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Keln, A. A., S. S. Schmidt, A. V. Kupchin, and B. A. Berdichevsky. "Active monitoring of contrast-accumulating kidney tumours." Urology Herald 8, no. 4 (2020): 53–61. http://dx.doi.org/10.21886/2308-6424-2020-8-4-53-61.
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Introduction. The incidence of kidney cancer (KC) in the world is increasing and today is about 3%, but the death rate from this type of malignancy does not increase proportionally. According to research by many authors, more than half of the patients are over 65 years old at the time of diagnosis. Patients at this age have a high incidence of high comorbidity and risk of death from cardiovascular or other intercurrent pathology that exceeds the risk of death from KC. Recently, there has been a positive trend in the detection of the disease in the early stages up to 61.80%. Most of the primary detected kidney tumours are diagnosed randomly as asymptomatically small (less than 4 cm) tumours without signs of visceral metastasis. These tumours have a high degree of differentiation and rarely require surgical treatment in addition to their small size, and in the case of surgery, these pathomorphological results are benign. Due to the slow progredient growth of kidney formations and an asymptomatic course, the method of dynamic observation of kidney tumours is relevant in elderly patients and avoids unnecessary risks of surgical treatment of localized KC.Purpose of the study. To trace the growth rate of kidney tumours accumulating contrast agent using the method of dynamic observation. This study will allow us to differentially approach the choice of surgical treatment, which is optimal for elderly patients with low somatic status.Materials and methods. In the Multidisciplinary clinical medical centre «Medical City» (Tyumen) database all cases of radiographically verified space-occupying lesions of the kidneys that accumulate contrast were selected in the period from 2009 to 2019. We studied 50 people: 23 women (46%) and 27 men (54%), aged from 58 to 90 years. The study group included patients with kidney neoplasms of size < 7cm. Patients whose follow-up period was less than 12 months were excluded from the analysis. Regularly, every 3 to 6 months, patients underwent computed tomography to assess the growth dynamics. The size of the tumour, which was assumed to be its diameter in the largest dimension, was carefully studied. The growth rate of the tumour was calculated as the average change in diameter for 1 year during the entire observation period.Results. The average age of patients was 74.8 ± 7.4 years according to the results of the study. The age of patients at the time of diagnosis also had no prognostic significance for the rate of growth of kidney tumours (p > 0.05). The primary diagnosis was made in 32 patients (64%) using CT, in 18 (36%) using ultrasound. The average size of the tumou at the time of detection was 35.0 ± 6.9 mm. Percutaneous kidney biopsy was performed in 2 patients for morphological verification of the tumour type. Moderate-differentiated light-cell renal cell carcinoma pT1bN0M0 was detected in both patients according to the results of histological differentiation. The average linear growth rate of the tumour was 6.6 ± 2.4 mm / year. The size of the tumour at the time of diagnosis was not correlated with the growth rate (p > 0.05). There was no correlation between the rate of increase in the size of formations depending on their structure — solid (median 6 mm / year; average — 10 mm / year) or cystic-solid (median 7 mm / year; average 9 mm / year; p > 0.05). The absence of tumour growth dynamics during the entire observation period was detected in 22 (44%) people, including 10 (20%) men and 12 (24%) women. Visceral metastasis was diagnosed in 3 cases: to the liver, spleen, and the appearance of a second tumour on the contralateral kidney. Surgical treatment was performed in 4 patients (8%), in 2 (4%) cases, the indication for surgery was the progression of the tumour in the form of the appearance of visceral metastases. One patient had chromophobic KC pT1bN0M1, the other had renal cell carcinoma, a light-cell variant of pT1bN0M1. The operation in the volume of kidney resection was performed in 2 (4%) patients, in both cases, morphologically confirmed renal cell carcinoma, light-cell variant pT1aN0M0. The presence of a cystic-solid component and the initial size of the tumour were potential radiographic signs that could predict the dynamics of an increase in renal parenchyma neoplasm.Conclusion. The tactic of actively observing the growth rates of kidney tumours that accumulate contrast material allowed us to better understand the biological behaviour of KC. It was found that most kidney malignancies have a slow growth rate when determining the linear growth rate of the tumour. This conclusion allows us to differentially approach the choice of surgical treatment, which is optimal for elderly patients with low somatic status. Because prognostic signs of KC have not yet been identified and are not fixed in international treatment protocols, all patients who are suitable candidates for surgery are shown operative treatment.
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&NA;. "Tumour-specific superantigens - super active." Inpharma Weekly &NA;, no. 896 (1993): 12. http://dx.doi.org/10.2165/00128413-199308960-00026.
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Sagnella, Sharon M., Joshua A. McCarroll, and Maria Kavallaris. "Drug delivery: Beyond active tumour targeting." Nanomedicine: Nanotechnology, Biology and Medicine 10, no. 6 (2014): 1131–37. http://dx.doi.org/10.1016/j.nano.2014.04.012.
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Bucella, Dario, Jean-Frédéric Limbosch, Frédéric Buxant, et al. "Recurrence of Mitotically Active Cellular Fibroma of the Ovary." Obstetrics and Gynecology International 2009 (2009): 1–3. http://dx.doi.org/10.1155/2009/803062.
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Background. 10% of ovarian fibromatous tumours typically exhibit increased cellularity, mitotic activity, and less frequently nuclear atypia. Therefore, the classification within the group of fibromatous tumours may represent some difficulties, thus, one or several of these features should appear.Case. We introduce the clinical and pathologic features based on one case of recurrence of a mitotically active cellular ovarian fibroma (MACF) in the pararectal fossa. This recurrence took place six years after primary surgery. Macroscopically, the tumour was firm, fibrous, well delimited, yellow-white without gross necrosis. On microscopic examination, it was composed of a densely cellular proliferation of fibrolastic-like cells with bland nuclear features and arranged in a fascicular pattern. There was no sign of significant atypia or necrosis.Conclusion. Recently, this case is the first report of a recurrence of MACF, following primary surgery with no tumoral rupture or surgical difficulty. The clinical outcome of ovarian cellular fibromas (CFs) and MACFs is typically uneventful. This case, however, strongly suggests maintaining a long-term clinical follow-up even though the principal tumour was surgically treated without tumour rupture or in the absence of adherence or any surgical difficulty.
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Shankar Dey, Bhabani, Manas Kumar Bera, and Binoy Krishna Roy. "Nonlinear active control of a cancerous tumour." International Journal of Engineering & Technology 7, no. 2.21 (2018): 72. http://dx.doi.org/10.14419/ijet.v7i2.21.11839.
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This paper deals with the control of a cancerous tumour growth. The model used is a Three-Dimensional Cancer Model (TDCM). The competition terms include tumour cells, healthy cells, and immune cells. Nature of the competition among the populations of tumour cells, healthy host cells, and immune cells results in a chaotic behaviour. In this paper, a nonlinear active control has been used to control the growth of a tumour. Effect of chemotherapy drug on the different cell populations has been studied. Our control objective is to control the tumour growth and minimize its population to a small value which can be considered as harmless.Along with the above objective, the normal cell population is also be maintained at a particular level. This work has been done completely inin-sillico environment. The simulation results are shown extensively to support the theoretical analysis and confirmed that the preliminary objectives of the paper are attained.
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Hirsjarvi, Samuli, Catherine Passirani, and Jean-Pierre Benoit. "Passive and Active Tumour Targeting with Nanocarriers." Current Drug Discovery Technologies 8, no. 3 (2011): 188–96. http://dx.doi.org/10.2174/157016311796798991.
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Salmaso, Stefano, Sara Bersani, Alessandra Semenzato, and Paolo Caliceti. "New cyclodextrin bioconjugates for active tumour targeting." Journal of Drug Targeting 15, no. 6 (2007): 379–90. http://dx.doi.org/10.1080/10611860701349752.
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Yan, Hengkang, Mary E. Vail, Linda Hii, et al. "Preferential Antibody and Drug Conjugate Targeting of the ADAM10 Metalloprotease in Tumours." Cancers 14, no. 13 (2022): 3171. http://dx.doi.org/10.3390/cancers14133171.
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ADAM10 is a transmembrane metalloprotease that sheds a variety of cell surface proteins, including receptors and ligands that regulate a range of developmental processes which re-emerge during tumour development. While ADAM10 is ubiquitously expressed, its activity is normally tightly regulated, but becomes deregulated in tumours. We previously reported the generation of a monoclonal antibody, 8C7, which preferentially recognises an active form of ADAM10 in human and mouse tumours. We now report our investigation of the mechanism of this specificity, and the preferential targeting of 8C7 to human tumour cell xenografts in mice. We also report the development of novel 8C7 antibody–drug conjugates that preferentially kill cells displaying the 8C7 epitope, and that can inhibit tumour growth in mice. This study provides the first demonstration that antibody–drug conjugates targeting an active conformer of ADAM10, a widely expressed transmembrane metalloprotease, enable tumour-selective targeting and inhibition.
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O'Rourke, N. P., E. V. McCloskey, and J. A. Kanis. "Tumour induced hypercalcaemia: A case for active treatment." Clinical Oncology 6, no. 3 (1994): 172–76. http://dx.doi.org/10.1016/s0936-6555(94)80057-x.
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Herrmann, Th. "Radiation oncology and functional imaging." Nuklearmedizin 44, S 01 (2005): S38—S40. http://dx.doi.org/10.1055/s-0038-1625213.
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Summary:PET/CT imaging is most likely to be of use in radiation oncology with patients who have poorly defined target volume areas, e.g. brain tumours, bronchogenic carcinoma, and cases of miscellaneous geographical miss. Other tumours that call for dose escalated radiotherapy, such as head and neck tumours, bronchogenic carcinoma, and prostate carcinomas may further benefit from an accurate delineation of the metabolically active tumour volume and its differentiation from surrounding healthy tissue, or tumour atelectasis.
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Bogdan, Michał J., and Thierry Savin. "Fingering instabilities in tissue invasion: an active fluid model." Royal Society Open Science 5, no. 12 (2018): 181579. http://dx.doi.org/10.1098/rsos.181579.
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Metastatic tumours often invade healthy neighbouring tissues by forming multicellular finger-like protrusions emerging from the cancer mass. To understand the mechanical context behind this phenomenon, we here develop a minimalist fluid model of a self-propelled, growing biological tissue. The theory involves only four mechanical parameters and remains analytically trackable in various settings. As an application of the model, we study the evolution of a two-dimensional circular droplet made of our active and expanding fluid, and embedded in a passive non-growing tissue. This system could be used to model the evolution of a carcinoma in an epithelial layer. We find that our description can explain the propensity of tumour tissues to fingering instabilities, as conditioned by the magnitude of active traction and the growth kinetics. We are also able to derive predictions for the tumour size at the onset of metastasis, and for the number of subsequent invasive fingers. Our active fluid model may help describe a wider range of biological processes, including wound healing and developmental patterning.
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Calvio, L., M. Feuerstein, J. Hansen, and G. M. Luff. "Cognitive limitations in occupationally active malignant brain tumour survivors." Occupational Medicine 59, no. 6 (2009): 406–12. http://dx.doi.org/10.1093/occmed/kqp094.
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Gielen, Marcel, Abdelaziz El Khloufi, Monique Biesemans, et al. "Synthesis, Characterization and High In Vitro Antitumour Activity of Novel Triphenyltin Carboxylates." Metal-Based Drugs 1, no. 4 (1994): 305–9. http://dx.doi.org/10.1155/mbd.1994.305.
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The synthesis and spectral characterization of six novel triphenyltin compounds are described. The in vitro antitumour activity of three of these compounds against two human tumour cell lines, MCF-7, a mammary tumour, and WiDr, a colon carcinoma, was determined. All three compounds are more active than cis-platin, etoposide and doxorubicin against both tumour cell lines. They are as active as mitomycin C against WiDr, but less active against MCF-7.
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Rahman, Muhammad M., Dimalee Herath, John C. Bladen, et al. "Differential expression of phosphorylated MEK and ERK correlates with aggressive BCC subtypes." Carcinogenesis 42, no. 7 (2021): 975–83. http://dx.doi.org/10.1093/carcin/bgab036.
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Abstract Basal cell carcinoma (BCC) is associated with aberrant Hedgehog (HH) signalling through mutational inactivation of PTCH1; however, there is conflicting data regarding MEK/ERK signalling in BCC and the signalling pathway interactions in these carcinomas. To address this, expression of active phospho (p) MEK and ERK was examined in a panel of 15 non-aggressive and 14 aggressive BCCs. Although not uniformly expressed, both phospho-proteins were detected in the nuclei and/or cytoplasm of normal and tumour-associated epidermal cells however, whereas phospho-MEK (pMEK) was present in all non-aggressive BCCs (14/14), phospho-ERK (pERK) was rarely expressed (2/14). In contrast pERK expression was more prevalent in aggressive tumours (11/14). Interestingly, pMEK was only localized to the tumour mass whereas pERK was expressed in tumours and stroma of aggressive BCCs. Similarly, pERK (but not pMEK) was absent in mouse BCC-like tumours derived from X-ray irradiated Ptch1+/− mice with stromal pERK observed in myofibroblasts of the aggressive variant as well as in the tumour mass. RNA sequencing analysis of tumour epithelium and stroma of aggressive and non-aggressive BCC revealed the upregulation of epidermal growth factor receptor- and ERK-related pathways. Angiogenesis and immune response pathways were also upregulated in the stroma compared with the tumour. PTCH1 suppressed NEB1 immortalized keratinocytes (shPTCH1) display upregulated pERK that can be independent of MEK expression. Furthermore, epidermal growth factor pathway inhibitors affect the HH pathway by suppressing GLI1. These studies reveal differential expression of pERK between human BCC subtypes that maybe active by a pathway independent of MEK.
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Kumar, Vikas. "Segmentation of Brain Images by Optimizing Clustering of Convolution Based Features." E3S Web of Conferences 229 (2021): 01034. http://dx.doi.org/10.1051/e3sconf/202122901034.
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Brain tumour segmentation aims to separate the various types of tumour tissues like active cells, necrotic core, and edema from normal brain tissues of substantia alba (WM), grey matter (GM), and spinal fluid (CSF). Magnetic Resonance Imaging based brain tumour segmentation studies are attracting more and more attention in recent years thanks to non-invasive imaging and good soft tissue contrast of resonance Imaging (MRI) images. With the event of just about two decades, the ingenious approaches applying computer-aided techniques for segmenting brain tumour are getting more and more mature and coming closer to routine clinical applications. the aim of this paper is to supply a comprehensive overview for MRIbased brain tumour segmentation methods. Firstly, a quick introduction to brain tumours and imaging modalities of brain tumours is given in this proposed research, convolution based optimization. These stepwise step refine the segmentation and improve the classification parameter with the assistance of particle swarmoptimization.
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Nowakowska, Anna, and Jolanta Tarasiuk. "Invasion and metastasis of tumour cells resistant to chemotherapy." Postępy Higieny i Medycyny Doświadczalnej 71, no. 1 (2017): 0. http://dx.doi.org/10.5604/01.3001.0010.3822.
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Metastatic tumours resistant to chemotherapy are the major cause of the clinical failure in the treatment of malignant diseases. It is observed often that drugs active against primary tumours do not exhibit the same efficacy towards metastatic tumour cells having modified signaling pathways. Among cellular factors involved in the development of the metastatic potential of multidrug resistant tumour cells are some oncoproteins, antiapoptotic proteins, mutated suppressor proteins, integrins and CD44 receptor. It was also demonstrated that numerous chemotherapeutics have the effect on the emergence of the metastatic potential and multidrug resistance (MDR) phenomenon of tumour cells. The results of numerous studies suggest that genes involved in the development of MDR and metastatic phenotype of tumour cells are regulated by the same signaling pathways. They lead to the activation of transcription factors e.g. HIF-1α, NF-κB, Ets1 and AP-1 controlling the expression of genes involved in the development of the metastatic potential of multidrug resistant tumour cells. The identification of key cellular factors responsible for the emergence of the metastatic potential of MDR tumour cells could lead to the development of new efficient strategies for the treatment of metastatic tumours resistant to the conventional chemotherapy.
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Kwan, Amy, Faith Howard, Natalie Winder, et al. "Macrophage Delivered HSV1716 Is Active against Triple Negative Breast Cancer." Future Pharmacology 2, no. 4 (2022): 444–59. http://dx.doi.org/10.3390/futurepharmacol2040029.
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Oncolytic viruses (OV) promote anti-tumour responses through the initiation of immunogenic cancer cell death which activates the host’s systemic anti-tumour immunity. We have previously shown that intravenously administered HSV1716 is an effective treatment for mammary cancer. However, intravenous administration of a virus has the potential to result in neutralization and sequestration of the virus which may reduce efficacy. Here, we show that the oncolytic virus HSV1716 can be administered within a cellular carrier (macrophages). PyMT and 4T1 murine mammary cancer cell lines were implanted into immuno-competent murine models (orthotopic primary, early metastatic and brain metastasis models). HSV1716 or macrophages armed with HSV1716 (M-HSV1716) were administered intravenously, and tumour size was quantified using caliper measurement or bioluminescence imaging. Administration of M-HSV1716 led to tumour shrinkage and increased the survival of animals. Furthermore, these results were achieved with a 100-fold lower viral load, which has the potential for decreased toxicity. Our results demonstrate that M-HSV1716 is associated with activity against murine mammary cancers and provides an alternative platform for the systemic delivery of OV.
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Peng, Xiang, Jinchao Chen, Jiangyi Wang, et al. "Natural history of renal tumours in von Hippel-Lindau disease: a large retrospective study of Chinese patients." Journal of Medical Genetics 56, no. 6 (2019): 380–87. http://dx.doi.org/10.1136/jmedgenet-2018-105567.
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BackgroundHistorically, renal cell carcinoma (RCC) is one of the main causes of death in von Hippel-Lindau (VHL) disease. However, the natural history of VHL-related RCC has not been thoroughly elucidated to date. This report described the natural history of VHL-related RCC in a large Chinese VHL cohort and might be helpful in the surveillance and treatment of VHL disease.MethodsIn this retrospective study, we included 196 renal tumours from 150 patients with VHL disease. Statistical analysis was used to evaluate the influence of age of onset, sex, family history, unilateral or bilateral tumour, VHL disease type, mutation type, mutation location, and tumour size on tumour growth, metastasis and survival in patients with VHL disease.ResultsThe mean age of onset was 38.8 years, and the mean initial tumour size was 3.1 cm. The mean linear growth rate was 0.49 cm/year. Patients experienced faster tumour growth when they had later age of onset, larger initial tumour size, missense mutation, mutations locating in exon 3, and when they were not affected by cerebral or retinal haemangioblastomas. Tumours larger than 4 cm grew faster than those smaller than 4 cm. Bilateral tumours, large initial tumours, fast tumour growth and metastasis were risk factors for poor prognosis in VHL-related RCC.ConclusionThis large study demonstrated that age of onset, initial tumour size, concomitant tumours, mutation type and mutation location had an effect on growth rate in VHL-related RCC. Active surveillance may be safe for patients with tumour size less than 4 cm, which is helpful in clinical decision-making.
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Casellas, F., M. Papo, F. Guarner, M. Antolín, J. R. Armengol, and J. R. Malagelada. "Intraluminal Colonic Release of Immunoreactive Tumour Necrosis Factor in Chronic Ulcerative Colitis." Clinical Science 87, no. 4 (1994): 453–58. http://dx.doi.org/10.1042/cs0870453.
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1. Tumour necrosis factor is a proinflammatory macrophage-derived polypeptide cytokine. Its participation in disease processes has been usually inferred from data obtained from experiments in vitro or from measurements of its plasma circulating levels. To investigate its role in chronic ulcerative colitis, we have quantified in vivo the steady-state release of tumour necrosis factor into the colonic lumen. 2. We studied 19 patients with untreated active ulcerative colitis and seven patients with irritable bowel syndrome as controls. A group of seven patients with active ulcerative colitis were studied before and after 4 weeks on treatment with oral 5-aminosalicylic acid. By means of an intracolonic double-lumen perfusion tube, an isotonic solution was continuously infused 50 cm from the anal verge at a rate of 5 ml/min, and was recovered 30 cm distally by siphonage. Effluents were assayed for tumour necrosis factor by a specific e.l.i.s.a. and for prostaglandin E2 and leukotriene B4 by specific r.i.a.s. 3. The intracolonic release of tumour necrosis factor was undetectable in patients with irritable bowel syndrome, whereas measurable release occurred in 15 out of 19 patients with active ulcerative colitis (P < 0.01). Prostaglandin E2 and leukotriene B4 release were also increased in active ulcerative colitis by comparison with irritable bowel syndrome (P < 0.01). Five out of seven patients with colitis improved with 5-aminosalicylic acid treatment, and tumour necrosis factor release became undetectable or decreased markedly (P < 0.05 compared with before treatment). However, tumour necrosis factor release remained high in the non-responder patients. 4. These findings indicate that intracolonic immunoreactive tumour necrosis factor release is enhanced in active chronic ulcerative colitis, becoming undetectable when mucosal lesions are healed. These results suggest that the luminal release of tumour necrosis factor may serve as an objective index of inflammatory activity in patients with chronic ulcerative colitis.
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Muller, Catherine. "Tumour-surrounding adipocytes are active players in breast cancer progression." Annales d'Endocrinologie 74, no. 2 (2013): 108–10. http://dx.doi.org/10.1016/j.ando.2013.02.007.
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Peters, MA, FH de Jong, KJ Teerds, DG de Rooij, SJ Dieleman, and FJ van Sluijs. "Ageing, testicular tumours and the pituitary-testis axis in dogs." Journal of Endocrinology 166, no. 1 (2000): 153–61. http://dx.doi.org/10.1677/joe.0.1660153.
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Dogs of different ages without testicular diseases were evaluated to study possible age-related changes in hormone concentrations in serum. Dogs with testicular tumours were also investigated to study the relation between tumour type and hormone concentrations; in this study, dogs with Sertoli cell tumours, Leydig cell tumours and seminomas were included. We measured testosterone, oestradiol, LH, FSH and inhibin-like immunoreactivity concentrations in peripheral venous and testicular venous blood of these animals. In normal dogs there appeared to be no age-related changes in the concentrations of the investigated hormones, except for a significant age-related decrease in oestradiol concentrations in testicular venous blood (P<0.02). Dogs with a Sertoli cell tumour had greater oestradiol concentrations and inhibin-like immunoreactivity in both peripheral and testicular venous blood than did dogs without a neoplasm (P<0. 05). Testosterone concentrations were reduced in dogs with Sertoli cell tumours, as were FSH and LH. Feminisation occurred in eight of 13 dogs with a Sertoli cell tumour and in two of 14 dogs with a Leydig cell tumour; it was accompanied by a significantly greater oestradiol concentration than in normal dogs and in dogs with Sertoli cell tumours without signs of feminisation. Dogs with a Leydig cell tumour had greater concentrations of oestradiol and inhibin-like immunoreactivity in both peripheral venous and testicular venous blood than did dogs without a neoplasm (P<0.05). The testosterone concentration in testicular venous blood of these dogs was lower than that in dogs with normal testes. The concentration of LH in peripheral venous blood was also reduced (P<0. 05). Hormone concentrations in dogs with a seminoma were not different from those in normal dogs. It was concluded that seminomas are not endocrinologically active. In contrast, both Sertoli cell tumours and Leydig cell tumours can cause increased oestrogen production leading to signs of feminisation. These tumours also have considerable amounts of inhibin-like immunoreactivity, but only in Sertoli cell tumours does this result in a reduction in FSH concentrations, suggesting that Sertoli cell tumours secrete dimeric inhibin, whereas Leydig cell tumours presumably produce loose alpha-subunits that cross-react in the inhibin assay but are not biologically active.
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Hadebe, Bawinile, Machaba Michael Sathekge, Colleen Aldous, and Mariza Vorster. "Current Status of 68Ga-Pentixafor in Solid Tumours." Diagnostics 12, no. 9 (2022): 2135. http://dx.doi.org/10.3390/diagnostics12092135.
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Chemokine receptor CXCR4 is overexpressed in neoplasms and its expression is related to tumour invasion, metastasis and aggressiveness. 68Ga-Pentixafor is used to non-invasively image the expression of CXCR4 in tumours and has been widely used in haematological malignancies. Recent evidence shows that therapies targeting CXCR4 can increase the chemosensitivity of the tumour as well as inhibit tumour metastasis and aggressiveness. 68Ga-Pentixafor has shown promise as an elegant radiotracer to aid in the selection of patients whose tumours demonstrate CXCR4 overexpression and who therefore may benefit from novel therapies targeting CXCR4. In addition, its therapeutic partners 177Lu- and 90Y-Pentixather have been investigated in the treatment of patients with advanced haematological malignancies, and initial studies have shown a good treatment response in metabolically active lesions. 68Ga-Pentixafor in solid tumours complements 18F-FDG by providing prognostic information and selecting patients who may benefit from therapies targeting CXCR4. This review summarises the available literature on the potential applications of 68Ga-Pentixafor in solid tumours.
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Newlands, E. S., L. Holden, and K. D. Bagshawe. "Tumour Markers and POMB/ACE Chemotherapy in the Management of Ovarian Germ Cell Tumours (GCTs)." International Journal of Biological Markers 3, no. 3 (1988): 185–92. http://dx.doi.org/10.1177/172460088800300307.
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The management of ovarian germ cell tumours (GCTs) has changed dramatically over the last 15 years. The combination of the introduction of tumour markers which accurately monitor the behaviour of the majority of germ cell tumours together with the introduction of newer chemotherapeutic agents has meant that few patients even with metastases should succumb from their disease. The tumour markers, human chorionic gonadotrophin (hCG) and alpha-foetoprotein (AFP) and, to a lesser extent, lactate dehydrogenase (LDH) and placental alkaline phosphatase (PLAP) are routinely used in assisting diagnosis, monitoring response to treatment and increasing the sensitivity of follow-up ofpatients after completing treatment. Analysis of our last 51 patients with all cell types of ovarian germ cell tumour has confirmed the importance of both hCG and AFP in that 45 (88%) of 51 patients had either or both of these tumour markers raised at the start of treatment for metastatic disease. Our data on LDH is incomplete since this has not been a routine assay until 1984 and, of the patients with active disease 10 (48%) had raised LDH at the start of treatment. PLAP has also been measured in a number of patients both on active treatment and in remission. 11 (50%) had raised levels of PLAP at the start of treatment but there was also a false positive rate of8 (24%) of the 33 patients who were in remission and had not subsequently relapsed.
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Setyono-Han, Buddy, Jörg Stürzebecher, Wolfgang Schmalix, et al. "Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1." Thrombosis and Haemostasis 93, no. 04 (2005): 779–86. http://dx.doi.org/10.1160/th04-11-0712.
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SummaryThe serine protease uPA (urokinase-type plasminogen activator) and its receptor uPAR (CD87) are often elevated in malignant tumours, hence, inhibition of this tumour-associated plasminogen activation system provides an attractive target for therapeutic strategies. WX-UK1, a derivative of 3-aminophenylalanine in the L-conformation with inhibitory antiproteolytic properties, was tested for its specificity spectrum using specific chromogenic paranitroanilide peptide substrates. The corresponding D-enantiomer of WX-UK1 was used as a control. The anti-tumour and anti-metastatic (number of lung foci and weight of the axillary lymph nodes) properties were studied by subcutaneous administration of WX-UK1 to Brown Norwegian (BN) rats carrying orthotopically transplanted BN472 rat breast tumours. WX-UK1 selectively inhibited tumour-related proteases from rats and humans such as uPA, plasmin, or thrombin in the sub or low micromolar range. The activity was stereoselective as the D-enantiomer of WX-UK1 inhibited uPA and plas-min at approximately 70-fold higher Ki values than the active L-form. Chronical administration of the L-enantiomer of WXUK1 impaired primary tumour growth and metastasis of BN472 rat breast cancer in a dose-dependent manner. The minimum inhibitory dosage with maximal effect was between 0.15 and 0.3 mg/kg/day. The inactive D-enatiomer of WX-UK1 was not active in this respect. Daily treatment with WX-UK1 for up to 35 days was well tolerated as judged by the unchanged body and organ weight development. In conclusion, our results provide evidence that WX-UK1 as a single agent inhibits breast tumour growth and metastasis in vivo, and thus is a promising candidate drug to treat human cancer.
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Raehaan, Nur Rahmi, Asvin Nurulita, and Mansyur Arif. "CARCInoeMBRYonIC AnTIGen (CEA) DI KANKER KOLOREKTAL." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 20, no. 3 (2016): 192. http://dx.doi.org/10.24293/ijcpml.v20i3.465.
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Colorectal cancer is a common gastrointestinal malignancy of the colon and rectum. According to the American Society of Clinical Oncology (ASCO) in 2006, preoperative CEA level is useful in dtermining the tumour stage, plan of action and monitoring therapeutic response during the active treatment. Several factors which influence CEA level in patients with colorectal cancer is the staging and the degree of tumour, liver function, and as well as its location. This retrospective study is aimed to know the preoperative CEA levels in 51 patients with colorectal cancer and to compare the levels of CEA based on tumour stage, degree of tumour based on histopathology and tumour location.. This study was carried out at the Dr.Wahidin Sudirohusodo Hospital (RSWS), Makassar during January 2009−December of 2011. The researchers found a significant difference between the levels of CEA with the tumour stage (p=0.000) and its relation with the degree of the tumour (p=0.002), however, based on the tumour location (p=0.585) there was no significant difference between the levels of CEA. In conclusion, it was found that the higher the tumour stage, the higher the levels of the produced CEA. A well differentiated tumour of colorectal cancer produced a higher level of CEA compared to the moderate or poor-differentiated tumours.
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Ewing, Ailith, and Colin Semple. "Breaking point: the genesis and impact of structural variation in tumours." F1000Research 7 (November 19, 2018): 1814. http://dx.doi.org/10.12688/f1000research.16079.1.
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Somatic structural variants undoubtedly play important roles in driving tumourigenesis. This is evident despite the substantial technical challenges that remain in accurately detecting structural variants and their breakpoints in tumours and in spite of our incomplete understanding of the impact of structural variants on cellular function. Developments in these areas of research contribute to the ongoing discovery of structural variation with a clear impact on the evolution of the tumour and on the clinical importance to the patient. Recent large whole genome sequencing studies have reinforced our impression of each tumour as a unique combination of mutations but paradoxically have also discovered similar genome-wide patterns of single-nucleotide and structural variation between tumours. Statistical methods have been developed to deconvolute mutation patterns, or signatures, that recur across samples, providing information about the mutagens and repair processes that may be active in a given tumour. These signatures can guide treatment by, for example, highlighting vulnerabilities in a particular tumour to a particular chemotherapy. Thus, although the complete reconstruction of the full evolutionary trajectory of a tumour genome remains currently out of reach, valuable data are already emerging to improve the treatment of cancer.
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Gupta, M., S. K. Sharma, R. Saxena, and S. Arora. "Analysis of machine learning algorithms in brain tumour prediction." Journal of Physics: Conference Series 2070, no. 1 (2021): 012090. http://dx.doi.org/10.1088/1742-6596/2070/1/012090.
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Abstract The tumour is fundamentally an excessive development of dangerous cells in any part of the body, while a tumour in a brain is an unreasonable development of cancerous cells in the brain. Brain tumour can be either benign or malignant. The benign brain tumour has structural consistency and does not include active (cancer) cells, but the malignant brain tumour has no structure consistency and includes active cells. The primary concern is to segment, detect, and extract the infected tumour area from magnetic resonance images (MRI) which are being performed by radiologists or medical experts, and their accuracy is totally dependent on their experience only. Thus, it becomes very essential to overcome these limitations by the use of artificial intelligence. The current paper uses various machine learning algorithms as well as their features to design a structure to predict brain tumour at an early phase by using different classifiers and comparing their respective accuracy parameters.
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Eftimie, R., and L. Gibelli. "A kinetic theory approach for modelling tumour and macrophages heterogeneity and plasticity during cancer progression." Mathematical Models and Methods in Applied Sciences 30, no. 04 (2020): 659–83. http://dx.doi.org/10.1142/s0218202520400011.
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The heterogeneity and plasticity of macrophages have become a topic of great interest, due to their role in various diseases ranging from cancer to bacterial infections. While initial experimental studies assumed an extreme polarisation situation, with the (anti-tumour) M1 and (pro-tumour) M2 macrophages representing the two extreme cell phenotypes, more recent studies showed a continuum of macrophages polarisation phenotypes. Here, we focus on tumour-macrophage interactions and develop a mathematical model based on kinetic equations for active particles to describe (i) the dynamics of macrophages with a continuum of diverse functional states, ranging from pro-tumour to anti-tumour states; and (ii) the dynamics of tumour cells with a variety of progression (i.e. mutation) states. With the help of this model we show that the growth of solid tumours is associated with an increased clonal heterogeneity, as well as with an increased macrophages phenotypic heterogeneity (caused by a shift from an initial anti-tumour M1-like phenotype to a mixed M1–M2 phenotype). Moreover, we show that the assumption of exponential tumour/immune cell growth leads to an unbounded macrophages growth, which is biologically unrealistic. In contrast, the assumption of logistic tumour/immune cell growth can lead to tumour dormancy (under the control of immune cells), or to tumour growth towards smaller/larger sizes which depend on various model parameters. Finally, we show that tumour dormancy is associated with an increase in the clonal heterogeneity of tumour cells and in the phenotypic heterogeneity of macrophages.
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Yacyshyn, BR, BM Longenecker, WA Biermann, D. McClure, S. Poppema, and MB Bowen-Yacyshyn. "Active Specific Immunotherapy in the Management of Adenocarcinoma of the Pancreas." Canadian Journal of Gastroenterology 9, no. 4 (1995): 213–16. http://dx.doi.org/10.1155/1995/491787.
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Active specific immunotherapy for pancreatic adenocarcinoma and subsequent immunohistochemical analysis of tumour tissue have not been previously reported. To date, the therapy of pancreatic adenocarcinoma has been largely unsuccessful. A patient treated with a therapeutic ‘cancer vaccine’ and the immunological impact on the primary tumour of this potential new therapy are described. To the authors’ knowledge, this is both the first patient to be treated with active specific immunotherapy for pancreatic adenocarcinoma and the first to be studied immunologically by flow cytometry and immunohistochemistry with an apparent positive clinical impact.
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Alam, Md Nur, and Fazlul Huq. "Comprehensive review on tumour active palladium compounds and structure–activity relationships." Coordination Chemistry Reviews 316 (June 2016): 36–67. http://dx.doi.org/10.1016/j.ccr.2016.02.001.
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Vauleon, Elodie, Tony Avril, Brigitte Collet, Jean Mosser, and Véronique Quillien. "Overview of Cellular Immunotherapy for Patients with Glioblastoma." Clinical and Developmental Immunology 2010 (2010): 1–18. http://dx.doi.org/10.1155/2010/689171.
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High grade gliomas (HGG) including glioblastomas (GBM) are the most common and devastating primary brain tumours. Despite important progresses in GBM treatment that currently includes surgery combined to radio- and chemotherapy, GBM patients' prognosis remains very poor. Immunotherapy is one of the new promising therapeutic approaches that can specifically target tumour cells. Such an approach could also maintain long term antitumour responses without inducing neurologic defects. Since the past 25 years, adoptive and active immunotherapies using lymphokine-activated killer cells, cytotoxic T cells, tumour-infiltrating lymphocytes, autologous tumour cells, and dendritic cells have been tested in phase I/II clinical trials with HGG patients. This paper inventories these cellular immunotherapeutic strategies and discusses their efficacy, limits, and future perspectives for optimizing the treatment to achieve clinical benefits for GBM patients.
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Real, Carla, Francisco Caiado, Catia Igreja, et al. "Delta Like 4 Expressing Bone Marrow-Derived Endothelial Progenitor Cells Regulate Tumour Angiogenesis." Blood 110, no. 11 (2007): 3728. http://dx.doi.org/10.1182/blood.v110.11.3728.3728.
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Abstract Bone marrow-derived endothelial progenitor cells (BM-EPCs) have been implicated in adult neoangiogenesis and consequently used as therapies for human pathologies with endothelial damage. The administration of these cells in human patients temporally improves endothelial function, although the engraftment of these cells in newly formed vessels is inefficient. Conversely, therapeutic stratagies to block EPC contribution during tumor angiogenesis have been proposed. In this work, we analysed the role of the Notch/Delta signalling pathway in EPC function during tumour neoangiogenesis, by regulating the expression of Notch ligand, delta-like 4 (Dll4) in these cells. Sublethally irradiated NOD-SCID mice received WT, Dll4+/− (Dll4 heterozygous mice) or Dll4 SiRNA-treated BM-EPCs and were subcutaneously inoculated with well established Human or murine tumor xenografts. Tumours growing in Dll4-depleted EPCs transplanted mice presented increased microvessel density when compared with WT EPCs transplanted mice or non-transplanted controls, regardless of VEGF expression. Although with increased vessel number, tumours of Dll4+/− EPC transplanted mice presented increased hypoxia and decreased tumour cell proliferation, suggesting an impairment in vessel function. In addition, these tumours present a diminished expression of PDGF, a vessel stabilizing factor, and increased expression of Ang2, known as a vessel destabilizing factor. We next verified whether the vessel destabilization observed in tumors after Dll4-depleted EPCs transplant might be due to a diferential endothelial differentiation or incorporation of EPCs in the tumour vasculature. In order to answer this question we quantified the incorporation of WT and Dll4-depleted EPCs in tumour vessels. Accordingly to our results, the presence of Dll4-depleted EPCs was reduced compared to WT EPCs, suggesting that Dll4-depleted EPCs might have reduced capacity to adhere to the renewing tumor vasculature, or to the underlying basement membrane. To test this, we used an in vitro endothelial differentiation assay, and observed a defect on the adhesion of of Dll4-depleted EPCs to extracellular matrix, which was correlated with a reduced expression of integrin subunits a3 and b1. These results suggest that the reduction of Dll4 on EPCs reduces integrin expression interfering with their ability to adhere, incorporate and stabilize the tumor vasculature during tumor neoangiogenesis. Therefore, EPCs have a major role in vessel stabilization in active neoangiogenic sites by the regulation of Dll4 expression. We propose that targeting the Notch/Dll4 pathway on EPCs, modulating vessel stability, may have therapeutic potential.
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Szostek, Arnika, Jakub Wydra, Izabella Czajka-Oraniec, and Wojciech Zgliczyński. "Two successful pregnancies in a woman with active acromegaly." Wiedza Medyczna 2, no. 2 (2020): 72–76. http://dx.doi.org/10.36553/wm.60.
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Acromegaly is a rare systemic disease, predominantly caused by growth hormone (GH)-secreting pituitary adenoma, leading to insulin-like growth factor-1 (IGF-1) overproduction. Pituitary adenoma extension and/or its treatment can cause infertility or subfertility in both sexes in different mechanisms. Pregnancies in women with active acromegaly are rarely observed but considered generally safe. Growth hormone and IGF-1 concentrations are usually stable during pregnancy and in most cases no significant tumour expansion emerges despite pharmacological therapy withdrawal.
 A 28 year-old woman with symptoms of acromegaly and amenorrhoea was admitted to the Department of Endocrinology. Diagnosis of acromegaly was made and treatment with somatostatin analogues (SSA) was initiated with subsequent surgical intervention. However, persistent acromegaly was diagnosed post-operatively due to residual tumour and the medical treatment was restarted. During follow-up the patient became pregnant twice and then treatment with somatostatin analogues was ceased. Both pregnancies were complicated by gestational diabetes and in the course of the second pregnancy treatment with dopamine agonist (DA) was commenced to alleviate persistent headaches and it was followed by clinical and biochemical improvement. The patient successfully delivered two healthy babies. After second labour treatment with SSA was resumed and the patient has achieved adequate disease control.
 The risk of pregnancy complications in women with acromegaly is slightly higher than in general population, especially if uncontrolled disease was present before conception or acromegaly was diagnosed during pregnancy. In rare cases pituitary tumour expansion during pregnancy occurs and then pharmacological or surgical interventions should be considered.
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Hayes, James R., Michael A. S. Jewett, and Robert J. Hamilton. "28-year late spermatic cord relapse of a testicular non-seminomatous germ cell tumour, managed robotically." Canadian Urological Association Journal 10, no. 7-8 (2016): 257. http://dx.doi.org/10.5489/cuaj.3492.
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We present a patient who relapsed symptomatically 28 years postorchiectomy, initially followed by active surveillance for clinical stage I non-seminomatous germ cell tumour (CSI NSGCT). His relapse was localized to the pelvis, managed with robotic surgery, and achieved a complete resection with tumour markers normalized. We highlight the current Princess Margaret guidelines for followup of CSI NSGCT and discuss the trade-off between lifelong radiographic surveillance to detect the very small risk of late relapse. We discuss the incidence and presentation of late relapse, treatment options, and outcomes, highlighting that these tumours are typically refractory to chemotherapy and can often be managed with surgery alone.
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Plank, M. J., and B. D. Sleeman. "Tumour-Induced Angiogenesis: A Review." Journal of Theoretical Medicine 5, no. 3-4 (2003): 137–53. http://dx.doi.org/10.1080/10273360410001700843.
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Angiogenesis, the formation of new blood vessels, has become a broad subject and is a very active area for current research. This paper describes the main biological events involved in angiogenesis and their importance in cancer progression. In the first section, a fundamental overview of tumour biology is presented. In the second section, the biology of healthy blood vessels is described and, in the third section, the mechanisms of cell migration and proliferation, which are crucial to angiogenesis, are discussed. In the fourth section, a detailed account of tumour-induced angiogenesis is given, whilst the pro- and anti-angiogenic factors involved are reviewed in the fifth section. Finally, the processes of tumour invasion and metastasis are examined in the sixth section.
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R. I. O., Nwoha, Onyegbula O., and Daniel G. I. "Treatment and Regression of Transmissible Venearal Tumour in Dogs." Sumerianz Journal of Agriculture and Veterinary, no. 43 (September 16, 2021): 92–96. http://dx.doi.org/10.47752/sjav.43.92.96.
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Antimicrobial resistance threatens the effective treatment of vast range of bacterial, fungi and viral diseases. Transmissible venereal tumour (TVT) is one of the highly contagious tumour in dogs commonly affecting sexually active stud and bitches. The disease was observed in a male and female Alsatian of about 3 years of age. Both dogs were sexually active and are utilized for breeding purposes. Samples were collected from the TVT growth on both the female and male genitalia. The samples were subjected to cytology and confirmatory diagnosis was made on the gross appearance of cauliformlike lesion and appearance of roundish cells with multiple vacuoles in the cytoplasm of the TVT tumour cells. Treatment was achieved by 3 doses of Vincristin sulphate injection USP1mg/ml Vinlon TM 1 intravenously through a cannula. There was no report of recrudesce of growth post treatment. Conclusion: TVT appear to exhibit genetic preference for sexually active Alsatian breed of dogs within the age bracket of 3 years and above. Despite the confronting challenge of drug resistance in medicine, intravenous administration of vincristine sulphate has remained efficacious in achieving complete regression of TVT the growth in dogs.
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Aung, Ei Thuzar, Umme Rubab, Mark Randon, Catherine Gilkes, Christina Daousi, and Sravan Thondam. "PMON120 Clinical Course Of Untreated Giant Invasive Macroprolactinomas- A Case Series." Journal of the Endocrine Society 6, Supplement_1 (2022): A535. http://dx.doi.org/10.1210/jendso/bvac150.1113.
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Abstract Introduction Giant invasive prolactinomas are rare pituitary tumours and have a male preponderance of 9: 1. In majority of cases, dopamine agonists (DA) are the treatment of choice in lowering prolactin and tumour shrinkage. Surgery may be opted in those with acute compressive symptoms or visual loss. Prolactinomas are known to invade the sellar floor, sphenoid sinus and clivus. Spontaneous CSF leak is rare in untreated patients with invasive prolactinomas compared to those on DA who respond with rapid tumour shrinkage that causes unplugging of the conduits resulting in CSF rhinorrhoea. We present 5 male patients with untreated giant invasive prolactinomas with skull base destruction where close surveillance was opted over DA treatment. Results Five male patients with median age of 73±10 years were studied. 1 patient presented with headache, vomiting and 6th nerve palsy which spontaneously resolved over weeks. 2 patients were diagnosed during work up of other hormonal deficiencies and in 2 patients giant tumours were incidentally found on imaging for head injury. Prolactin values ranged from 55,641 to 835,800 mIU/L. Hormonal deficiency was present in 3/5; anterior hypopituitarism (1) and symptomatic secondary hypogonadism (2). MRI imaging in all patients showed extensive skull base bony erosion, with tumour invasion into sphenoid sinus and clivus. Additionally, the patient with largest tumour had invasion into right orbital roof and floor of right anterior cranial fossa. In other patients, tumour had also invaded occipital condyles (1), bilateral cavernous sinus (1). All patients were discussed in tertiary neurosurgical MDT. As the risk of CSF leakage due to tumour shrinkage outweighed the benefits of tumour reduction, a decision not for medical treatment was agreed with patients and planned for active surveillance with MRI scans and regular clinical and visual fields assessments. The mean follow-up period was 4±1 years. One patient was very frail and decided not for radiological surveillance. DA treatment is being considered for the patient with the largest tumour which has grown further causing frontal lobe invasion. There was no significant tumour size increase in other 4 patients and none had spontaneous CSF leak. Discussion Risk stratification for CSF leak with DA treatment is difficult as it depends on the invasion, tumour response to DAs and the extent of underlying bony destruction. This may cause a dilemma on whether or not to treat some patients with DAs. The risk of CSF leak, bacterial meningitis and the subsequent need for urgent surgical repair may outweigh the benefits of tumour reduction with DAs particularly in some patients with low symptom burden. In our experience, patient counselling, active radiological surveillance and considering treatment with change in symptoms (visual deterioration, compressive pathology) could be an appropriate management option in such patients. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
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Ebrahimi-Nik, Hakimeh, Arvin Iracheta-Vellve, Kira E. Olander, et al. "Abstract A41: Small molecule inhibition of PTPN2/1 inflames the tumour microenvironment and unleashes potent CD8+ T cell immunity." Cancer Immunology Research 10, no. 12_Supplement (2022): A41. http://dx.doi.org/10.1158/2326-6074.tumimm22-a41.
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Abstract Immune checkpoint blockade is effective for a subset of patients across many cancers, but most patients are refractory to current immunotherapies and new approaches are needed to overcome resistance. The protein tyrosine phosphatase PTPN2 is a central regulator of inflammation, and genetic deletion of PTPN2 on either tumour cells or host immune cells promotes anti-tumour immunity. However, inhibitors of PTPN2 with suitable pharmacokinetic properties for oral administration have not been described. Here, we present the characterization of ABBV-CLS-484 (A484), a potent active site inhibitor of PTPN2 and the closely related phosphatase PTPN1. A484 treatment in vitro amplifies the response to interferon gamma, and monotherapy A484 treatment generates robust anti-tumour immunity in several murine cancer models. Through in vivo studies and single cell transcriptional profiling of tumour-infiltrating lymphocytes (TIL) from A484-treated mice, we show that A484 inflames the tumour microenvironment and promotes CD8+ T cell function by enhancing cytokine signaling and decreasing T cell exhaustion and dysfunction. Our results demonstrate that oral administration of small molecule inhibitors of PTPN2/N1 can induce potent anti-tumour immunity in mouse models. PTPN2/N1 inhibitors offer a promising new strategy for cancer immunotherapy and are currently being evaluated clinically in patients with advanced solid tumours (NCT04777994). More broadly, our study shows that small molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to current antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge A484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics targeting this important class of enzymes. Citation Format: Hakimeh Ebrahimi-Nik, Arvin Iracheta-Vellve, Kira E. Olander, Thomas R.G. Davis, Sarah Y. Kim, Mitchell D. Yeary, James C. Patti, Tyler M. Balon, Omar Ismail Avila, Cun Lan Chuong, Meng-Ju Wu, Christina K. Baumgartner, Keith M. Hamel, Kathleen A. McGuire, Rebecca Mathew, Carey Backus, Ian C. Kohnle, Zhaoming Xiong, Elliot P. Farney, Jennifer M. Frost, Geoff T. Halvorsen, Matthew Rees, Andrew Boghossian, Melissa Ronan, Jennifer A. Roth, Todd R. Golub, Gabriel K. Griffin, Nabeel El-Bardeesy, Clay C. Beauregard, Philip R. Kym, Kathleen B. Yates, Robert T. Manguso. Small molecule inhibition of PTPN2/1 inflames the tumour microenvironment and unleashes potent CD8+ T cell immunity [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr A41.
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Wang, Xiaojuan, Xing Sun, Hua He, et al. "A two-component active targeting theranostic agent based on graphene quantum dots." Journal of Materials Chemistry B 3, no. 17 (2015): 3583–90. http://dx.doi.org/10.1039/c5tb00211g.
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Kaufmann, J., G. Pronk, K. Giese, and A. Klippel. "Identification of novel effectors of invasive cell growth downstream of phosphoinositide 3-kinase." Biochemical Society Transactions 32, no. 2 (2004): 355–59. http://dx.doi.org/10.1042/bst0320355.
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Conventional approaches to identifying cancer targets are complicated by the chromosomal instability of tumour cells, and typically result in a large number of differentially expressed candidate genes with uncertain disease relevance. Here we present a novel approach which aims to elucidate the molecular changes that are induced after loss of tumour suppressor function. Using gene silencing tools, we mimic the loss of tumour suppressor function to identify key regulators of tumour initiation and progression. Loss of function of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10) correlates with increased invasive cell growth due to the resulting chronic activation of the PI 3-kinase (phosphoinositide 3-kinase) pathway. Induced activation of PI 3-kinase either by inhibiting PTEN expression or by using p110*, a constitutively active PI 3-kinase, increased signalling and the invasive growth potential of cells. Using this unbiased approach we have identified novel downstream effectors of PI 3-kinase/PTEN signalling that mediate the behaviour of cells with a hyperactive PI 3-kinase pathway. These molecules represent candidate targets for therapeutic intervention in patients with PTEN-deficient tumours.
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Pang, Lisa Y., Emma A. Hurst, and David J. Argyle. "Cyclooxygenase-2: A Role in Cancer Stem Cell Survival and Repopulation of Cancer Cells during Therapy." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/2048731.
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Cyclooxygenase-2 (COX-2) is an inducible form of the enzyme that catalyses the synthesis of prostanoids, including prostaglandin E2 (PGE2), a major mediator of inflammation and angiogenesis. COX-2 is overexpressed in cancer cells and is associated with progressive tumour growth, as well as resistance of cancer cells to conventional chemotherapy and radiotherapy. These therapies are often delivered in multiple doses, which are spaced out to allow the recovery of normal tissues between treatments. However, surviving cancer cells also proliferate during treatment intervals, leading to repopulation of the tumour and limiting the effectiveness of the treatment. Tumour cell repopulation is a major cause of treatment failure. The central dogma is that conventional chemotherapy and radiotherapy selects resistant cancer cells that are able to reinitiate tumour growth. However, there is compelling evidence of an active proliferative response, driven by increased COX-2 expression and downstream PGE2release, which contribute to the repopulation of tumours and poor patient outcome. In this review, we will examine the evidence for a role of COX-2 in cancer stem cell biology and as a mediator of tumour repopulation that can be molecularly targeted to overcome resistance to therapy.
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Reubi, J. C. "Central nervous system-mediated growth inhibition of a rat prostate carcinoma by an opioid." Journal of Endocrinology 107, no. 2 (1985): 247–50. http://dx.doi.org/10.1677/joe.0.1070247.
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ABSTRACT Long-term treatment for more than 3 months with a central nervous system (CNS)-active drug, the opioid agonist bremazocine, at a dose of 1 mg/kg per day elicited an 80% inhibition of the volume of the subcutaneously transplanted rat prostate adenocarcinoma Dunning R3327H. Whereas, under this therapy, prostate tumour and prostatic weights were decreased, testes and pituitary weights remained normal. Bremazocine inhibited not only the growth of freshly transplanted tumours but also that of well-grown Dunning prostate carcinomas since, after 41 days of treatment, such tumours showed a volume inhibition of 52%. In these experiments bremazocine decreased LH and testosterone plasma levels significantly. Bremazocine, therefore, probably acts mainly through suprapituitary CNS-opiate receptor sites, which indirectly, rather than locally, mediate LH inhibition. Indeed, no specific receptors for bremazocine could be found in the Dunning tumour, which makes a local action of bremazocine in this tissue unlikely. The efficient tumour growth inhibition through the supra-pituitary action of bremazocine makes such opiate drugs, which lack respiratory and side effects due to improper use, of potential interest for treatment of prostatic tumours. J. Endocr. (1985) 107, 247–250
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Marra, Giancarlo, Marco Oderda, Marco Allasia, Stefania Munegato, Steven Joniau, and Paolo Gontero. "A Review on the Management of Small Renal Masses: Active Surveillance Versus Surgery." Anti-Cancer Agents in Medicinal Chemistry 18, no. 7 (2018): 940–50. http://dx.doi.org/10.2174/1871520617666171113123443.
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Despite the rise of small renal tumour (SRMs) diagnosis and related surgeries, death rate of kidney cancer is increasing, suggesting a non-optimal management of SRMs. Active Surveillance (AS) for kidney cancer was introduced to deal with this paradox. However, incertitude remains on whether and when AS can replace surgery in selected patients. We performed a literature search, reviewed and discussed the evidence in favour of AS or surgery for SRMs. Histopathology and natural history of SRMs, including the percentage of benign tumours amongst SRMs, tumour growth rate, life expectancy of SRMs patients being generally older, and current results of AS series seem to support its use in selected groups. However, kidney cancer is a heterogeneous entity, metastasis and ≥T3a status can be found also for SRMs and no biomarkers or other parameters are available to identify lethal SRMs. Despite the recent improvement in the diagnostic and prognostic work through imaging modalities, renal biopsies and nomograms, the interpretation of a survival plot subjectively is still not possible. The majority of AS studies are retrospective and extensive level 1 evidence cohorts with long term follow up are lacking. No unanimity is present regarding inclusion and exclusion criteria to undergo AS, follow up timings and AS exit criteria. Surgery is the only definitive treatment and remains the current standard. A better understanding of kidney cancer biology and SRMs behaviour is needed to clarify the role of AS and its indications.
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GARCKE, HARALD, and KEI FONG LAM. "Well-posedness of a Cahn–Hilliard system modelling tumour growth with chemotaxis and active transport." European Journal of Applied Mathematics 28, no. 2 (2016): 284–316. http://dx.doi.org/10.1017/s0956792516000292.
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We consider a diffuse interface model for tumour growth consisting of a Cahn–Hilliard equation with source terms coupled to a reaction–diffusion equation. The coupled system of partial differential equations models a tumour growing in the presence of a nutrient species and surrounded by healthy tissue. The model also takes into account transport mechanisms such as chemotaxis and active transport. We establish well-posedness results for the tumour model and a variant with a quasi-static nutrient. It will turn out that the presence of the source terms in the Cahn–Hilliard equation leads to new difficulties when one aims to derivea prioriestimates. However, we are able to prove continuous dependence on initial and boundary data for the chemical potential and for the order parameter in strong norms.
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Därr, Roland, Jonas Kater, Peggy Sekula, et al. "Clinical decision making in small non-functioning VHL-related incidentalomas." Endocrine Connections 9, no. 8 (2020): 834–44. http://dx.doi.org/10.1530/ec-20-0208.
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The optimal treatment strategy for patients with small non-functioning VHL-related incidentalomas is unclear. We searched the Freiburg VHL registry for patients with radiologic evidence of pheochromocytoma/paraganglioma (PHEO/PGL). In total, 176 patients with single, multiple, and recurrent tumours were identified (1.84 tumours/patient, range 1–8). Mean age at diagnosis was 32 ± 16 years. Seventy-four percent of tumours were localised to the adrenals. Mean tumour diameter was 2.42 ± 2.27 cm, 46% were <1.5 cm. 24% of tumours were biochemically inactive. Inactive tumours were significantly smaller than active PHEO/PGL at diagnosis (4.16 ± 2.80 cm vs 1.43 ± 0.45 cm; P < 0.025) and before surgery (4.89 ± 3.47 cm vs 1.36 ± 0.43 cm; P < 0.02). Disease was stable in 67% of 21 patients with evaluable tumours ≤1.5 cm according to RECIST and progressed in 7. Time till surgery in these patients was 29.5 ± 20.0 months. A total of 155 patients underwent surgery. PHEO/PGL was histologically excluded in 4 and proven in 151. Of these, one had additional metastatic disease, one harboured another tumour of a different type, and in 2 a second surgery for suspected disease recurrence did not confirm PHEO/PGL. Logistic regression analysis revealed 50% probability for a positive/negative biochemical test result at 1.8 cm tumour diameter. Values of a novel symptom score were positively correlated with tumour size (Rs = 0.46, P < 0.0001) and together with a positive biochemistry a linear size predictor (P < 0.01). Results support standardised clinical assessment and measurement of tumour size and metanephrines in VHL patients with non-functioning incidentalomas <1.5 cm at one year following diagnosis and at individualised intervals thereafter depending on evolving growth dynamics, secretory activity and symptomatology.
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Ripamonti, M., G. Pezzoni, E. Pesenti, et al. "In vivo anti-tumour activity of FCE 23762, a methoxymorpholinyl derivative of doxorubicin active on doxorubicin-resistant tumour cells." British Journal of Cancer 65, no. 5 (1992): 703–7. http://dx.doi.org/10.1038/bjc.1992.148.
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Nagaraju, Santhosh, Ion Boiangiu, Ian Brown, Hussien El-Maghraby, and U. Pohl. "Intracranial myxoid mesenchymal tumour with EWSR1-ATF1 fusion mimicking high grade glioma." Neuro-Oncology 23, Supplement_4 (2021): iv23—iv24. http://dx.doi.org/10.1093/neuonc/noab195.059.
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Abstract Aims Molecular profiling is increasingly used in the diagnosis of CNS and non-CNS neoplasms. More than a quarter of all soft tissue tumours are characterized by specific recurrent chromosomal translocations which can be used as molecular signatures. With increasing frequency, EWSR1 rearrangements are found on both mesenchymal tumours and primary glial/neuronal tumours. Here we present a case of intracranial myxoid mesenchymal tumour (IMMT), a rare tumour which is becoming more recognised in recent years, affecting mainly children and young adults, and rarely older adults. It can be found in intraaxial and extraaxial location, with frequent dural connection. The tumour is defined by the genetic hallmark of EWSR1-CREB family gene fusion. Including our case, 16 intracranial tumours with this gene fusion have been reported to date. Our goal is to contribute further to the characterisation of the morphological spectrum, fusion partners and biological behaviour of rare EWSR1-CREB (non-ETS)-rearranged tumours of the CNS. Method Case: The patient is a 27 year old woman with a frontal lobe lesion, radiologically described as a tumour with dural attachment. She underwent surgical debulking, and tumour tissue was histologically examined with conventional immunohistochemistry. Additional genetic testing included targeted mutation screening, FISH, EPIC (Illumina BeadChip) methylation array and next generation sequencing. Histology showed a mitotically active neoplasm with relatively uniform cells, round nuclei and oligodendroglioma-like clear cell change, but no myxoid change. Glomeruloid microvascular proliferation and large areas of tumour necrosis were present. Immunohistochemistry was focally positive for GFAP, and negative or normal for synaptophysin, IDH1 R132H mutation, ATRX and p53. The ki-67 index reached ~20%. Sequencing of IDH1 and IDH2 did not reveal rare IDH mutations, and FISH did not show 1p19q codeletion. Testing for BRAF V600 mutation was negative. Results Although the histology initially suggested a diagnosis of oligodendroglioma, the integrated diagnosis was compatible with glioblastoma, IDH wildtype. Methylation array analysis by EPIC array did not result in classification of currently known entities, neither confirming glioblastoma, nor providing a new diagnosis, when analysed on both brain tumour and sarcoma classifier. This suggested a novel tumour entity not yet represented in the classifier algorithm. Additional testing including next generation sequencing revealed EWSR1 gene rearrangement with fusion partner ATF1 (EWSR1-ATF1 fusion). Based on this, the diagnosis was revised to the emerging new entity of ‘intracranial myxoid mesenchymal tumor’ (IMMT) characterised by EWSR1 fusion with members of the cAMP response element binding protein (CREB) family (ATF1, CREB1 and CREM). Subsequent immunohistochemistry demonstrated positive staining for CD99 and EMA but not desmin. The patient underwent various oncological treatments and is recurrence-free 3 years after initial diagnosis. Conclusion Histologically, IMMT demonstrates a spectrum of features that overlaps with other tumours, but often displays circumscribed growth, uniform cellularity, cytoplasmic clearing and variable myxoid change. The clinical behaviour of these tumours is not fully understood, however provisionally considered intermediate grade. EWSR1-CREB family fusion is not specific but shared with a diverse group of extracranial tumours including soft tissue, salivary gland, odontogenic and myoepithelial tumours. Therefore, clinico-radiologico-pathological correlation is essential to achieve the final diagnosis, and ensure the absence of a primary tumour elsewhere. Familiarisation with IMMT, its characteristic genetic profile and its as yet underreported natural course is crucial, as it can clinically mimic other intracranial tumours such as malignant meningioma or glioma but appears to behave less aggressively than high grade glioma. It is also important to further our understanding of its optimal treatment through review of larger case series and global comparison of patient management.
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Shiono, Junko, Hitoshi Horigome, Seiyo Yasui, et al. "Electrocardiographic changes in patients with cardiac rhabdomyomas associated with tuberous sclerosis." Cardiology in the Young 13, no. 3 (2003): 258–63. http://dx.doi.org/10.1017/s1047951103000507.
Full textAbstract:
Background:Cardiac rhabdomyomas associated with tuberous sclerosis induce various abnormalities in the electrocardiogram. Electrocardiographic evidence of ventricular hypertrophy may appear if the tumour is electrically active. To our knowledge, electrocardiographic evidence of ventricular hypertrophy has been reported only in association with congestive heart failure. Follow-up studies of changes in electrocardiographic findings are also lacking.Methods:We studied 21 consecutive patients with cardiac rhabdomyoma associated with tuberous sclerosis, 10 males and 11 females, aged from the date of birth to 9 years at diagnosis. The mean period of follow-up was 53 months. None of the patients developed congestive heart failure. We evaluated the electrocardiographic changes during the follow-up, and their association with echocardiographic findings.Results:Of the 21 patients, 12 showed one or more abnormalities on the electrocardiogram at presentation, with five demonstrating right or left ventricular hypertrophy. In all of these five cases, the tumours were mainly located in the respective ventricular cavity. In one patient with a giant tumour expanding exteriorly, there was marked left ventricular hypertrophy on the electrocardiogram. Followup studies showed spontaneous regression of the tumours in 12 of 19 patients, with abnormalities still present in only 7 patients. A gradual disappearance of left ventricular hypertrophy as seen on the electrocardiogram was noted in the patient with marked left ventricular hypertrophy at presentation in parallel with regression of the tumour.Conclusions:The presence of cardiac rhabdomyomas in patients with tuberous sclerosis might explain the ventricular hypertrophy seen on the electrocardiogram through its electrically active tissue without ventricular pressure overload or ventricular enlargement, although pre-excitation might affect the amplitude of the QRS complex. Even in cases with large tumours, nonetheless, the electric potential might not alter the surface electrocardiogram if the direction of growth of the tumour is towards the ventricular cavity. In many cases, electrocardiographic abnormalities tend to disappear, concomitant with regression of the tumours.
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Kutlvasr, K., K. Bukovjan, and R. Kodet. "Bilateral low grade serous adenocarcinoma of the ovaries in a badger (Meles meles L.) and its association with a borderline serous ovarian tumour: a case report." Veterinární Medicína 59, No. 1 (2014): 44–50. http://dx.doi.org/10.17221/7245-vetmed.
Full textAbstract:
Here, we describe a case of a wild female badger (a sow) with disseminated serous adenocarcinoma of the ovary which corresponds to a group of low grade serous carcinomas of the ovary in humans. Beside grossly apparent dissemination of the disease we observed a scale of histological features classifiable as a precursor lesion &ndash; borderline serous tumour of the ovary with implant metastases at the peritoneum, and features of the borderline tumour transformation in the carcinoma. The latter features included invasion of some of the metastatic peritoneal implants into the adipose tissue of the mesentery, retroperitoneum, and in the muscle of diaphragm with lymphangioinvasion and with blood-borne metastatic disease in the lungs. The primary tumour and its metastases had a uniform cytological appearance without atypia of the tumour cells. Mitotic activity was exceptional. The proliferation activity as demonstrated by immunohistochemical investigation of Ki-67 protein expression (revealing all active phases of the cell cycle &ndash; G1, S, G2, M) showed a low proliferation activity of the tumour cells, comparable with findings in low grade carcinomas or borderline tumours of the ovaries in women. WT1 protein was expressed in the whole tumour cell population. All these features were diagnostic of serous carcinoma of the ovary with low grade malignant potential. Tumours of the ovaries in wildlife have been described previously but they are infrequent and are rarely classified histopathologically. This case report offers a parallel with serous carcinomas in human pathology including features of transformation from a precursor lesion of a borderline serous tumour into a serous low grade carcinoma. &nbsp;
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NATHER, A., and I. H. SUTHERLAND. "Malignant Transformation of a Benign Cutaneous Mixed Tumour." Journal of Hand Surgery 11, no. 1 (1986): 139–43. http://dx.doi.org/10.1016/0266-7681_86_90039-2.
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Whilst benign cutaneous mixed tumour is common, malignant cutaneous mixed tumour is rare. There are only eleven accepted cases of the malignant counterpart in the literature. In none was there residual benign tumour tissue present to suggest that they arose from malignant transformation of the benign tumour. We report a very rare case of a malignant transformation of a benign cutaneous mixed tumour in an eighty-four year old female. Other unusual features in this case included considerable involvement of bone in the primary lesion and the histological picture of extreme pleomorphism and active mitoses, not seen in other reported cases of the malignant tumour.