences was not significant (p = 0.2743). Conclusions Cancer in the apex or base of the prostate may be less conspicuous than mid-gland tumours. Similarly, TZ cancer appears to have reduced conspicuity compared to PZ cancer, however, meta-analysis did not show a significant difference between DOR. Future larger studies with prospective datasets are required to clarify the relationship between tumour position and conspicuity.
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Pariyar, Jitendra, and Binuma Shrestha. "Clinical presentation and management of malignant germ cell ovarian tumours in BPKMCH." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685406.

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Background: Germ cell malignancies account for about 5% of all ovarian cancers. These tumours grow rapidly and often produce symptoms quicker than the slow growing epithelial tumour. Commonly seen in the first two decades of life germ cell malignancies are highly chemosensitive and are potentially curable with surgery and chemotherapy. This study is the first of its kind regarding the epidemiology, management and outcome of patients with malignant germ cell tumour in Nepal. Objective: To analyze the clinical presentation and management outcomes of malignant germ cell tumours managed in B.P. Koirala Memorial Cancer Hospital, Nepal. Methodology: Descriptive study conducted in B.P. Koirala Memorial Cancer Hospital, Nepal. Case records of malignant germ cell tumours attending the hospital from January 1999 to December 2009 were analyzed regarding their illness history, clinical examination, investigations, treatment, follow-up and outcomes measured. Observations: Total 65 cases of malignant germ cell tumours with age range from 2 to 58 years (mean 21.7 years) were received. 42% cases were Tibeto-Burmese; 30% were Indo-Aryans. There were 15 cases (23%) of dysgeminoma, 21 endodermal sinus tumor (32%), 16 Immature Cystic Teratoma (24.5%), 9 (14%) Mixed Germ Cell, 2 unclassified GCT (3.5%) and 2 malignant transformation in teratoma (3.5%). 33 (49.5%) patients had early stage disease, 37 (57%) underwent fertility preserving surgery. 4 cases (9%) due to disseminated disease, underwent neoadjuvant chemotherapy followed by debulking surgery. 51 cases (78.5%) received adjuvant chemotherapy (BEP or EP regimen). The overall survival was 70%. Conclusion: Early stage germ cell malignancies can be safely managed by fertility preserving surgery followed by, chemotherapy if indicated. For advanced diseases, neoadjuvant chemotherapy followed by surgery can be undertaken with curable intent.
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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685289.

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Methods: Matched samples of ascites and tumor tissue were taken from patients undergoing surgery for epithelial ovarian cancer. Tumor samples were formalin fixed and paraffin embedded (FFPE); ascites samples were used to generate primary cultures (PC). HR status was determined in PCs as previously described.[1] IC50 for the PARP inhibitor Rucaparib was estimated using SRB assays. DNA was extracted from the FFPE tissue. The following techniques were evaluated in PCs or paired FFPE samples: DR-GFP reporter assay, PARP activity assay, BRCA1 expression on immunohistochemistry, BRCA1 methylation status and BRCA1/2 mutation analysis. A next generation sequencing based assay was used to detect mutations and other genomic alterations in a large panel of cancer-associated genes, including BRCA1/2. Results: Paired samples were collected from 64 patients and characterized for HR function. 47/64 (76%) were high grade serous. 44% (28/64)) were HR defective (HRD) by Rad51 assay and correlated with Rucaparib sensitivity (PPV-92%, NPV-100%). Molecular analysis revealed that all mutations and other genomic alterations detected in ascites derived PCs were also found in matched FFPE tumor tissues. All tumors with serous histology contained p53 mutations, whilst the remaining tumors without p53 mutations were non-serous in histology. DR-GFP assay was unreliable in PC due to poor transfection. In a subset of 50 cancers there was reduced BRCA1 expression in the HRD vs. HRC tumours (34.8% vs. 22.7%, ns) whilst in a further subset of 30 cases there was no difference in endogenous or stimulated PARP activity between HRD and HRC tumours. Deleterious BRCA2 mutations were identified in 7 tumors, 6 of which were HRD. Only 1 deleterious BRCA1 mutation was detected but methylation of BRCA1 was identified in 13 of 64 (20%) tumors, 7 of which were HRD. Mutation of BRCA2 was mutually exclusive to methylation of BRCA1. HRD vs. HRC tumours showed BRCA1 methylation (25% vs. 17%) and BRCA1/2 mutation (21% vs. 0.3%). 14/28 (50%) HR defective tumors do not have BRCA1/2 mutations or BRCA1 methylation, suggesting other mechanisms can also result in a HR defective phenotype. 28/64 (43%) of samples demonstrated the HR defective phenotype. In all cases HR status correlated with sensitivity to Rucaparib. Conclusion: As expected, deleterious BRCA2 mutations conferred a HRD phenotype in cells but methylation of BRCA1 was not universally associated with HRD. This may be as a result of only partial silencing of the gene by methylation and further work is required to identify thresholds of methylation which may predict HR status. The use of BRCA1/2 mutation testing alone is unlikely to identify the majority of HR defective ovarian tumors. Assessment of functional status of HRD is the preferred option and further technologies should be developed to simplify the Rad51 assay.
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Iqbal, S. A., H. Shukla, V. Jain, S. Giri, R. Sekhon, and S. Rawal. "Synchronous primary ovarian sex cord tumor and endometrial cancer." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685384.

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Synchronous primary tumors of female genital tract are rare with a rate of about 0.7-1.8% of all gynaecological tumours. Most common primary tumours presenting as synchronous lesions are ovary and endometrium. However, sex cord stromal tumors are rare variety of primary ovarian tumor and synchronous with endometrium is even much rarer. These tumors are detected usually in younger, overweight, nulliparous and perimenopausal female. Synchronous primary tumors of endometrium and ovary have a better prognosis than the either of above alone because these are usually low grade and diagnosed at early stage. We present a report of four cases of synchronous endometrial and sex cord stromal tumors of ovary.
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Kamaruzaman, Hanin Farhana, Atikah Shaharudin, Sharifa Ezat Wan Puteh, Zafar Ahmed, and Junainah Sabirin. "BONE TARGETING AGENTS IN PREVENTION OF SKELETAL-RELATED EVENTS IN METASTATIC CANCERS OF SOLID TUMOURS: AN ECONOMIC EVALUATION." In International Conference on Public Health. The International Institute of Knowledge Management (TIIKM), 2019. http://dx.doi.org/10.17501/23246735.2019.5102.

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Focke, CM, T. Decker, and PJ van Diest. "Abstract P1-03-02: Intratumoral heterogeneity of Ki67 expression in early breast cancers exceeds variability between individual tumours." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p1-03-02.

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Manuchehrabadi, N., A. Attaluri, H. Cai, R. Edziah, E. Lalanne, C. Bieberich, R. Ma, A. M. Johnson, and L. Zhu. "Visualization and Quantification of Gold Nanorods Distribution in Prostatic Tumors Using MicroCT Imaging." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80317.

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One uncertainty in use of gold nanorods for laser photothermal therapy is the non-uniform spreading of gold nanorods in tissue after either systemic delivery or intratumoral injections. High concentration of gold nanorods in certain areas influences the resulted optical absorption of the laser and thermal damage to tumors. This also provides challenges in designing optimal heating protocols via modeling thermal transport in laser photothermal therapy. For successful cancer treatment, the tissue should be heated with minimum thermal dosage to induce tumor cell damage, while minimizing overheating in the surrounding healthy tissues. Thus, one of the main challenges for reliable cancer therapy is to precisely control loading and distribution of gold nanorods in the tumour tissue. The critical mass transport processes are the distribution of gold nanorods after injection to the tumor and the redistribution of gold nanorods during laser treatment. Since tumors are opaque, nanostructure distribution in tissue is often studied either by theoretical modeling approaches1, or via dye enhanced imaging on superficial layers of tumors.2 It is important to find a technique which can directly visualize and analyze three-dimensional nanostructure distribution of tumors. Three-dimensional reconstructions of tumors with the ability to trace gold nanorod spreading have the potential for precise theoretical simulation of temperature fields. Previous studies showed that computer tomography (CT) scan is a promising technique to be utilized to characterize the distribution of intratumorally injected magnetic nanoparticles in tumors 3.
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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Clinico-pathological correlation of homologous recombination status in epithelial ovarian cancer: Surgeon’s perspective." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685292.

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Background: TCGA data using expensive multi-modality diagnostic platforms have shown that 50% epithelial ovarian cancers (EOCs) are estimated to be homologous recombination (HR) deficient (HRD). We developed a functional assay for HR using gamma H2AX-Rad51 immunofluoresence.[1] Methods: Primary cultures were developed in 50 consecutive EOCs from ascetic fluid and HR assay was performed. Results: 50% patients were HRD based on the functional assay and show improved ex-vivo chemosensitivity to PARP inhibitor (PARPi) (PPV = 92%, NPV = 100%). HRD patients showed improved platinum sensitivity (53.8% vs 16.7%), survival (12 month OS - 41.7% vs. 11.5%) and optimal cytoreduction (80% vs. 62%) rates compared to HR competent (HRC) tumours which are less responsive and represent an unmet clinical need. Conclusions: Personalised surgical and chemotherapeutic strategies may be developed for HR stratified EOCs. Primary surgery may be the preferred approach in HRC due to poor chemoresponse; surgical expertise/environment should be optimised to ensure optimal surgical outcome. Intra-operative hyperthermic treatment and selective HR inhibitors may improve subsequent chemoresponse in HRC and are currently being investigated.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Stigliano, Robert V., Fridon Shubitidze, and P. Jack Hoopes. "Magnetic Nanoparticle Hyperthermia Cancer Therapy Temperature Distribution Modeling and Validation." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93123.

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The use of magnetic nanoparticles (mNP’s) in hyperthermia therapy for the treatment of cancer has been receiving increasing interest in the past few decades. It is known that heating cancerous tissues to temperatures above physiologically normal levels will cause cytotoxicity. In mNP hyperthermia, mNP’s are either injected intravenously or directly into the tumor site. In many tumor types the nanoparticles are invaginated into the cancer cells and aggregated into endosomes. Local temperature increases are achievable by exposing tumors containing mNP’s to an alternating magnetic field (AMF). The proximity of the mNP’s has a strong influence on their ability to generate heat due to inter-particle magnetic interaction effects [1, 2]. Taking this effect into account is important when modeling the heating characteristics of mNP’s.
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Reports on the topic "Tumours; Cancers"

1

Andrews, Jack, and Jeffrey Karnes. Treating the primary tumour in oligometastatic prostate cancer. BJUI Knowledge, September 2020. http://dx.doi.org/10.18591/bjuik.0737.

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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403397.

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Shyam, E., and P. Reddy. Tumor Suppressors and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada412779.

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Tenniswood, Martin P. Apoptosis and Tumor Progressionin Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada443063.

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Tiwari, Raj. Tumor Associated Antigenic Peptides in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada383084.

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Tyner, Angela L. Breast Tumor Kinase Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417996.

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Tiwari, Raj K. Tumor Associated Antigenic Peptides in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2002. http://dx.doi.org/10.21236/ada406458.

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Tenniswood, Martin P. Apoptosis and Tumor Progression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423481.

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Chin, Arnold I. Regulation of the Prostate Cancer Tumor Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580499.

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Tenniswood, Martin. Apoptosis and Tumor Progression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada467940.

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You might also be interested in the extended bibliographies on the topic 'Tumours; Cancers' for particular source types:
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