Relevant bibliographies by topics / Metastatic cancer

Academic literature on the topic 'Metastatic cancer'

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

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Journal articles on the topic "Metastatic cancer"

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Yuk, Hyeong-Dong, Kyoung-Hwa Lee, Hye-Sun Lee, Seung-Hwan Jeong, Yongseok Kho, Chang-Wook Jeong, Hyeon-Hoe Kim, Ja-Hyeon Ku, and Cheol Kwak. "PDLIM2 Suppression Inhibit Proliferation and Metastasis in Kidney Cancer." Cancers 13, no. 12 (June 15, 2021): 2991. http://dx.doi.org/10.3390/cancers13122991.

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We evaluated the expression of PDLIM2 in human kidney cancer cell lines from primary or metastatic origins and found that PDLIM2 expression was highly elevated in metastatic kidney cancers. We evaluated the effect of PDLIM2 inhibition by RNA interference method. PDLIM2 knockdown showed the decreased proliferation and metastatic character in human metastatic kidney cancer cells. By repeated round of orthotopic injection of RenCa mouse kidney cancer cell line, we obtained metastatic prone mouse kidney cancer cell lines. PDLIM2 expression was highly expressed in these metastatic prone cells comparing parental cells. In addition, we evaluated the in vivo efficacy of PDLIM2 knockout on the tumor formation and metastasis of kidney cancer cells using a PDLIM2 knockout mice. The experimental metastasis model with tail vein injection and orthotopic metastasis model injected into kidney all showed reduced lung metastasis cancer formation in PDLIM2 knockout mice comparing control Balb/c mice. Overall, our findings indicate that PDLIM2 is required for cancer formation and metastasis in metastatic kidney cancer, indicating that PDLIM2 may be a new therapeutic target for metastatic kidney cancer.
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Singh Randhawa, Amritjot. "Metastatic Breast Cancer to the Uterine Cervix Mimicking Cervical Cancer." Indian Journal of Cancer Education and Research 8, no. 1 (June 1, 2020): 49–52. http://dx.doi.org/10.21088/ijcer.2321.9815.8120.8.

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Chen, Chao, Haozhen Liu, Qumiao Xu, Xiuqing Zhang, Feng Mu, and Jixian Liu. "Association of PTPRT Mutations with Cancer Metastasis in Multiple Cancer Types." BioMed Research International 2022 (June 25, 2022): 1–9. http://dx.doi.org/10.1155/2022/9386477.

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Metastasis is one of the characteristics of advanced cancer and the primary cause of cancer-related deaths from cancer, but the mechanism underlying metastasis is unclear, and there is a lack of metastasis markers. PTPRT is a protein-coding gene involved in both signal transduction and cellular adhesion. It is also known as a tumor suppressor gene that inhibits cell malignant proliferation by inhibiting the STAT3 pathway. Recent studies have reported that PTPRT is involved in the early metastatic seeding of colorectal cancer; however, the correlation between PTPRT and metastasis in other types of cancer has not been revealed. A combined analysis using a dataset from the genomics evidence neoplasia information exchange (GENIE) and cBioPortal revealed that PTPRT mutation is associated with poor prognosis in pan-cancer and non-small-cell lung cancer. The mutations of PTPRT or “gene modules” containing PTPRT are significantly enriched in patients with metastatic cancer in multiple cancers, suggesting that the PTPRT mutations serve as potential biomarkers of cancer metastasis.
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Ganguly, Debolina, Marcel Schmidt, Morgan Coleman, Tuong-Vi Ngo, Noah Sorrelle, Adrian Dominguez, Jason Toombs, et al. "Abstract B016: Pleiotrophin drives a pro-metastatic immune niche within the breast tumor microenvironment." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): B016. http://dx.doi.org/10.1158/1538-7445.metastasis22-b016.

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Abstract Metastatic cancer cells adapt to thrive in secondary organs. To investigate metastatic adaptation, we performed transcriptomic analysis of metastatic and non-metastatic murine breast cancer cells. We found that pleiotrophin (PTN), a neurotrophic cytokine, is a metastasis-associated factor that is expressed highly by aggressive breast cancers. Moreover, elevated PTN in plasma correlated significantly with metastasis and reduced survival of breast cancer patients. Mechanistically, we find that PTN activates NF-kB in cancer cells leading to altered cytokine production, subsequent neutrophil recruitment and an immune suppressive microenvironment. Consequently, inhibition of PTN, pharmacologically or genetically, reduces the accumulation of tumor associated neutrophils and reverts local immune suppression resulting in increased T cell activation and attenuated metastasis. Furthermore, inhibition of PTN significantly enhanced the efficacy of immune checkpoint blockade + chemotherapy in reducing metastatic burden in mice. These findings establish PTN as a previously unrecognized driver of a pro-metastatic immune niche and thus represents a promising therapeutic target for the treatment of metastatic breast cancer. Citation Format: Debolina Ganguly, Marcel Schmidt, Morgan Coleman, Tuong-Vi Ngo, Noah Sorrelle, Adrian Dominguez, Jason Toombs, Cheryl Lewis, Yisheng Fang, Fatima Mora, David Ortega, Anton Wellstein, Rolf Brekken. Pleiotrophin drives a pro-metastatic immune niche within the breast tumor microenvironment [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr B016.
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Park, Jinkyung, Dahee Jeong, Meeryoung Song, and Bonglee Kim. "Recent Advances in Anti-Metastatic Approaches of Herbal Medicines in 5 Major Cancers: From Traditional Medicine to Modern Drug Discovery." Antioxidants 10, no. 4 (March 27, 2021): 527. http://dx.doi.org/10.3390/antiox10040527.

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Metastasis is the main cause of cancer-related death. Despite its high fatality, a comprehensive study that covers anti-metastasis of herbal medicines has not yet been conducted. The aim of this study is to investigate and assess the anti-metastatic efficacies of herbal medicines in the five major cancers, including lung, colorectal, gastric, liver, and breast cancers. We collected articles published within five years using PubMed, Google Scholar, and Web of Science with “cancer metastasis” and “herbal medicine” as keywords. Correspondingly, 16 lung cancer, 23 colorectal cancer, 10 gastric cancer, 10 liver cancer, and 18 breast cancer studies were systematically reviewed. The herbal medicines attenuated metastatic potential targeting various mechanisms such as epithelial mesenchymal transition (EMT), reactive oxygen species (ROS), and angiogenesis. Specifically, the drugs regulated metastasis related factors such as matrix metalloproteinase (MMP), serine-threonine protein kinase/extracellular regulated protein kinase (AKT/ERK), angiogenic factors, and chemokines. Overall, the present study is the first review, comprehensively investigating the anti-metastasis effect of herbal medicines on five major cancers, providing the experimental models, doses and durations, and mechanisms. Herbal medicines could be a potent candidate for anti-metastatic drugs.
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Cheng, Liang, David G. Bostwick, Guang Li, Shaobo Zhang, Alexander O. Vortmeyer, and Zhengping Zhuang. "Conserved Genetic Findings in Metastatic Bladder Cancer." Archives of Pathology & Laboratory Medicine 125, no. 9 (September 1, 2001): 1197–99. http://dx.doi.org/10.5858/2001-125-1197-cgfimb.

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Abstract Context.—Molecular analysis of microsatellite alterations of biologically distinct tumor cell subpopulations from the same patient may aid in the determination of tumor origin and further our understanding of the genetic basis of cancer progression. Design.—The authors examined the pattern of allelic loss with polymorphic microsatellite markers on chromosome 9p21 (D9S161, D9S171, IFNA), regions of putative tumor suppressor gene p16, and on chromosome 17p13 (TP53), the p53 locus, in matched primary and metastatic bladder cancers from 9 patients. All patients underwent cystectomy for bladder cancer and had regional lymph node metastases at the time of surgery. Genomic DNA was prepared from primary cancers and matched synchronous lymph node metastases using a microdissection method. Results.—The overall frequency of allelic loss was 78% in primary cancer and 89% in paired metastatic cancer. The frequency of allelic loss in the primary cancer was 86% with D9S161, 67% with D9S171, 71% with IFNA, and 80% with TP53. The frequency of allelic loss in matched metastatic cancer was 100% with D9S161, 62% with D9S171, 71% with IFNA, and 80% with TP53. An identical pattern of allelic imbalance (allelic loss or retention) at multiple DNA loci was observed in matched primary and metastatic carcinoma in 8 (88%) cases. One case showed allelic loss in the metastasis, but not in the primary cancer. Conclusions.—The pattern of allelic loss at chromosome 9p21 (p16) and 17p13 (p53) was generally maintained during cancer progression to metastasis, and identical allelic loss in primary cancer was conserved in paired metastatic carcinoma. These data suggest that these genetic changes may be useful in establishing a diagnosis and determining tumor origins in difficult cases.
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Wan, Xiaochun, and Junxin Li. "DcR3 acts as a tumor marker of metastatic cancers." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 178.45. http://dx.doi.org/10.4049/jimmunol.200.supp.178.45.

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Abstract Decoy receptor 3 (DcR3) is a soluble protein that competitively binds Fas ligand and has an anti-apoptotic role. Abnormally elevated DcR3 in malignant tumors may help cancer cells metastasize by suppressing immune responses and establishing metastatic lesions. However, whether DcR3 is valuable in differentiating cancer metastasis from non-metastasis remains largely unclear. In this study, we produced anti-DcR3 monoclonal antibodies and established a sensitive ELISA (11–12000 pg/ml, R2= 0.9941) to measure serum levels of DcR3 in cancer patients. DcR3 was significantly elevated in gastric cancer (2.04 ± 1.01, P = 0.0061), lymphoma (1.62 ± 0.75, P = 0.041) and breast cancer (1.53 ± 0.51, P = 0.023). ROC (Receiver Operating Characteristic) analysis suggested DcR3 was a suitable biomarker for the diagnosis of gastric cancer (Sensitivity = 85.7%, Specificity = 90.0%, AUC = 82.3%). Importantly, serum DcR3 was positively correlated with platelet distribution width (PDW) (P = 2.45×10−6, R = 0.63) in metastatic cancers while negatively correlated with hemoglobin (HGB) (P = 0.002, R = −0.59) and hematocrit (HCT) (P = 0.001, R = −0.62) in non-metastatic cancers. DcR3×PDW÷(HGB×HCT), the novel indicator could be used to differentiate cancer metastasis from non-metastasis (Sensitivity = 75.0%, Specificity = 80.9%, AUC = 79.0%). These results reveal that DcR3 has a predictive value for cancer metastasis in combination with hematological traits.
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Tarragó-Celada, Josep, and Marta Cascante. "Targeting the Metabolic Adaptation of Metastatic Cancer." Cancers 13, no. 7 (April 1, 2021): 1641. http://dx.doi.org/10.3390/cancers13071641.

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Metabolic adaptation is emerging as an important hallmark of cancer and metastasis. In the last decade, increasing evidence has shown the importance of metabolic alterations underlying the metastatic process, especially in breast cancer metastasis but also in colorectal cancer metastasis. Being the main cause of cancer-related deaths, it is of great importance to developing new therapeutic strategies that specifically target metastatic cells. In this regard, targeting metabolic pathways of metastatic cells is one of the more promising windows for new therapies of metastatic colorectal cancer, where still there are no approved inhibitors against metabolic targets. In this study, we review the recent advances in the field of metabolic adaptation of cancer metastasis, focusing our attention on colorectal cancer. In addition, we also review the current status of metabolic inhibitors for cancer treatment.
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Park, Misung, Dohee Kim, Sunghyub Ko, Ayoung Kim, Kyumin Mo, and Hyunho Yoon. "Breast Cancer Metastasis: Mechanisms and Therapeutic Implications." International Journal of Molecular Sciences 23, no. 12 (June 18, 2022): 6806. http://dx.doi.org/10.3390/ijms23126806.

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Breast cancer is the most common malignancy in women worldwide. Metastasis is the leading cause of high mortality in most cancers. Although predicting the early stage of breast cancer before metastasis can increase the survival rate, breast cancer is often discovered or diagnosed after metastasis has occurred. In general, breast cancer has a poor prognosis because it starts as a local disease and can spread to lymph nodes or distant organs, contributing to a significant impediment in breast cancer treatment. Metastatic breast cancer cells acquire aggressive characteristics from the tumor microenvironment (TME) through several mechanisms including epithelial–mesenchymal transition (EMT) and epigenetic regulation. Therefore, understanding the nature and mechanism of breast cancer metastasis can facilitate the development of targeted therapeutics focused on metastasis. This review discusses the mechanisms leading to metastasis and the current therapies to improve the early diagnosis and prognosis in patients with metastatic breast cancer.
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Pein, Maren, and Thordur Oskarsson. "Microenvironment in metastasis: roadblocks and supportive niches." American Journal of Physiology-Cell Physiology 309, no. 10 (November 15, 2015): C627—C638. http://dx.doi.org/10.1152/ajpcell.00145.2015.

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In many cancers, malignant cells can spread from the primary tumor through blood circulation and initiate metastasis in secondary organs. Metastatic colonization may depend not only on inherent properties of cancer cells, but also on suitable microenvironments in distant sites. Increasing evidence suggests that the nature of the microenvironment may determine the fate of disseminated cancer cells, providing either hindrance or support for cancer cell propagation. This can result in strong selective pressure where the vast majority of cancer cells, invading a secondary organ, are either eliminated or maintained in a dormant state. The ability of cancer cells to fend off or circumvent anti-metastatic signals from the stroma and the capacity to manipulate the local microenvironment towards a supporting environment, a metastatic niche, may be essential for metastatic growth. The molecular interactions between cancer cells and the stroma are still enigmatic, but recent studies are beginning to reveal their nature. Here, we discuss the interactive relationship between metastatic cancer cells and host stroma, involving selection and adaptation of metastasis-initiating cells and host tissue remodeling. Understanding the dynamic and continuously evolving cross talk between metastatic cancer cells and the stroma may be crucial when developing cancer treatments.
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Dissertations / Theses on the topic "Metastatic cancer"

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Wander, Seth A. "p27 and Metastatic Progression: Molecular Mechanisms Underlying Bone Metastasis." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/690.

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The complex PI3K/mTOR pathway regulates tumor progression via effects on cellular proliferation, apoptosis, autophagy, and motility. New drugs that inhibit the catalytic site of both PI3K and mTOR have shown promise in clinical trials. Here, we report the first use of a novel, dual PI3K/mTOR catalytic site inhibitor (PF-04691502, PF1502) in a xenograft model of breast cancer metastasis to bone. Metastatic MDA-MB-1833 cells showed PI3K/mTOR activation relative to parental MDA-MB-231. Low-dose PF1502 significantly impaired tumor cell motility and invasion in vitro without causing cell cycle arrest, apoptosis, or reduced proliferation. Pre-treatment of tumor cells at this dose reduced bone metastatic outgrowth in vivo. The atypical tumor suppressor, p27KIP1, is phosphorylated in its C-terminal region by multiple AGC kinases downstream of PI3K/mTOR. These phosphorylation events promote cytoplasmic mislocalzation of p27 which, in turn, facilitates inhibition of the RhoA cytoskeletal regulatory protein. The resulting turnover of the actin cytoskeleton is thought to underlie the increased cellular motility attributed to cytoplasmic p27. In MDA-MB-1833 cells, PI3K/mTOR inhibition reduced p27 C-terminal phosphorylation at T157 and T198 and reduced cytoplasmic p27 levels. Overexpression of a p27T157D/T198D phospho-mimetic mutant conferred resistance to the anti-motility effects of PF1502 in vitro. MDA-MB-1833 cells demonstrate p27-dependent inhibition of RhoA-ROCK signaling, as well as p27-dependent motility and invasion in vitro, however, RhoA knockdown did not confer resistance to the anti-motility effects of PF1502. p27shRNA dramatically impaired the bone metastatic outgrowth of MDA-MB-1833 in vivo. In an effort to explore potentially novel RhoA-independent mechanisms whereby cytoplasmic p27 might drive tumor cell motility and metastasis, we turned to the process known as epithelial-to-mesenchymal transition (EMT). The EMT program has been implicated as a critical driver of tumor metastasis in a variety of cancer models. PI3K/mTOR inhibition and shRNA p27 treatment both reversed expression of EMT markers in MDA-MB-1833. Thus, PI3K/mTOR appears to drive p27-dependent motility and metastasis at least in part by induction of an EMT-like phenotype, a novel mechanism through which p27 might act to promote tumor progression. These results provide an important new clinical rationale supporting the use of PI3K/mTOR inhibitors as anticancer agents via their inhibition of tumor invasion and metastasis.
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Nordman, Ina IC Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Surrogate endpoints of survival in metastatic carcinoma." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/42791.

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In most randomised controlled trials (RCTs), a large number of patients need to be followed over many years, for the clinical benefit of the drug to be accurately quantified (1). Using an early proxy, or a surrogate endpoint, in place of the direct endpoint of overall survival (OS) could theoretically shorten the duration of RCTs and minimise the exposure of patients to ineffective or toxic treatments (2, 3). This thesis examined the relationship between surrogate endpoints and OS in metastatic colorectal cancer (CRC), advanced non-small cell lung cancer (NSCLC) and metastatic breast cancer (MBC). A review of the literature identified 144 RCTs in metastatic CRC, 189 in advanced NSCLC and 133 in MBC. The publications were generally of poor quality with incomplete reporting on many key variables, making comparisons between studies difficult. The introduction of the CONSORT statement was associated with improvements in the quality of reporting. For CRC (337 arms), NSCLC (429 arms) and MBC (290 arms) there were strong relationships between OS and progression free survival (PFS), time to progression (TTP), disease control rate (DCR), response rate (RR) and partial response (PR). Correlation was also demonstrated between OS and complete response (CR) in CRC and duration of response (DOR) in MBC. However, while strong relationships were found, the proportion of variance explained by the models was small. Prediction bands constructed to determine the surrogate threshold effect size indicated that large improvements in the surrogate endpoints were needed to predict overall survival gains. PFS and TTP showed the most promise as surrogates. The gain in PFS and TTP required to predict a significant gain in overall survival was between 1.2 and 7.0 months and 1.8 and 7.7 months respectively, depending on trial size and tumour type. DCR was a better potential predictor of OS than RR. The results of this study could be used to design future clinical trials with particular reference to the selection of surrogate endpoint and trial size.
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Solberg, Arne. "Outcome Assessments in Non- Metastatic Prostate Cancer." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for kreftforskning og molekylær medisin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-13881.

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Metoder for å måle utfall av behandling hos pasienter med prostatakreft uten spredning. Prostatakreft uten påvist spredning kan behandles med operasjon, strålebehandling med eller uten hormonbehandling, eller hormonbehandling alene. Svært mange menn med nylig påvist prostatakreft vil imidlertid kunne leve i mange år uten plager av sykdommen også uten behandling, og en stor andel dør til slutt av helt andre årsaker enn prostatkreft. Man mangler imidlertid helt sikre metoder for å velge ut pasienter som ikke trenger behandling, men i noen tilfeller hvor sykdommen er i tidlig fase er et regelmessig kontrollopplegg hvor kurativ behandling iverksettes først hvis sykdomen viser tegn til utvikling, forsvarlig. Imidlertid kan prostatakreft også være en agressiv sykdom med stor risiko for spredning og forkortet levetid. Pasienter med nylig påvist prostatakreft uten spredning og intermediær til høy risiko for progresjon regnes derfor å være behandlingstrengende. Det kan ta mange år før man merker symptomer på et tibakefall etter en behandling som ikke har gitt ønsket kurasjon. Da vil sykdommen ofte ha kommet for langt til å kunne helbredes. Påvisning av manglende behandlingseffekt før et tilbakefall av sykdommen gir symptomer er imidlertid kun viktig hvis det da finnes effektiv tileggsbehandling. Siden overlevelse vanligvis ansees som det viktigste effektmålet ved kurativ kreftbehandling, blir det også viktig å avklare om det å påvise et tidlig tilbakefall eller manglende behandlingseffekt virkelig kan forutsi om pasienten på sikt vil utvikle plager av kreftsykdommen og i verste fall dø av den. I tillegg er det også svært viktig at bivirkningene ved utredning og behandling er så lite plagsomme som mulig. Denne avhandlingen omhandler metoder for å måle effekt/utfall av behandling hos pasienter med prostatakreft uten spredning. Avhandlingen inbefatter 4 studier hvor hovedvekten er lagt på resultater av vevsundersøkelser av prostatkjertelen etter åpen radikal prostatectomi (operasjon) samt resultater i form av overlevelse og bivirkninger når kombinert strålebehandling og hormonbehandling sammenlignes med hormonbehandling alene. Videre undersøkes hvor hyppig det påvises kreftceller i systematiske vevsprøver fra prostata 3-4 år etter at de to sistnevne behandlingene ble iverksatt. Endelig undersøkes bivirkninger av vevsprøvetakning etter kombinert strålebehandling og hormonbehandlig sammenlignet med hormonbehandling alene. Resultatene av studiene viser at andel pasienter som fikk prostatakreften fullstendig fjernet ved operasjon bedømt ut fra kirurgiske marginer gradvis økte de første årener etter at operasjonsmetoden ble innført. Det gir en indikasjon på at operasjonsteknikken bedret seg vesentlig i samme periode. Strålebehandling kombinert med hormonbehandling ga vesentlig bedre totaloverlevelse enn hormonbehandling alene. Kombinasjonsbehandlingen ga en lett øktning av bivirkninger, men bivirkningene var akseptable. De pasientene som fikk denne kombinasjonsbehandlingen hadde vesentlig skjeldnere gjenværende kreftceller i vevsprøvene sammenlignet med de som bare fikk hormonbehandling. Videre hadde pasienter med gjennværende kreftceller i prostatakjertelen vesentlig høyere risiko for tilbakefall påvist med blodprøve (stigende PSA) . Bivirkningene ved å ta systematiske vevsprøver fra prostata etter hormonbehandling med eller uten stråleterapi var små og gikk stort sett over i løpet av en uke.
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Paon, Lenaic Marie Pierre. "Gene expression profiling of metastatic gastric cancer." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490659.

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Gastric cancer is one of the main cancers in the world, and is responsible for a large number of deaths each year. In Europe, the main issue is that it is only detected at latter stages, when metastases have developed. Although metastasis is the main cause of death from such tumours, the process is a very complex one and still not fully understood. In order to unravel this mechanism, microarrays have been used to study the expression pattern of a large number of genes in primary tumours and metastatic samples. These studies aim at indentifying genes that may playa role in metastasis. A number of microarray studies have already been carried out on gastric cancer to pursue knowledge. However, they have been mainly carried out in Asian populations, which are thought to present different gastric tumours than Europeans, possibly due to genetic and environmental parameters. The present thesis therefore aimed to carry out the first microarray study on gastric tumours from a European population, to identify genes that might playa role in gastric cancer metastasis, and assess whether there were any differences between Asian and European samples. In order to achieve this aim, the printing of in-house microarrays and methods to amplify and hybridise the samples first needed to be developed. This included the development of a new amplification method, the SMARTff7 protocol. Results showed that this method allowed more genes to be amplified than with an .established protocol. In addition, a microarray study published in 2003 identified a metastasis specific gene expression signature that could differentiate between metastatic and nonmetastatic primary tumours from different sites. However, this study did not include samples from gastric cancer. It was thus decided to test whether this signature could be applied to primary gastric tumours, using the new MetriGenix® platform. Although the analysis seemed to indicate that the signature did not apply to gastric tumours, technical issues meant that the results were inconclusive. On the other hand, a larger microarray analysis using the techniques developed during this project allowed the indentification of a number of genes of interest which may playa role in the metastatic spread of gastric cancer.
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Pelon, Floriane. "Fibroblastic heterogeneity and metastatic spread in breast cancers Fibroblast heterogeneity drives metastatic spread in breast cancer through distinct mechanisms." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2392&f=17330.

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Les cancers du sein, premiers cancers féminins et causes aujourd’hui encore de nombreux décès, sont classés en 3 sous-types moléculaires : luminaux –les plus répandus, HER2 et triple-négatifs (TN) –les plus agressifs. Lors du diagnostic, l’envahissement des ganglions lymphatiques axillaires par les cellules tumorales est établi. Il s’agit, en plus de la classification moléculaire, d’un marqueur pronostique utilisé en clinique pour stratifier les patientes, car il informe sur le risque de développement ultérieur de métastases, cause majeure des décès à l’heure actuelle. Les tumeurs solides, et notamment les cancers du sein, sont des écosystèmes complexes comprenant de nombreux types cellulaires qui interagissent avec les cellules cancéreuses. Parmi eux, les fibroblastes associés au cancer (CAF) sont les plus abondants et participent activement à de nombreux aspects de la tumorigenèse dont la croissance, l’invasion, l’angiogenèse, l’immunosuppression. Cependant, ils constituent une population hétérogène et à ce jour, très peu d’études ont analysé cette hétérogénéité tout en la liant aux diverses fonctions décrites des CAF. Dans ce projet, nous nous sommes intéressés au rôle de cette hétérogénéité fibroblastique dans la dissémination métastatique des cancers du sein. En combinant l’étude de plusieurs marqueurs de CAF, nous avons montré que les ganglions lymphatiques envahis par les cellules tumorales sont constitués de 4 sous-populations de CAF (CAF-S1, S2, S3 et S4), similaires à celles identifiées dans les tumeurs primaires appariées. De façon intéressante, ce sont les deux sous-types de CAF myofibroblastiques (αSMA+), CAF-S1 et particulièrement CAF-S4, qui s’accumulent préférentiellement dans les ganglions métastatiques. Ils présentent les mêmes signatures transcriptomiques entre les deux localisations tissulaires (ganglions envahis et tumeurs primaires correspondantes). Or, ces deux populations CAF-S1 et CAF-S4 augmentent le phénotype invasif des cellules tumorales, en régulant des fonctions complémentaires. D’un côté, les CAF-S1 sont hautement motiles, et stimulent la prolifération, la migration, l’invasion et l’initiation d’une transition épithélio-mésenchymateuse des cellules de cancer du sein. De l’autre, les CAF-S4 sont très contractiles, capables de remodeler la matrice extracellulaire et promeuvent ainsi l’invasion et la motilité des cellules tumorales dans des systèmes en 3 dimensions. Des expériences fonctionnelles suggèrent que l’action des CAF-S1 implique CXCL12 et TGFβ tandis que celle des CAF-S4 dépend de la voie NOTCH. En accord avec ces résultats, l’accumulation des CAF et leur identité dans les ganglions envahis constituent deux nouveaux facteurs pronostics dans les cancers du sein, indépendants du sous-type de cancers du sein et de l’envahissement ganglionnaire. En effet, un fort contenu en CAF-S4 y est associé avec un développement ultérieur de métastases à longue distance. Ainsi, analyser le contenu fibroblastique des ganglions axillaires au diagnostic pourrait constituer une information nouvelle et utile à la prise en charge des patientes
Breast cancers are the most common cancers in women and despite great improvements in treatments, they are still responsible for many deaths worldwide. They are classified into 3 main molecular subtypes: Luminal cancers are the most frequent ones, while HER2 and TN are the most aggressive. At diagnostic, lymph node involvement is also assessed as it constitutes, in addition to molecular classification, a strong prognostic marker. Indeed, it informs on the risk to develop further distant metastases, which is the main cause of death by cancer. Solid tumors, including breast cancers, are complex ecologies comprising numerous different cell types that interact with cancer cells. Among them, cancer-associated-fibroblasts (CAF) are the most abundant and actively participate in many tumor hallmarks such as tumor growth, invasion, immunosuppression and angiogenesis. However, they do not constitute a homogeneous population but so far, only few studies have characterized this heterogeneity and linked it to CAF previously described functions. In this project, we focused on the potential involvement of CAF heterogeneity in breast cancer metastatic spread. Combining the analysis of several CAF markers, we showed that invaded LN comprise 4 CAF subsets (CAF-S1, S2, S3 and S4), similar to those found in primary tumors. Interestingly, the two myofibroblastic subsets (αSMA+) CAF-S1 and especially CAF-S4 preferentially accumulate in metastatic LN and present the same transcriptomic profiles in both tumors and LN. Importantly, both CAF-S1 and CAF-S4 display pro-invasive properties, by acting at different levels on tumor cells. On the one hand, highly motile CAF-S1 stimulate breast cancer cell proliferation, migration and EMT initiation. On the other hand, CAF-S4 exhibit an important contractility and by remodeling the matrix they are able to promote tumor cell invasion in 3D. Functional studies highlight a CXCL12/TGFβ involvement in CAF-S1 functions while CAF-S4 pro-invasive phenotype appears to be Notch-dependent. In agreement with these data, we found that CAF accumulation and subset enrichment in involved LN were two new prognostic factors, independent of breast cancer molecular subtypes and LN status at diagnosis. Indeed, stromal rich LN with a predominance of CAF-S4 are associated with long distance metastases development and poor overall survival. Thus, we propose that analyzing LN fibroblastic content at diagnosis could constitute new and useful information to breast cancer patients’ care
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Chiang, Yan Ting. "Identification of metastasis-driving genes as potential therapeutic targets/ biomarkers for metastatic prostate cancer." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52901.

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Metastatic prostate cancer is currently incurable. Metastasis is thought to result from changes in the expression of specific metastasis-driving genes, leading to a cascade of activated downstream genes setting the metastatic process in motion. As such, metastasis-driving genes could provide effective therapeutic targets and prognostic biomarkers for improved disease management. In search of potential metastasis-driving genes, genes with elevated expression in patient-derived metastatic LTL-313H prostate cancer tissues, as distinct from non-metastatic LTL-313B tissues, were identified. Among these genes, TIMELESS and DLX1 were promising. Unfortunately, their silencing and overexpression in prostate cancer cells did not lead to inhibition of metastatic properties, indicating that they were not metastasis-driving genes. A different, novel approach was used based on the notion that metastasis-driving genes can activate genes in an amplification cascade fashion. Accordingly, I used the IPA’s Upstream Regulator Analysis tool to analyze the differential gene expression profile of the metastatic and non-metastatic tissues to predict the upstream master regulatory (metastasis-driving) genes accountable for the differential expression. Six candidate genes were identified, including GATA2, a pioneer factor-encoding gene. Elevated GATA2 expression in clinical metastatic prostate cancer specimens correlated with poor patient prognosis. Furthermore, GATA2 gene silencing in human prostate cancer LNCaP cells led to marked reduction in cell proliferation, cell migration, tissue invasion, focal adhesion disassembly and a dramatic change in transcriptional activity, indicating that GATA2 plays a critical role in prostate cancer metastasis. As such, GATA2 could represent a metastasis-driving gene and a potential therapeutic target for inhibiting the growth and metastasis development in prostate cancer. Further analysis of GATA2-regulated genes led to the development of a GATA2-based metastatic gene signature. Its prognostic value was confirmed using two prostate cancer patient cohorts. In addition, it was shown to be a prognostic factor for risk assessment of metastasis development, independent of the widely used D’Amico prognostic classification system. However, a thorough validation is critical and, if successful, the GATA2-based gene signature could lead to a paradigm shift in the management of early prostate cancer. In conclusion, the findings of this study appear to be potentially useful for improved management of metastatic prostate cancer.
Medicine, Faculty of
Graduate
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Nielsen, S. R. "Metastasis-associated macrophages orchestrate the formation of a hospitable metastatic niche in pancreatic cancer." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3007527/.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with an overall 5-year survival rate < 5%, a rate that has not improved for a long time. The dismal prognosis for PDAC is part due to late detection, often at advanced stages of the disease where patients have developed distant metastases, but also due to chemotherapeutical resistance. Patients eligible for surgical resection of the pancreatic tumour has the best prognosis, but even when resection is successful, patients often relapse with distant metastases within 2 years after surgery. Macrophages promote tumourigenesis and enhance metastasis in many cancer types; however, the role of macrophages in PDAC metastasis is poorly understood. Using an experimental mouse model of liver metastasis, we find that PDAC liver metastasis critically depends on the early recruitment of granulin-secreting metastasis-associated macrophages (MAMs) to the liver that promote metastatic colonisation. Mechanistically, we demonstrate that granulin secretion by MAMs activates resident hepatic stellate cells (HSTCs) into myofibroblasts that secrete extracellular matrix components, including periostin, resulting in a fibrotic microenvironment that sustains metastatic tumour growth. Disruption of MAM recruitment in PI(3)Kγ-deficient mice, chemical depletion of MAMs from established lesions or genetic ablation of granulin reduces HSTC activation and liver metastasis. Adjuvant CTX is standard for patients after surgical resection to eliminate any residual cancer cells, and it improves survival for patients after resection. We find that 45% of mice with metastatic lesions respond to gemcitabine treatment with a reduction in metastatic burden. The metastatic lesions in these mice are characterised by a reduction in αSMA+ myofibroblasts. HSTCs do not seem to promote cancer cell survival in the presence of chemotherapy, but rather constitutes a protective niche that promotes relapse by promoting the growth of pancreatic cancer cells after gemcitabine treatment.
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Reed, Elizabeth. "The experience of living with metastatic breast cancer." Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/344746/.

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Over the last 10-15 years the medical management of metastatic breast cancer has improved survival, so women are living longer with progressive disease. Little is understood about women’s problems and needs and how they live their everyday lives. This study aimed to explore the experience of women with metastatic breast cancer by applying three phases: a cross-sectional survey exploring quality of life, experience of care and where they turned for support; exploration of the narratives of 30 women considering the social consequences of living with progressive breast cancer on identity; and finally triangulating medical and nursing documentation, a measure of physical functioning and ten women’s narratives to define the illness trajectory of metastatic breast cancer. Phase 1: Quality of life was found to be poor with women experiencing a significant symptom burden. Experience of care was poor with unmet information and support needs. There was little evidence of General Practitioner or palliative care involvement in care. Phase 2: In weathering the oscillations of progressive disease, women faced threats to their social identity. Women sought ways to maintain their social roles and social order to avoid social isolation. To do this they adopted contingent identities: stoicism or absolved responsibility. Women used these contingent identities to mediate any discontinuity between the self, the body and social order. These self-representations were used by women to maintain their social roles and social order and in doing so avoiding being discredited and socially isolated. Phase 3: Mapping women’s illness trajectories identified three typical trajectories. The illness trajectories demonstrated the complexity of living over time with progressive disease, through phases which give definition to a previously ill-defined pathway. Living with metastatic breast cancer challenges the personal resources of the individual and poses interesting questions about how healthcare professionals provide information, effective symptom control, and emotional and practical support to women. Current models of care are not meeting women’s needs and new approaches to care provision need to be considered.
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He, Felicia Jane. "Targeting Metastatic Breast Cancer Using Dual-Ligand Nanoparticles." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499699087340348.

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Donald, Carlton Dewitt. "Metastatic characteristics of tumor progression in Prostate Cancer." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 1995. http://digitalcommons.auctr.edu/dissertations/3299.

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Tumor biologist have long appreciated that both cell to cell and cell to extracellular matrix (ECM) interactions are involved in the invasive and metastatic events that are characteristic of malignancy. Cancer cell attachment to and invasion of an ECM has been associated with metastatic potential of cell lines of the Dunning rat prostate model. It was postulated that differences observed in the metastatic potential of four Dunning cell lines may correlate with cell-matrix interactions. Four cell lines, highly metastatic ML, MLL, AT-3 and non-metastatic AT-1 were studied. The adhesive, invasive and chemoinvasive capability of each cell line was compared. Cell adhesion was examined by plating the cells on plastic dishes coated with various components of the ECM (fibronectin, laminin and collagen) as well as EHS Natrix (a natural ECM) . Invasion was determined by examining cells ability to traverse a matrigel barrier. Correlations were found between the cells' adhesive and invasive abilities in response to the ECM. These observations suggest that ECM components are highly involved in prostate cancer cell activities and loss may contribute to tumor progression and metastasis.
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Books on the topic "Metastatic cancer"

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Swanton, Charles, and Stephen R. D. Johnston. Handbook of metastatic breast cancer. 2nd ed. New York: Informa Healthcare, 2011.

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Sherbet, G. V. The Metastatic Spread of Cancer. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-09577-3.

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Kaufmann, M. Therapeutic management of metastatic breast cancer. Berlin: Walter de Gruyter & Co, 1989.

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Leong, Stanley P. L., ed. From Local Invasion to Metastatic Cancer. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8.

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Metastatic cancer: Clinical and biological perspectives. Austin, Texas, USA: Landes Bioscience, 2013.

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1952-, Wick Mark R., ed. Metastatic carcinomas of unknown origin. New York: DEMOS, 2008.

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Chu, Edward. New treatment strategies for metastatic colorectal cancer. [Manhasset, NY]: CMP Medica, 2008.

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New treatment paradigms in metastatic breast cancer. [Manhasset, NY]: CMPMedica, 2008.

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Chu, Edward. New treatment strategies for metastatic colorectal cancer. [Manhasset, NY]: CMP Medica, 2008.

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Evans, Clive W. The metastatic cell: Behaviour and biochemistry. London: Chapman and Hall, 1991.

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Book chapters on the topic "Metastatic cancer"

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Szmulewitz, Russell, Jennifer Taylor, and Carrie Rinker-Schaffer. "Metastatic Colonization." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3676-2.

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Szmulewitz, Russell, Jennifer Taylor, and Carrie Rinker-Schaffer. "Metastatic Colonization." In Encyclopedia of Cancer, 2797–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_3676.

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Szmulewitz, Russell, Jennifer Taylor, and Carrie Rinker-Schaffer. "Metastatic Colonization." In Encyclopedia of Cancer, 2271–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3676.

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Field, Kathryn M., and John R. Zalcberg. "Chemotherapy: Metastatic Disease." In Rectal Cancer, 189–222. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-567-5_12.

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Sumpter, K., and D. Cunningham. "Metastatic Rectal Cancer." In Modern Management of Cancer of the Rectum, 157–77. London: Springer London, 2001. http://dx.doi.org/10.1007/978-1-4471-0331-8_14.

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Halfdanarson, Thorvardur R., and Joleen M. Hubbard. "Metastatic Rectal Cancer." In Modern Management of Cancer of the Rectum, 287–310. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6609-2_20.

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Patel, Tejal A., and Edith A. Perez. "Metastatic Breast Cancer." In Management of Breast Diseases, 425–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-69743-5_23.

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Stephens, Frederick O., and Karl Reinhard Aigner. "Metastatic (Secondary) Cancer." In Basics of Oncology, 299–303. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-92925-3_22.

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Stephens, Frederick O., and Karl Reinhard Aigner. "Metastatic (Secondary) Cancer." In Basics of Oncology, 331–34. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23368-0_22.

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Harris, Louise, Caitlin Bowen, Satish Kumar, Bernadette Coles, and Malcolm Mason. "Metastatic bladder cancer." In Evidence-Based Urology, 383–89. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119129875.ch32.

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Conference papers on the topic "Metastatic cancer"

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Yoshimoto, T., T. Ishikawa, N. Matsuki, H. Fujiwara, Y. Imai, H. Ueno, M. Takeda, and T. Yamaguchi. "Rheology of Cancer Cells With Different Metastatic Properties." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206593.

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Cancer is the leading cause of death in Japan as well as many other countries. One of the most serious problem of cancer is that cancer cells often migrate to a distant part of the body, referred to as metastasis. The rheological properties of cancer cells have been investigated by some reserchers [1,2]. However, the correlations between the metastasis and the rheological properties are still unclear, because of limited number of experimental cases reported so far. In this study, we used two kinds of human breast cancer cell lines, MCF-7 and KPL-4. It is known that KPL-4 has much higher metastatic property than MCF-7. The rheological properties of these cells were measured by a micropipette aspiration method [3,4]. By comparing Young’s modulus between two kinds of cancer cells, we discuss the correlations between the metastasis and the cell deformability.
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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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Inufusa, H., N. Sagara, K. Nakano, and M. Yasutomi. "CHARACTERISATION OF PLATELET AGGREGATING MATERIAL EXTRACTED FROM HUMAN LUNG ADENOCARCINOMA CELL LINE WHICH METASTASIZED IN NUDE MICE S,C, IMPLANTATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643199.

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It has been reported in animal experimental system that Platelet Aggregating Material (PAM) of cancer cell play important role in cancer metastasis. Many human cancer cell lines has been also studied the platelet aggregation activity of PAM. But correlation between the platelet aggregation activity and metastatic potential of human cancer cells were usually unkncwn. We established a human lung adenocarcinoma cell line KUM-LK-2 which produce spontaneous lung metastasis when cells implanted into subcutaneous of nude mice. PAM was extracted from KUM-LK-2 cells following the method of D.Mbhanty and P.Hilgard. Platelet aggregation study of PAM was performed by human Heparinized platelet rich plasma useing NIKO Hematracer PACT2D. Character of PAM were examined by physical and chemical treatment. KUM-LK-2 PAM shew 80% of platelet aggregation in maximum after 150 sec lag time, and aggregation was not found by Citrated PRP.It is concluded that PAM is high moleculer protein and contain Phospholipid and aggregation activity is concerning with ATP composition of platelet. PAM dose not contain Fibrinogen and Sialic acid, and not concern with Throrriboxan composition. This study is first case of platelet aggregation activity of PAM extracted human canoer cells which contain metastatic potential.
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Hoskins, Meghan H., Shile Liang, Robert F. Kunz, and Cheng Dong. "Cellular Mechanics and Biology of Tumor Cell-Leukocyte Interactions in the Near Wall Region Under Shear Flow Conditions." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176376.

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Malignant melanoma has a high propensity for metastatic spread, making it the most deadly form of skin cancer. Currently, no effective treatment exists to prevent melanoma metastasis or to inhibit metastatic tumors growing in distant organs [1,2].
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Shareef, Sarah J., Mihai Nita-Lazar, and Maria A. Kukuruzinska. "E-cadherin N-glycosylation Modulates the Strength of Adherens Junctions." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13013.

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Metastasis, the spread of cancer cells throughout the body, claims 90% of solid tumor deaths. During metastasis, cancer cells undergo discohesion. An understanding of how to control and strengthen cell adhesion through junction formation could lead to methods for decreasing metastatic tendencies.
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Sayyad, Megan, Madhavi Puchalapalli, Chris Canal, Theresa Swift-Scanlan, Andrew Ottens, and Jennifer E. Koblinski. "Abstract 1988: Metastatic v non-metastatic cancer exosomes in brain metastasis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1988.

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Sayyad, Megan, Madhavi Puchalapalli, Chris Canal, Theresa Swift-Scanlan, Andrew Ottens, and Jennifer E. Koblinski. "Abstract 1988: Metastatic v non-metastatic cancer exosomes in brain metastasis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1988.

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McClain, Jacob, Sara L. Tuell, and Susan N. Thomas. "Tumors Change the Elastic and Viscoelastic Properties of Draining Lymph Node Tissues." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14419.

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Changes in tissue mechanical properties are often the first indication of malignant disease, with the detection of a stiff lump by a patient. These changes include growth-induced solid stresses, increased matrix stiffness, high fluid pressure, and increased interstitial flow, which in turn enhance fluid flux away from the tumor to downstream lymph nodes (LNs). But in addition to changing the way a tumor feels to a patient, altered tumor tissue mechanics promote cancer cell invasion into lymphatic vessels, allowing their metastatic dissemination to draining LNs. LN swelling and stiffening is another common indicator of tumor growth, and the presence of metastatic cells in the sentinel LN, or tumor draining lymph node (TDLN), is used clinically to stage disease. Recent studies indicate the LN microenvironment determines whether metastatic cancers can spread to the sentinel LNs. Yet despite the known correlation of LN swelling and stiffening with tumorigenesis and the role of the LN microenvironment in metastasis, our understanding of how changes in LN mechanical properties relate to tumor progression, anti-tumor immune response and metastatic colonization of the LN is limited. This lack of a quantitative understanding limits functional analyses of the role of LN mechanics in determining cancer cell colonization of the TDLN, their influence on immune suppression taking place within the TDLN, as well as the development of strategies to mitigate these effects.
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Cruz, Marcelo Ribeiro da Luz, Valeria Fernandes Roppa Cruz, Alfredo Almeida Cunha, and Renato Souza Bravo. "CAN AXILLARY ULTRASONOGRAPHY WITH CORE NEEDLE BIOPSY BE A USEFUL TOOL IN THE APPROACH OF BREAST CANCER PATIENTS?" In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1004.

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Introduction: Metastatic involvement of axillary lymph nodes in patients with breast cancer is an important prognostic factor and it also has therapeutic implications. Nevertheless, the use of ultrasound for evaluating axillary lymph node status has been questioned. Objective: Evaluate the performance of ultrasound with core needle biopsy in the diagnosis of axillary metastasis. Patients and Method: A diagnostic validation study was performed to compare axillary ultrasound with core biopsy versus the surgical procedure. The scenario was a quaternary hospital in Rio de Janeiro where breast cancer patients were treated. The surgical procedure was the gold standard. Performance was assessed by calculating sensitivity, specificity, positive predictive value, negative predictive value, and estimated nodal disease burden. Result: Specificity and positive predictive values were 100% for the presence of axillary metastasis. The false negative rate was only 1.69% with a negative predictive value of 98.31% for the involvement of three or more lymph nodes. Conclusion: Axillary ultrasound with core needle biopsy shows excellent performance in assessing axillary metastatic impairment in patients with breast cancer, proving to be an effective tool in different clinical contexts.
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Freitas, Paola Ferreira de, Renata Borges de Aquino, Andre Mattar, Jorge Yoshinori Shida, and Luiz Henrique Gebrim. "CASE REPORT: PATHOLOGICAL COMPLETE RESPONSE IN BREAST IN A PATIENT WITH METASTATIC BREAST CANCER TREATED WITH ANASTROZOLE." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2088.

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Background: De novo metastatic breast cancer is seldomly encountered in patients visiting doctor’s clinics for the first time. This article reports a case of cervical/submandibular metastatic breast cancer treated with neoadjuvant endocrine therapy (NET) with anastrozole (ANA). Case description: We herein report on a patient affected by HR+, HER2−, and metastatic breast cancer treated with NET that presented after 6 months with the possibility of breast-conserving surgery due to clinical and radiological complete response, revealing after surgery pathological complete response. Conclusion: Even for patients with metastatic luminal breast cancer, NET with an aromatase inhibitor, especially ANA, is a good option for postmenopausal women with fewer side effects and allowing for breast-conserving surgery with less morbidity when comparing with chemotherapy and yet yielding good results.
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Reports on the topic "Metastatic cancer"

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Tinker, Anna V., Neesha C. Dhani, Prafull Ghatage, Deanna McLeod, Vanessa Samouëlian, Stephen A. Welch, and Alon D. Altman. Immune Checkpoint Inhibitors in Pretreated Metastatic Endometrial Cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0038.

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Review question / Objective: Efficacy and safety of immune checkpoint inhibitors alone or in combination with tyrosine kinase inhibitors in patients with pretreated advanced, persistent, or recurrent metastatic endometrial cancer. Condition being studied: Advanced, persistent, or recurrent metastatic endometrial cancer. Study designs to be included: Non-randomized studies of monotherapy in populations selected for relevant biomarkers such as MMR, microsatellite stability, and PD-L1 expression status and randomized trials of ICI combinations in unselected patients.
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Khan, Shafiq. Biomarkers for Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada427158.

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Williams, Myron N. Biomarkers for Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416624.

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Deisseroth, Albert B. Vectors for Treatment of Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada448903.

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Deisseroth, Albert B. Vectors for Treatment of Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada429189.

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Takeshita, Kenichi. Retinoic Acid Receptors in Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada413284.

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Marchetti, Dario. Heparanase Mechanisms in Brain-metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada585985.

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Pang, Shen. Gene Delivery for Metastatic Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada390852.

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Takeshita, Kenichi. Retinoic Acid Receptors in Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada392639.

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Marchetti, Dario. Heparanase Mechanisms in Brain-Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada596541.

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