Relevant bibliographies by topics / Tumour metastasis

Academic literature on the topic 'Tumour metastasis'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Tumour metastasis"

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Tang, Phua Hwee, and Sameema Nisa. "MEDB-10. Comparing pediatric medulloblastoma with and without spinal metastasis." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i106. http://dx.doi.org/10.1093/neuonc/noac079.385.

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Abstract AIM: To compare pediatric medulloblastoma with and without spinal metastasis METHODOLOGY: Pediatric medulloblastoma cases from 1999 to 2021 were retrospectively reviewed in this Institutional Review Board approved study. Imaging reports, presence of spinal drop metastases at diagnosis, degree of tumor excision, treatment given and survival status were captured. RESULTS: Brain and spine imaging at diagnosis was available in 54 medulloblastoma patients with no drop metastasis and in 7 with drop metastasis. Largest tumor dimension at presentation is 4.54 ± 0.94 cm with those with drop metastasis, similar to the 4.43 ± 0.94 cm in those without drop metastasis (p = 0.79). For the 54 medulloblastomas with no drop metastasis, 44 (81%) were completely excised, 9 (17%) partially excised and there was no follow up for 1. For the 7 medulloblastomas with drop metastasis, 3 (43%) of the primary tumours were completely excised, 3 (43%) partially excised and there was no follow up for 1. Post operative chemo/radiotherapy was given to 48 of the 54 with no drop metastasis, not given for 1 with no information available for 5. Chemo/radiotherapy was given to 6 of the 7 with drop metastasis with no information available for 1. At 1 year follow up of the 54 with no spinal drop metastasis at diagnosis , 42 remain tumour free, 3 have tumour, 4 are deceased and 5 are lost to follow up. At 1 year follow up of the 7 with drop metastasis, 2 are free of tumour, 2 have tumour and 3 are lost to follow up. Higher percentage of medulloblastomas without drop metastasis are completely excised (p<0.01). No significant difference between postoperative chemotherapy/radiation rates between groups CONCLUSION: Most medulloblastomas do not have spinal drop metastasis at diagnosis and complete excision is more frequently in those without drop metastasis.
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Honma, K., K. Hara, and T. Sawai. "Tumour-to-tumour metastasis." Virchows Archiv A Pathological Anatomy and Histopathology 416, no. 2 (March 1989): 153–57. http://dx.doi.org/10.1007/bf01606320.

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Pickford, Ian, and G. D. Birnie. "Tumour metastasis." Lancet 340, no. 8815 (August 1992): 372–73. http://dx.doi.org/10.1016/0140-6736(92)91447-g.

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Ferronika, Paranita, Joost Hof, Gursah Kats-Ugurlu, Rolf H. Sijmons, Martijn M. Terpstra, Kim de Lange, Annemarie Leliveld-Kors, Helga Westers, and Klaas Kok. "Comprehensive Profiling of Primary and Metastatic ccRCC Reveals a High Homology of the Metastases to a Subregion of the Primary Tumour." Cancers 11, no. 6 (June 12, 2019): 812. http://dx.doi.org/10.3390/cancers11060812.

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While intratumour genetic heterogeneity of primary clear cell renal cell carcinoma (ccRCC) is well characterized, the genomic profiles of metastatic ccRCCs are seldom studied. We profiled the genomes and transcriptomes of a primary tumour and matched metastases to better understand the evolutionary processes that lead to metastasis. In one ccRCC patient, four regions of the primary tumour, one region of the thrombus in the inferior vena cava, and four lung metastases (including one taken after pegylated (PEG)-interferon therapy) were analysed separately. Each sample was analysed for copy number alterations and somatic mutations by whole exome sequencing. We also evaluated gene expression profiles for this patient and 15 primary tumour and 15 metastasis samples from four additional patients. Copy number profiles of the index patient showed two distinct subgroups: one consisted of three primary tumours with relatively minor copy number changes, the other of a primary tumour, the thrombus, and the lung metastases, all with a similar copy number pattern and tetraploid-like characteristics. Somatic mutation profiles indicated parallel clonal evolution with similar numbers of private mutations in each primary tumour and metastatic sample. Expression profiling of the five patients revealed significantly changed expression levels of 57 genes between primary tumours and metastases, with enrichment in the extracellular matrix cluster. The copy number profiles suggest a punctuated evolution from a subregion of the primary tumour. This process, which differentiated the metastases from the primary tumours, most likely occurred rapidly, possibly even before metastasis formation. The evolutionary patterns we deduced from the genomic alterations were also reflected in the gene expression profiles.
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Tulotta, Claudia, and Penelope Ottewell. "The role of IL-1B in breast cancer bone metastasis." Endocrine-Related Cancer 25, no. 7 (July 2018): R421—R434. http://dx.doi.org/10.1530/erc-17-0309.

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Approximately 75% of patients with late-stage breast cancer will develop bone metastasis. This condition is currently considered incurable and patients’ life expectancy is limited to 2–3 years following diagnosis of bone involvement. Interleukin (IL)-1B is a pro-inflammatory cytokine whose expression in primary tumours has been identified as a potential biomarker for predicting breast cancer patients at increased risk for developing bone metastasis. In this review, we discuss how IL-1B from both the tumour cells and the tumour microenvironment influence growth of primary breast tumours, dissemination into the bone metastatic niche and proliferation into overt metastases. Recent evidence indicates that targeting IL-1B signalling may provide promising new treatments that can hold tumour cells in a dormant state within bone thus preventing formation of overt bone metastases.
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Gründker, Carsten, Matthias Läsche, Johanna Hellinger, and Günter Emons. "Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism." Geburtshilfe und Frauenheilkunde 79, no. 02 (February 2019): 184–88. http://dx.doi.org/10.1055/a-0805-9113.

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AbstractTumour metastasis is responsible for more than 90% of tumour-associated mortality. About one third of breast cancer patients in the early stage develop metastases. The transformation in tumour development referred to as the “metastatic cascade” or “metastatic cycle” is a complex and multi-stage event. While it is generally recognised that epithelial-mesenchymal transformation (EMT) plays a crucial role in cancer progression and metastasis, the metabolic events in this process have received little attention to date. We would therefore like to provide a brief overview here of the influence of the metabolism on the progression and metastasis of tumours.
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Zheng, Xiuli, Mingli Wu, Limian Er, Huiyan Deng, Gongning Wang, Lingyao Jin, and Shengmian Li. "Risk factors for lymph node metastasis and prognosis in colorectal neuroendocrine tumours." International Journal of Colorectal Disease 37, no. 2 (January 8, 2022): 421–28. http://dx.doi.org/10.1007/s00384-021-04082-7.

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Abstract Purpose The detection rate of colorectal neuroendocrine tumours (CR-NETs) is increasing, but their treatment is still controversial. Lymph node metastasis is an important reference index for the selection of treatment. The aim of our study was to investigate the factors associated with lymph node metastasis and prognosis of CR-NETs. Methods The case characteristics of patients with colorectal neuroendocrine tumours from January 2011 to December 2020 were retrospectively analysed, including age, gender, tumour size, tumour location, lymph node metastasis, pathological grade and follow-up. Results A total of 195 cases of CR-NETs were included in this study. When 15 mm was used as the cut-off value, the sensitivity, specificity and area under the curve (AUC) of lymph node metastases were 95.9%, 95.2% and 0.986, respectively. Multivariate analysis suggested that tumour size ≥ 15 mm (OR: 30.517, 95% CI: 1.250 ~ 744.996, p = 0.036) and lymphovascular invasion (OR: 42.796, 95% CI: 2.882 ~ 635.571, p = 0.006) were independent risk factors for lymph node metastasis. Age ≥ 56 (HR: 7.434, 95% CI: 1.334 ~ 41.443, p = 0.022) and distant metastasis (HR: 24.487, 95% CI: 5.357 ~ 111.940, p < 0.001) were independent prognostic factors in multivariable analyses. Conclusions When the size of a CR-NET is ≥ 15 mm, the risk of lymph node metastasis is higher, and it is recommended to choose the surgical method carefully. Tumour size and lymphovascular invasion were independent risk factors for lymph node metastasis. Age ≥ 56 and distant metastasis were independent prognostic factors.
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Melis, Céline, Florence Ballaux, and Claire Bourgain. "Curious Residents of the Thyroid Gland: Two Case Reports of Colorectal Carcinoma Metastasis by Fine-Needle Aspiration Diagnosis." Acta Cytologica 62, no. 5-6 (2018): 443–49. http://dx.doi.org/10.1159/000490367.

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Background: The most frequent metastases to the thyroid originate in the kidney, lung or breast. Colorectal adenocarcinoma represents less than 4% of metastases to the thyroid gland. Solitary metastases of colorectal cancer with no other manifestation of disseminated cancer disease are exceedingly rare. Within the Bethesda Classification for Reporting ­Thyroid Cytopathology, metastases are included in Diagnostic Categories “Suspicious for Malignancy” and “Malignant.” Cases: We present 2 cases of colorectal adenocarcinoma metastatic to the thyroid gland, diagnosed by fine-needle aspiration (FNA). One metastasis occurred in normal thyroid parenchyma; the other was a tumour-to-tumour metastasis into a follicular carcinoma of the thyroid. The latter is the first published tumour-to-tumour metastasis of a colorectal carcinoma in the thyroid from which both components were diagnosed by FNA. Conclusion: Diagnosing a metastasis to the thyroid is challenging. On FNA, a dual cell population should raise suspicion. Immunocytochemical and molecular analysis may be helpful. Clinical information is essential in guiding specific ancillary technique panels in scant cellular material.
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Bashyam, A., V. Grammatopoulou, T. Crook, S. Di Palma, and VS Sunkaraneni. "Tumour-to-tumour metastasis: breast carcinoma to an olfactory neuroblastoma." Annals of The Royal College of Surgeons of England 102, no. 6 (July 2020): e118-e121. http://dx.doi.org/10.1308/rcsann.2020.0038.

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Tumour-to-tumour metastasis is a rare phenomenon. It occurs when a primary tumour is a recipient of a separate tumour within the same individual. We present a case of a 66-year-old woman with known breast cancer who presented with one-sided nasal symptoms. Examination and imaging revealed a unilateral polyp arising from the skull base. She underwent endoscopic polypectomy with the histology demonstrating tumour-to-tumour metastasis from a breast carcinoma to an olfactory neuroblastoma, a rare sinonasal tumour. Clinicians should be cautious of distant metastases in any patient presenting with head and neck symptoms and a known primary tumour. This is the first documented case of this type.
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Srirajaskanthan, R., K. Desai, A. Jayaratnam, E. Carras, C. Toumpanakis, T. Meyer, and M. Caplin. "Uncommon sites for metastasis of neuroendocrine tumor in adults." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e15683-e15683. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e15683.

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e15683 Background: Neuroendocrine tumours are relatively slow growing tumours. They often present with significant metastatic disease affecting liver, lymph nodes, lungs and bone. However tumour masses may be found at unusual/uncommon sites e.g. breast, orbital soft tissue and the heart raising the possibility of this being metastatic focus or presence of another primary tumour. Detection of these sites could have a significant impact on the available treatment options. Aim: to determine the most appropriate imaging modality and type of tumour metastases. Methods: We reviewed 300 consecutive clinic patients. We identified 18 patients with metastasis at uncommon sites i.e. breast, orbital and cardiac. We retrospectively evaluated clinical notes and recent radiological investigations of these patients. To characterise these lesions additional investigations included cross sectional imaging, PET imaging (68Gallium DOTA Octreotate PET and 18F- FDG PET) and histological evaluation of the metastasis where appropriate. Patients with breast metastasis underwent bilateral mammogram, patients with peri-ocular involvement underwent MRI of the brain and the orbit. Results: 18 patients had tumour masses at uncommon sites. Of these 15 masses were in the breast; 4 were in the orbital muscles and 2 patients had pericardial metastasis. Of the 15 patients with breast lesions 12 had confirmed neuroendocrine tumour metastases and 3 had breast cancer. It should be noted that breast cancer lesions were positive on the 68Gallium Octreotate PET imaging. One patient who had a defined metastasis in the pericardium showed avid uptake on the 68Gallium DOTA Octreotate PET and scan and cardiac MRI, the other patient had pericardial metastases confirmed at post mortem. Conclusions: Clear knowledge of these uncommon sites of metastasis is useful in terms of arranging further investigations and excluding other cancers. It is also important to realise that although somatostatin receptor scintigraphy especially 68Gallium DOTA Octreotate PET is very useful in detecting NET metastasis, it may also show avid uptake in patients with breast cancer and hence histological evaluation of these lesions are important. Undoubtedly within our cohort of patients and generally there is an under-diagnosis of lesions in uncommon sites. No significant financial relationships to disclose.
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Dissertations / Theses on the topic "Tumour metastasis"

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Clark, S. R. "The investigation of tumour metastasis." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370241.

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Knight, C. Rosamund L. "Transglutaminase activity, tumour growth and metastasis." Thesis, Nottingham Trent University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278115.

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Hand, D. "The importance of transglutaminase in tumour growth and metastasis." Thesis, Nottingham Trent University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382575.

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Chen, Dongsheng. "Transcriptional regulation of the p9Ka gene in metastatic and non-metastatic rat mammary epithelial cells." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266488.

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Li, Chao. "Investigation of the influence of tissue factor on tumour metastasis." Thesis, University of Hull, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441584.

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Royston, Daniel John. "The role of LYVE-1 in tumour metastasis and inflammation." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558401.

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The lymphatic metastasis of tumours to lymph nodes (LN) is a frequent event in many cancers and heralds a poor clinical outcome. Comparison of lymphatic endothelial cells (LECS) from metastasizing murine T-241/VEGF-C fibrosarcomas and normal dermis revealed a tumour-specific LEC profile, characterized by the elevated expression of functionally significant molecules such as endothelial specific adhesion molecule (ESAM) and the TGF-~ coreceptor endoglin (CD105). Moreover, similar induction of ESAM and endoglin by human tumour Iymphatics was seen to dramatically correlate with LN metastasis. To further investigate interactions between tumour cells and Iymphatics, the role of lymphatic endothelial hyaluronan receptor LYVE-1 in LN metastasis was investigated. Using LYVE-1 mAbs and LYVE-1-1- mice, it was shown that a deficiency or perturbation of LYVE-1 expressed by tumour Iymphatics potentiated the lymphatic spread of spontaneously metastasizing T-241/VEGF-C fibrosarcomas and induced de novo metastasis by indolent parental T-241 tumours. Subsequent in vitro experiments using mAbs suggested that LYVE-1 exerts a blocking or 'gatekeeper' function, preventing pro-metastatic tumour cell-LEC interactions. Although largely restricted to the Iymphatics, LYVE-1 is also expressed in murine lung by type I alveolar epithelial cells (AECs). Using a bleomycin model of lung inflammation it was shown that LYVE-1-1- mice are unable to clear infiltrating leukocytes following acute lung injury. Furthermore, in vivo and in vitro experiments using blocking mAb reveal a critical role for LYVE-1 in the transepithelial migration of leukocytes across the alveolar epithelium, an essential step in the resolution of acute lung inflammation. These findings identify a specific role for LYVE-1 in cancer metastasis and the resolution of acute inflammation in the lung.
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Texler, Michael Lutz. "Aetiology of tumour cell movement during laparoscopic surgery : patterns of movement and influencing factors." Title page, table of contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09MD/09mdt355.pdf.

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Accompanying CD-ROM contains image files and software. Bibliography: leaves 259-286. Explores the factors affecting the movement of tumour cells from a primary malignancy across the peritoneal cavity to the port-site following laparoscopic intervention. Filter methods and radio-labelled tumour cells provided the most useful way of following cell movement. Concludes spread of tumour cells to the port-site is more likely in the presence of disseminated disease, as well as with inappropriate surgical technique. Metastasis may be reduced by the use of intraperitoneal lavage and appropriate surgical technique.
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Jack, A. S. "A study of the factors which affect the growth of tumour cells at distant sites." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381493.

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Lundberg, Owe. "Laparoscopy and tumour growth : a clinical and experimental study." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-227.

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Balathasan, Lukxmi. "Characterising the role of circulating immune cells in brain metastasis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:e7620d30-7e4a-468b-b819-db4cf27eaef6.

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Brain metastasis is a frequent occurrence in cancer patients and carries a high mortality rate. The incidence of brain metastasis is on the rise, highlighting the need for improved therapeutic intervention. Immune cells have been shown to promote disseminated tumour cells to colonise the lung and liver. Therefore, we aim to determine whether immune cells also facilitate brain metastasis by describing the host immune response to tumour cells attached to the brain vasculature. We developed a model of brain metastasis by using ultrasound guidance to perform intracardiac injection of tumour cells. Using this method, we identified highly and weakly brain metastatic cell lines. To understand how cancer cells develop into brain metastases, we analysed brains harvested 4 h- 14 d after tumour injections. At 4 h after intracardiac injection, only cell lines that developed into brain metastases were found adhered to the brain vasculature in high numbers. A small number of arrested tumour cells clustered with CD45⁺ immune cells. These tumour-CD45 clusters persisted over time whilst the frequency of solitary tumour cells declined. Tumour-associated CD45⁺ immune cells were identified to be Ly6G⁺Gr-1⁺CD11c⁻ myeloid cells. Considerably more tumour-CD45⁺ immune cell clusters were found within the brain vasculature when tumour cells were injected into mice bearing a primary tumour. Increased tumour-CD45⁺ immune cells clusters correlated with an increased number of brain metastases in the same group of mice. We also found a positive association between increased tumour-immune clusters and levels of tumour and host derived G-CSF. To establish a causal relationship between tumour cell-CD45 clusters and metastases, we developed an experimental setup for transcranial imaging. Our results suggest that tumour recruited immune cells may promote tumour cell colonisation of the brain and provides a framework for further investigation.
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Books on the topic "Tumour metastasis"

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Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Carcinogenesis and tumour progression. Budapest: Akadémiai Kiadó, 1987.

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Windle, J. M. The role of transglutaminase in tumour growth and metastasis. Birmingham: University of Birmingham, 1985.

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M, Chadwick C., ed. Receptors in tumour biology. Cambridge: Cambridge University Press, 1986.

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Banfalvi, Gaspar. Homeostasis - Tumor - Metastasis. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7335-6.

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T, Galeotti, ed. Cell membranes and cancer: Proceedings of the Second International Workshop on Membranes in Tumour Growth, Rome, Italy, June 17-20, 1985. Amsterdam: Elsevier Science, 1985.

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Dickson, Robert B., and Marc E. Lippman, eds. Mammary Tumor Cell Cycle, Differentiation, and Metastasis. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1259-8.

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Motomichi, Torisu, Yoshida Takeshi, and International Symposium on Basic Mechanisms and Clinical Treatments of Tumor Metastasis (1982 : Fukuoka-shi, Japan), eds. Basic mechanisms and clinical treatment of tumor metastasis. New York: Academic Press, 1985.

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Akira, Watanabe, ed. Cancer metastases research. New York: Nova Science Publishers, 2008.

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Cardona, Kenneth, and Shishir K. Maithel, eds. Primary and Metastatic Liver Tumors. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91977-5.

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E, Abrey Lauren, Chamberlain Marc C, and Engelhard Herbert H, eds. Leptomeningeal metastases. New York: Springer, 2005.

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Book chapters on the topic "Tumour metastasis"

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Teh, Catherine S. C. "Multidisciplinary Liver Tumour Board." In Colorectal Liver Metastasis, 511–20. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-09323-4_54.

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Hou, Jing, Zhipeng Han, Naping Zhao, and Lixin Wei. "Autophagy and Tumour Metastasis." In Autophagy: Biology and Diseases, 315–38. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-4272-5_22.

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Tille, Jean-Christophe, Riccardo Nisato, and Michael S. Pepper. "Lymphangiogenesis and Tumour Metastasis." In Novartis Foundation Symposia, 112–36. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470856734.ch9.

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Schiller, Erich. "Tumour Proliferation and Metastasis." In Free Radicals and Inhalation Pathology, 735–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18619-6_20.

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Millican, A., T. S. Baker, N. R. A. Beeley, M. Birch, B. A. Boyce, S. Chander, M. Cockett, et al. "Gelatinase inhibitors and tumour metastasis." In Peptides 1994, 73–74. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_24.

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Lefebvre, Karen J., Sarah Assadian, Wissal El-Assaad, and Jose G. Teodoro. "Regulation of Angiogenesis by Tumour Suppressor Pathways." In Experimental and Clinical Metastasis, 79–99. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3685-0_8.

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Raz, Avraham. "Adhesive Properties of Metastasizing Tumour Cells." In Ciba Foundation Symposium 141 - Metastasis, 109–22. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513736.ch7.

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Kandel, Jessica J., Darrell J. Yamashiro, and Jan Kitajewski. "Angiogenesis in Tumour Development and Metastasis." In Therapeutic Angiogenesis for Vascular Diseases, 81–93. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9495-7_4.

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Sherbet, G. V. "Oncogenes in Tumour Development and Metastasis." In The Metastatic Spread of Cancer, 81–122. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-09577-3_5.

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Eichten, Alexandra, Karin E. de Visser, and Lisa M. Coussens. "Macrophages in tumour development and metastasis." In Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response, 115–37. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7_8.

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Conference papers on the topic "Tumour metastasis"

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Ricetti, M. M., A. Samaden, V. Fregoni, M. Vigotti, F. Piovella, and E. Ascari. "TUMOR CELLS INTERACTIONS WITH SUBENDOTHELIAL EXTRACELLULAR MATRIX IN A PERFUSION SYSTEM: ROLE OF PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643197.

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It has been suggested that platelets may facilitate tumor metastasis by increasing tumour cell (TC) adhesion to vascular endothelium mainly through the formation of platelet/TC aggregates. In order to further investigate this we have utilized an in vitro model combining extracellular matrices (EM) from cultured vascular endothelial cells and two neoplastic clones from a mFS6 murine fibrosarcoma: one expressing high metastatic potency (M4) and one with low metastatic potential (M9). These two sublines express an in vitro platelet aggregating activity which has previously been characterized and which correlates with in vivo metastasizing capacity. To reproduce the in vivo flow conditions a flat perfusion chamber was used (*). Glass coverslips, carrying the EM were perfused for 10’ at a wall shear rate of 450 sec™1 with reconstituted heparinized human blood containing 3×10s/ml TC, with or without platelets. Coverage of the EM with adherent TC was evaluated by a morphometric method and expressed as percent TC coverage. M4 cells adhered to EM more than did M9 cells: 4.3% TC coverage for M4, versus 2.5% TC coverage for M9. In the presence of platelets, TC adherence was greatly increased, being 9.7% for M4 and 7.8% for M9. In the experiments performed in the presence of thrombocytes no platelet/TC thrombi were found onto the EM and no TC-induced platelet aggregation was detected in blood after perfusion. Our results confirm that platelets favour the occurrence of metastasis and suggest that other mechanisms than platelet/TC aggregates formation might be involved in this process.(*) K.S. Sakarlassen et al. J.Lab.Cl in.Med. 102:522, 1983
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Satyaprakash, Mathur Neha, Pratibha Singh, and Suyasha Vyas. "Early stage adenocarcinoma of cervix with ovarian micrometastasis." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685281.

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Introduction: Adenocarcinoma of cervix is a rare malignancy of cervix. It is an aggressive tumour with high incidence of metastasis. Ovarian metastasis in early stage adenocarcinoma is rare. Metastasis is usually seen when there is some other coexisting finding. In premenopausal patient and low risk category, ovarian metastasis is very rare. Case Report: The present case is a 40 yrs old parous women, with complaints of discharge per vaginum. Her colposcopy showed an erosion on the lower lip. Radical hysterectomy with bilateral oophorectomy was planned. The histopathology was a well differentiated adenocarcinoma with surface ovarian metastasis on one side. Discussion: Early stage adenocarcinoma of cervix can rarely present with ovarian metastasis. Thus radical surgery with oophorectomy is a an aggressive but practical approach in these patients.
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Parish, Christopher, David Armitt, Ligong Liu, Craig Freeman, Anna Bezos, Vito Ferro, and Martin Banwell. "SULFATED OLIGOSACCHARIDE-BASED INHIBITORS OF TUMOUR GROWTH AND METASTASIS." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.367.

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Costa, Rafael Everton Assunção Ribeiro da, Fergus Tomás Rocha de Oliveira, Eduarda Norberto Siqueira, Ana Lúcia Nascimento Araújo, and Sabas Carlos Vieira. "CUTANEOUS AND BONE METASTASIS OF OCCULT BREAST CANCER: CASE REPORT." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2078.

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Introduction: Occult breast cancer (OBC) is defined as a metastatic carcinoma that occurs mainly in the axillary lymph nodes, derived from a primary malignant breast tumor undetectable by clinical and radiological analyses. OBC is a rare disease accounting for 0.3%–1.0% of all breast cancers, which occurs more commonly at the age of around 55 years. The OBC represents a rare event (especially with the manifestation of systemic metastases) and a major diagnostic challenge. Thus, the aim of this study was to report a case of OBC with the primary manifestation of cutaneous metastases and the subsequent detection of bone metastasis. Case report: A 70-year-old female patient, G1P0A0, nonsmoker, nonalcoholic, with hypertension, and sedentary lifestyle, exhibited multiple metastatic cutaneous lesions in the left cervical region (2 cm), of the left breast (3 cm), left axilla (0.5 cm), left subscapular region (3 cm), and in the second and fifth left chirodactyls (using anastrozole for 1 month). Mammography, ultrasonography, and magnetic resonance imaging of the breast were performed, and no structural alterations were detected in any of these tests. Biopsy of the skin lesion of the left cervical region and immunohistochemistry also indicated positive estrogen receptors (ER), progesterone receptors (PR), and GATA-binding protein 3 (GATA-3; compatible with breast cancer metastasis), establishing the diagnosis of occult breast cancer with cutaneous metastasis. The use of anastrozole was maintained. The scintigraphy was performed, indicating bone metastasis in the right coastal arcs 8 and 9 considered stable in a new test performed 8 months later. All cutaneous metastatic lesions disappeared 2 years later, with the exception of a lesion in the left cervical region, where surgical resection was indicated. The study was approved by a Research Ethics Committee, under CAAE No 30154720.0.0000.5209. Conclusion: The patient exhibited an excellent response to anastrozole and is in excellent general condition with the stability of bone metastasis.
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Tang, Xin, and Taher Saif. "In Vitro Cancer Metastasis Induced by Mechanical Force." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93130.

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Based on the American Cancer Society’s report at 2004, after 50-year’s efforts in bio-chemical medicine development, the U.S.A. cancer mortality is 193.9 per 100,000 persons, which is not significantly reduced from that at 1950, 185.8 per 100,000 persons. One critical reason for the clinical inefficacy is that it is not identified what signals trigger the onset of metastasis. 90% of cancer deaths are caused by metastases (1–6). During metastasis, malignant cancer cells detach from the parent cancer tumor to invade new organs (5–7). Although the primary tumor can be readily removed by surgery if detected in time, metastasis cannot be cured effectively due to the presence of numerous secondary tumors. Here we present, for the first time, that cancer cells can exhibit metastasis like phenotype (MLP) in vitro when they are experiencing appropriate mechanical stimuli.
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Cydenova, I. A., M. M. Cyganov, M. K. Ibragimova, A. A. Nushtaeva, and N. V. Litvyakov. "MECHANISMS OF ESCAPE FROM REPLICATIVE SENESCENCE OF TUMOUR CELLS AFTER EXPOSURE TO CHEMOTHERAPY." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-147.

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In 25% of patients with breast cancer, tumor cells after neoadjuvant chemotherapy (NAHT) leave the state of replicative aging and form macrometastases. In patients with breast cancer, it was shown that the exit from replicative aging with metastasis is observed only in those patients in whose tumor WNT signaling is ectopically activated due to amplification of activator genes and deletions of negative regulators of this signaling pathway. Purpose: in a direct experiment on cell cultures differing in ectopic activation of WNT signaling due to CNA (Copy Number Aberration) WNT signaling genes, to study the ability of tumor cells to exit replicative senescence after exposure to chemotherapy drugs.
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Liu, Ping, Xiaomin Ren, and Lisa X. Xu. "Alternate Cooling and Heating Thermal Physical Treatment: An Effective Strategy Against MDSCs in 4T1 Mouse Mammary Carcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80229.

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An alternate thermal physical treatment was developed to destroy tumor tissue using liquid nitrogen cooling and RF heating treatment in our pervious study. Our pervious reports had shown that anti-tumor immunity was induced by the alternate treatment. Myeloid derived suppressor cells (MDSCs) are a subset of heterogeneous, bone marrow derived hematopoietic cells that accumulate in the spleen, bone marrow, blood and tumor sites of tumor-bearing mice and cancer patients. MDSCs are one of the key suppressor cells that regulate anti-tumor immune responses in tumor-bearing hosts. MDSCs have been shown to inhibit the function of various types of cells mediating anti-tumor immunity, such as T cells, B cells, NK cells and dendritic cells. MDSCs are recruited specifically to the tumors and contribute indirectly to angiogenesis, growth and metastasis. MDSCs also exert resistance to cancer therapies, such as anti-VEGF strategies and cancer immunotherapy. Given the role of MDSCs in tumor invasion and metastasis and anti-tumor immune responses, therapeutics targeting MDSCs might offer a new strategy for cancer treatment. In this study, the therapeutic effect and MDSCs changes after the alternate cooling and heating treatment was studied using the 4T1 murine mammary carcinoma, a common animal model of human metastatic breast cancer. Due to its highly invasive and poorly immunogenic characters, the 4T1 tumor could cause death even after the primary tumor was surgically removed. The treatment was carried out when micro-metastases were well established. Comparisons were made with the results from the surgery and hyperthermia groups, respectively. The results showed that MDSCs in blood increased rapidly with time after tumor inoculation, and in 66 days, all the mice died in the control group. The statistical results indicated a significant increase in circulating MDSC numbers at different tumor growth stages. In the surgical resection group, MDSCs in blood did not decrease, but increased rapidly to a level much higher that of the control group in 39 day after tumor inoculation. In the hyperthermia group, MDSCs in blood increased rapidly with time after tumor inoculation, and in 39 day, MDSCs was up to 3 times higher than that of the control group. Mice died in 45 day after initial tumor inoculation. But in the alternate treatment group, the number of MDSCs decreased rapidly and recovered to the normal healthy level in 11 days after the treatment. No metastatic tumor could be observed in these mice, and they were in good physiological conditions as observed in the following 3 month. In conclusion, the alternate treatment was found extremely effective against MDSCs in the very aggressive and highly metastatic mouse mammary carcinoma. The good prognosis was expected in relation to the significant decrease in MDSCs and thus the relief of the immune suppression, induced by the alternate cooling and heating treatment. It could be further developed as a novel therapeutic method against metastatic tumor. On the other hand, combining the alternate treatment with other strategies, such as anti-VEGF and cancer immunotherapy, the best therapeutic effect would be achieved through synergy.
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Lorentzen, A., PF Becker, M. Saini, D. Mihic-Probst, U. Protzer, A. Trumpp, CA Klein, B. Polzer, L. Borsig, and M. Heikenwalder. "PO-187 Liquid-phase polarity facilitates attachment, adhesion and metastasis of tumour cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.226.

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Chiu, Kuo-Liang, Ting-Ting Kuo, Qian-Yu Kuok, Liang-Chuan Lai, and Yuh-Pyng Sher. "ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumour metastasis." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2842.

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Batista, Silvia A., Louise Reynolds, Bernardo Tavora, and Kairbaan Hodivala-Dilke. "Abstract 517: Deficiency of FAK in the bone marrow compartment enhances tumour metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-517.

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Reports on the topic "Tumour metastasis"

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Prestwich, Glenn D. Targeted Chemotherapy of Tumors and Metastases With Hyaluronic Acid-Anti-Tumor Bioconjugates. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada398191.

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Prestwich, Glenn D. Targeted Chemotherapy of Tumors and Metastases With Hyaluronic Acid-Anti-Tumor Bioconjugates. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada383364.

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Nie, Daotai. Targeting Tumor Oct4 to Deplete Prostate Tumor and Metastasis Initiating Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613791.

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Price, Janet. Tumor-Host Interaction in Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada446814.

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Zhan, Xi. The Role of Actin Polymerization in Tumor Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada431324.

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Zhan, Xi. The Role of Actin Polymerization in Tumor Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411545.

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Price, Janet E. Tumor-Host Interactions in Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418048.

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Zhan, Xi. The Role of Actin Polymerization in Tumor Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada420763.

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Condeelis, John. Metastatic Tumor Cell Behavior in Situ. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada361604.

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Condeelis, John. Metastatic Tumor Cell Behavior In Situ. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada336000.

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