Literatura científica selecionada sobre o tema "Instabilité microsatellites"
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Artigos de revistas sobre o assunto "Instabilité microsatellites"
Collura, Ada, Jérémie H. Lefevre, Magali Svrcek, David Tougeron, Aziz Zaanan e Alex Duval. "Instabilité des microsatellites et cancer". médecine/sciences 35, n.º 6-7 (junho de 2019): 535–43. http://dx.doi.org/10.1051/medsci/2019093.
Texto completo da fonteNshizirungu, J., M. Rui, V. Marta, P. Sónia, I. Mellouki, L. Chbani, H. Jalila e S. Bennis. "Instabilité des microsatellites et infection par le virus d’Epstein–Barr dans les carcinomes gastriques". Revue d'Épidémiologie et de Santé Publique 68 (setembro de 2020): S141. http://dx.doi.org/10.1016/j.respe.2020.03.084.
Texto completo da fonteParaf, François. "Comment et quand rechercher une instabilité des microsatellites dans les cancers colorectaux en 2008 ?" Annales de Pathologie 27, n.º 6 (dezembro de 2007): 433–38. http://dx.doi.org/10.1016/s0242-6498(07)71415-3.
Texto completo da fonteFléjou, J. F., O. Lascols, N. Mourra, M. Svrcek, Y. Parc, E. Tiret e R. Hamelin. "Expression des protéines MMR et instabilité de microsatellites dans une série consécutive de 1 555 cancers colorectaux". Annales de Pathologie 26 (novembro de 2006): 127. http://dx.doi.org/10.1016/s0242-6498(06)78428-0.
Texto completo da fonteBorie, Claire, Martine Raphaël, Richard Hamelin e Alex Duval. "Instabilité des microsatellites : un nouveau mécanisme de carcinogenèse associé à l’immunodépression dans les lymphomes non hodgkiniens chez l’homme". médecine/sciences 20, n.º 6-7 (junho de 2004): 641–42. http://dx.doi.org/10.1051/medsci/2004206-7641.
Texto completo da fonteBurel-Vandenbos, F., F. Pedeutour, V. Paquis, P. Paquis, N. Cardot-Leccia, J. Haudebourg, M. C. Saint-Paul e J. F. Michiels. "Association de deux anomalies génétiques rares dans un glioblastome à cellules géantes : un caryotype tumoral haploïde et une instabilité des microsatellites". Annales de Pathologie 26, n.º 3 (junho de 2006): 239. http://dx.doi.org/10.1016/s0242-6498(06)77316-3.
Texto completo da fonteYang, Guang, Ru-yi Zheng e Zai-shun Jin. "Correlations between microsatellite instability and the biological behaviour of tumours". Journal of Cancer Research and Clinical Oncology 145, n.º 12 (15 de outubro de 2019): 2891–99. http://dx.doi.org/10.1007/s00432-019-03053-4.
Texto completo da fonteGadgil, Rujuta Yashodhan, Eric J. Romer, Caitlin C. Goodman, S. Dean Rider, French J. Damewood, Joanna R. Barthelemy, Kazuo Shin-ya, Helmut Hanenberg e Michael Leffak. "Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication". Journal of Biological Chemistry 295, n.º 45 (1 de setembro de 2020): 15378–97. http://dx.doi.org/10.1074/jbc.ra120.013495.
Texto completo da fonteLong, Dustin R., Adam Waalkes, Varun P. Panicker, Ronald J. Hause e Stephen J. Salipante. "Identifying Optimal Loci for the Molecular Diagnosis of Microsatellite Instability". Clinical Chemistry 66, n.º 10 (24 de setembro de 2020): 1310–18. http://dx.doi.org/10.1093/clinchem/hvaa177.
Texto completo da fonteHaiduk, Tiffany, Michael Brockmann, Christoph Schmitt, Ramona-Liza Tillmann, Monika Pieper, Jessica Lüsebrink, Oliver Schildgen e Verena Schildgen. "Are Microsatellite Patterns Specific for Tumor Types? A Pilot Investigation". Journal of Molecular Pathology 1, n.º 1 (4 de setembro de 2020): 3–8. http://dx.doi.org/10.3390/jmp1010002.
Texto completo da fonteTeses / dissertações sobre o assunto "Instabilité microsatellites"
Bodo, Sahra. "Induction d'un processus d'instabilité des microsatellites du génome dans des modèles murin et cellulaire : intérêt physiopathologique et clinique". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066565/document.
Texto completo da fonteInactivation of the MMR (mismatch repair) system promotes the oncogenic process of microsatellite instability (MSI). During my PhD, I firstly investigated the role of azathioprine (Aza) in the induction of MSI tumors in mice. Epidemiological studies reported a correlation between the occurrence of late MSI cancers in humans and long-term treatment with this immunosuppressant whose cytotoxicity was shown in vitro to be mediated by MMR activity. Using a dose-response study, I observed the occurrence of rare late-onset MSI lymphomas in wild-type mice treated with Aza, but not with ciclosporin (another immunosuppressant used for comparison). These results established in vivo that long-term Aza exposure is a risk factor for the emergence of MSI tumors. Secondly, I was interested in the CMMRD syndrome (constitutional MMR deficiency), a major and rare predisposition to MSI cancers. Since CMMRD patients are carriers of biallelic germline mutations of a MMR gene, diagnosis is based on constitutional genotyping, a method that was found non-contributory when a variant of unknown significance is detected (30% patients). In this context, I developed a complementary approach for the detection of this syndrome in at-risk patients, based on the hypothesis that two functional features of MMR-deficient tumor cells, i.e. the MSI phenotype and the tolerance to genotoxic agents such as Aza, can be demonstrated in non-neoplastic tissues of CMMRD patients. We provided a sensitive and specific method that may constitute a valuable tool when diagnosis of CMMRD could not be confirmed by genetic testing
Micelli, Lupinacci Renato. "Caractérisation anatomo-clinique et phénotypique des adénocarcinomes canalaires du pancréas avec instabilité des microsatellites". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066311/document.
Texto completo da fontePancreatic ductal adenocarcinoma (PDAC) is a major health problem in France and around the world. PDAC is developed mainly from two precursor lesions: pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm (IPMN). There are several molecular mechanisms underlying pancreatic oncogenesis. Particularly, we were interested in the MSI (MicroSatellite Instability) which is due to a defective DNA Mismatch Repair (MMR) system, which normally functions to recognize and repair erroneous insertions, deletions, and mis-incorporation of bases that can arise during DNA replication and recombination. The MSI phenotype was first described in the familial cancer condition known as Lynch syndrome (LS), where the MMR genes MLH1, MSH2, MSH6 or PMS2 harbor germline mutations. Interest in MSI tumors has recently increased after studies have highlighted the concomitant expression of multiple active immune checkpoint (ICK) markers including PD-1 and PD-L1 and the role of the MSI status to predict clinical benefit from immune checkpoint blockade. A Our results indicate that the MSI phenotype occurs in PDAC with a frequency of 1-2%. Our data showed that IHC using antibodies against the four MMR proteins was more sensitive for the assessment of MSI status than PCR-based methods. In addition, we demonstrate for the first time a statistically significant positive association between MSI and IPMNs in PDAC. MSI PDAC, including IPMN, are unlikely to be sporadic since they display molecular features that are usually observed in LS-related neoplasms. Also, our results highlight that an MSI-driven immunogenic pathway to cancer is active in MSI PDACs but suggest that MSI-driven somatic events may be tissue-specific. We observed a stronger lymphocytic tumor infiltration by activated TCD8 cells in MSI PDAC compared to MSS PDAC and found a positive association between PD-L1 expression and MSI status, suggesting that MSI PDAC could be responsive to ICK blockade therapy
Greene, Malorie. "Étude des conséquences génomiques et fonctionnelles de l'instabilité des microsatellites dans le cancer colorectal". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066592/document.
Texto completo da fonteSince the discovery of a link between mismatch repair (MMR) deficiency and cancer, microsatellite instability (MSI) is thought as a process underlying cell transformation and tumour progression and invasion. MSI tumours are a subset of frequent human neoplasms, both inherited and sporadic, associated with several primary locations (colon, stomach, endometrium…). In MMR-deficient cells, MSI generates hundreds of frameshift mutations in genes (MSI Target Genes, MSI-TGs) containing coding microsatellite sequences (e.g. -1/+1 bp, insertions/deletions, i.e. indels). Some of these mutations affect genes with a role in human carcinogenesis and are thus expected to promote the MSI-driven tumorigenic process. During my PhD, I aimed to decipher the role of MSI in colon tumorigenesis. I exploited exome-sequencing data available in my lab that were generated from the analysis of a series of 47 human MSI primary colorectal cancer (CRC). Through biostatistics analysis and mathematical models that we designed to interpret mutation rates in the context of the high background for instability characterizing MSI in CRC, we identified a few microsatellites containing genes coding mutations that were negatively selected in MSI colon tumours (N=13). Under the hypothesis that these events may have a negative impact in colon tumorigenesis, I demonstrated that the silencing of these MSI target genes (siRNA/shRNA) was deleterious for MSI cancer cells using in vitro and in vivo models (impairment of proliferation and/or migration and/or response to chemotherapy and/or tumour growth) (Jonchère*, Marisa*, Greene* et al., submitted)
Borie, Claire. "Instabilité des microsatellites et cancers : recherche et description de ce phénotype tumoral dans les cancers du patient immunodéprimé". Paris 7, 2011. http://www.theses.fr/2011PA077067.
Texto completo da fonteMSI cancers arise as a consequence of loss of fonction of the DNA Mismatch repair system ("MMR" System). Inactivation of this system results in accumulation of replication errors in the genome of these tumors, in particular in repetitive séquences of the DNA called microsatellites; these tumors are therefore called MSI for " Instable Microsatellite". MSI cancers are inherited diseases associated with familial the colorectal cancer (Lynch syndrom or HNPCC), and represent 15-20 % of sporadic colorectal, gastric and endometrial cancers. Recently, the MSI phenotype was reported in other sporadic cancers. In particular owing to the works realized in our laboratory; this phenotype was described in non Hodgkin lymphomas (NHLs), but only in the NHL arising in an immuno-suppression context ( ID-RL), i. E. HIV-related or after organ transplantation. The objectives of my thesis were in this context: i) to specify the incidence of MSI in the ID-RL and establish the clinical and biological characteristics of these lymphomas compared with the other ID-RL (ID-RL not -MSI); ii) to search for a possible association between MSI and other frequent immuno-supression related tumoral types, e. G. In the squamous cell carcinomas cancers (ID-SCC) and the Kaposi's sarcomas (ID-KS). We established that the MSI phenotype is rarely observed in the ID-RL, representing 2-5 % of HIV-related NHL and approximately 10 % of PTLD. Briefly, MSI PTLD are characterized by their late occurrence after organ transplantation (median > 5 years), rare association with EBV (< 50 %), and frequent T phenotype (50 % of the PTLD T are MSI). MSI is significantly associated in these tumors after Azathioprine (Imurel) treatement. Further, loss of expression of the MMR proteins is heterogeneous in the ID-RL : MLH1, as well MSH2 or MSH6 can be involved. Loss of expression of O6 methyl guanine transferase (MGMT), a repair enzyme whose inactivation helps in selection of MMR deficient clones, was significantly associated with MSI in ID-RL. Finally, ID-RL MSI are characterized by few chromosomal rearangements and frequent mutations of the oncogene BRAF (Borie and al. , Int. J Cancer on 2010). My work involved the study of large series of tumors ID-RL, SCC and KS, to better understand the role of MSI in the oncogenetic process. Interestingly, I contributed to the identification of original clinical and molecular features of ID-RL MSI. Prospectives studies are needed to better define prognostic factors and therapeutic protocols of these tumors as compared with to the other ID-RL. This would be in particular interest, in PTLD-T. Following the example of what has been reported in other tumors, MSI could indeed be a factor to take into account in the treatment of these lymphomas
El-Murr, Nizar. "Étude de l'impact des microARNs sur la carcinogenèse des cancers colorectaux instables sur les séquences répétées microsatellites du génome". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2014. http://tel.archives-ouvertes.fr/tel-00990895.
Texto completo da fonteBoulagnon-Rombi, Camille. "Etude du récepteur d’endocytose LRP1 dans les adénocarcinomes coliques : caractéristiques cliniques, pathologiques et moléculaires associées et valeur pronostique". Thesis, Reims, 2017. http://www.theses.fr/2017REIMM203/document.
Texto completo da fonteLRP1 (low-density lipoprotein receptor–related protein 1), a multifunctional endocytic receptor, has recently been identified as a hub in a biomarker network for multi-cancer clinical outcome prediction. Its role in côlon cancer has not been characterized. Here, we investigate the relationship between LRP1 and colon cancer.LRP1 mRNA expression was determined in colon adenocarcinoma and paired colon mucosa samples, and in stromal and tumoral cells obtained after laser capture microdissection. The clinical potential was further investigated by immunohistochemistry in a population-based colon cancer series (n = 307). LRP1 methylation, mutation and miR-205 expression were evaluated and compared to LRP1 expression levels.LRP1 mRNA levels are significantly decreased in colon adenocarcinoma cells compared to colon mucosa and stromal cells. Low LRP1 immunohistochemical expression in adenocarcinomas was associated with higher age, right-sided tumor, loss of CDX2 expression, Annexin A10 expression, CIMP-H, MSI-H and BRAFV600E mutation. Low LRP1 expression correlates with poor clinical outcome, especially in stage IV patients. LRP1 expression was downregulated by LRP1 mutation. LRP1 expression was slightly modified by miR-205 expression. LRP1 promoter was never methylated.Loss of LRP1 expression is associated with peculiar clinocopathological and molecular characteristics and with worse colon cancer outcomes
Chalastanis, Alexandra. "Etude des facteurs associés à l'instabilité des microsatellites dans l'initiation et la progression des tumeurs déficientes dans le système de réparation des mésappariements de bases de l'ADN". Paris 6, 2009. http://www.theses.fr/2009PA066580.
Texto completo da fonteViguier, Jérôme. "Identification de facteurs moléculaires prédictifs de la chimiosensibilité des cancers colorectaux". Paris 6, 2006. http://www.theses.fr/2006PA066324.
Texto completo da fonteMiquel, Catherine. "Caractérisation des mutations des gènes cibles de l' instabilité des séquences répétées microsatellites dans les cancers colorectaux humains". Paris 6, 2005. http://www.theses.fr/2005PA066336.
Texto completo da fonteMajed, Zeina. "Elaboration d'un nouveau modèle pour la caractérisation de nouveaux gènes impliqués dans la stabilité des sites fragiles". Montpellier 1, 2009. http://www.theses.fr/2009MON1T022.
Texto completo da fonteCommon fragile sites are chomosomal regions involved in recurrent breaks, which are "expressed" under various physiological stresses, most of them are known to disturb DNA replication. A direct link between fragile sites and emergence of various types of chromosomal rearrangement has been established, even in early stages of tumorigenesis. However, only few genes involved in genome stability at fragile sites have been identified. The aim of this study is to identify new genes involved in the expression of fragile sites and to elucidate molecular processes that affect their stability. We established a cell based system on a mismatch repair deficient background. 20 candidate genes were targeted in this study. We examined the incidence of frameshift mutations in 32 mononucleotide repeats of these genes. 17 frameshift mutations were found. We demonstrate that frameshift mutations affecting coding mononucleotide repeat of ATR, inactivate one of the two alleles leading to formation of breaks at fragile sites. This collection of clones gives us a unique cellular model to study precisely the maintenance of genome stability at fragile sites. Furthermore, we have investigated the effects of the deregulation of the expression of MCPH1/BRIT1 on common fragile site stability. MCPH1/BRIT1 acts as a regulator of both the intra-S and G2/M keckpoints. We show that deregulation of the expression of MCPH1/BRIT1 increase H2AX phosphorylation suggesting the accumulation of DNA double-strand breaks. This leads to formation of breaks at fragile sites. These findings demonstrate a critical role for the MCPH1/BRIT1 in regulating chromosome stability, and in particular, common fragile site
Livros sobre o assunto "Instabilité microsatellites"
Millar, Anna L. Frequency estimation of endometrial cancer associated with microsatellite instability and mismatch repair gene defects. Ottawa: National Library of Canada, 1999.
Encontre o texto completo da fonteGryfe, Robert. Colorectal cancer microsatellite instability. 2001.
Encontre o texto completo da fonteUmar, A. Lynch Syndrome (HNPCC) and Microsatellite Instability. Ios Pr Inc, 2004.
Encontre o texto completo da fonteUmar, A. Lynch Syndrome (HNPCC) and Microsatellite Instability Analysis Guidelines, Part 2. IOS Press, 2006.
Encontre o texto completo da fonteLeahy, Dermot T. Clinicopathological significance of p53, bcl-2 and microsatellite instability in colorectal carcinoma. 1998.
Encontre o texto completo da fonteCurran, Bernie. Microsatellite instability and loss of heterozygosity distinguish two phenotypes in colorectal carcinoma and identity a subgroup with poor prognosis. 1996.
Encontre o texto completo da fonteTumor microsatellite instability, mismatch repair deficiency and response to chemotherapy: A molecular reanalysis of randomized adjuvant chemotherapy trials in colon cancer. Ottawa: National Library of Canada, 2001.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Instabilité microsatellites"
Patel, Nisha R., Michael L. Wong, Anthony E. Dragun, Stephan Mose, Bernadine R. Donahue, Jay S. Cooper, Filip T. Troicki et al. "Microsatellite Instability". In Encyclopedia of Radiation Oncology, 502. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_211.
Texto completo da fonteAhlquist, Terje C., e Ragnhild A. Lothe. "Microsatellite Instability". In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3731-2.
Texto completo da fonteAhlquist, Terje C., e Ragnhild A. Lothe. "Microsatellite Instability". In Encyclopedia of Cancer, 2842–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_3731.
Texto completo da fonteAhlquist, Terje, e Ragnhild A. Lothe. "Microsatellite Instability". In Encyclopedia of Cancer, 2305–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3731.
Texto completo da fontePrasad, Meena A., e Barbara Jung. "Microsatellite Instability and Intestinal Tumorigenesis". In Intestinal Tumorigenesis, 29–53. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19986-3_2.
Texto completo da fonteLi, Jinhong, e Fan Lin. "Lower Gastrointestinal Tract and Microsatellite Instability". In Handbook of Practical Immunohistochemistry, 423–33. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-8062-5_25.
Texto completo da fonteChen, Guoli, Jianhong Li, Zongming Eric Chen, Jinhong Li e Fan Lin. "Lower Gastrointestinal Tract and Microsatellite Instability (MSI)". In Handbook of Practical Immunohistochemistry, 701–14. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-83328-2_29.
Texto completo da fonteElfimova, Natalia, Wafa Amer e Margarete Odenthal. "Analysis of Microsatellite Instability by Microfluidic-Based Electrophoresis". In Methods in Molecular Biology, 287–96. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-029-8_25.
Texto completo da fonteViana-Pereira, Marta, Chris Jones e Rui Manuel Reis. "Pediatric High-Grade Glioma: Role of Microsatellite Instability". In Pediatric Cancer, Volume 3, 205–10. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4528-5_22.
Texto completo da fonteLiu, Yuqing, Weiwen Wang, Chuan-Xian Ren e Dao-Qing Dai. "MetaCon: Meta Contrastive Learning for Microsatellite Instability Detection". In Medical Image Computing and Computer Assisted Intervention – MICCAI 2021, 267–76. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-87237-3_26.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Instabilité microsatellites"
Singh, Sukhi, Janez Kokosar, Jan Otonicar e Luka Ausec. "179 Profiling microsatellite instability using RNA sequencing data". In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0179.
Texto completo da fontePaulose, Assoc Prof Roopa, Prof Roopa Paulose, Divya Ail, Shital Biradar e K. Sundaram. "PTU-054 Microsatellite instability in stage II colorectal carcinoma". In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.395.
Texto completo da fonteKIM, Jee Hung, Chang-gon Kim, Joong Bae Ahn, MinKyu Jung, Seung Hoon Beom, Joo Hoon Kim, Soo Jin Heo e Sang Joon Shin. "Abstract 808: Microsatellite instability in metastatic colorectal cancer (mCRC)". In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-808.
Texto completo da fonteSamara, Katerina D., Eirini Neofytou, Nikolaos Tzanakis, Alexandros D. Karatzanis, Dimitra Papandrinopoulou, Nikolaos Siafakas e Eleni G. Tzortzaki. "Perforin Expression In COPD Patients With Microsatellite DNA Instability". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3879.
Texto completo da fonteBond, Catherine E., Aarti Umapathy, Ron L. Buttenshaw, Leesa Wockner, Barbara A. Leggett e Vicki LJ Whitehall. "Abstract 106: Chromosomal instability inBRAFmutant, microsatellite stable colorectal cancers". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-106.
Texto completo da fonteWang, Huilin, Jiang Zhu, Guanbiao Liang, Yongyong Wang, Jianji Guo, Min Zheng, Qin Fu e Weiwei Shi. "Abstract 4316: Frequent microsatellite instability in Chinese solid tumor patients". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4316.
Texto completo da fonteSussman, Daniel A., Shivali Berera, Peter Hosein, Feng Miao, Tulay Koru-Sengul, Jacob McCauley, Erin Kobetz-Kerman, Olveen Carrasquillo e Maria T. Abreu. "Abstract B45: Microsatellite instability among disenfranchised minority colorectal cancer patients". In Abstracts: Sixth AACR Conference: The Science of Cancer Health Disparities; December 6–9, 2013; Atlanta, GA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7755.disp13-b45.
Texto completo da fonteAbbas, Basman F., Ahmed S. Abood, Ghufran H. Abed, Nidhal A. Mohammad e Alaa D. Kadhim. "BAT26 marker as detector of microsatellite instability in breast tumors". In 1ST SAMARRA INTERNATIONAL CONFERENCE FOR PURE AND APPLIED SCIENCES (SICPS2021): SICPS2021. AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0121227.
Texto completo da fonteKurata, K., M. Kubo, H. Mori, H. Kawaji, Y. Motoyama, L. Kuroki, M. Yamada, K. Kaneshiro, M. Kai e M. Nakamura. "Abstract P1-06-11: Microsatellite instability in triple negative breast cancers". In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p1-06-11.
Texto completo da fonteBhattacharya, Priyanjali, Naveed Anjum Chikan, Arati Sharma, Dhimant Desai, Charyguly Annageldiyev, Pinaki Patel e Trupti N. Patel. "Abstract 1741: Identification of microsatellite instability in hematologic malignant cell lines". 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.sabcs18-1741.
Texto completo da fonteRelatórios de organizações sobre o assunto "Instabilité microsatellites"
Baranovskaya, Svetlana. Microsatellite and Chromosomal Instability in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 2004. http://dx.doi.org/10.21236/ada430384.
Texto completo da fonteBaranovskaya, Svetlana. Microsatellite and Chromosomal Instability in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 2003. http://dx.doi.org/10.21236/ada418690.
Texto completo da fonteMichelmore, Richard, Eviatar Nevo, Abraham Korol e Tzion Fahima. Genetic Diversity at Resistance Gene Clusters in Wild Populations of Lactuca. United States Department of Agriculture, fevereiro de 2000. http://dx.doi.org/10.32747/2000.7573075.bard.
Texto completo da fonte