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Homojen Glioblastoma Örneklerinin Yüksek Çözünürlüklü Genetik Teknolojiler ile Analizi

Year 2018, Volume: 6 Issue: 2, 63 - 71, 03.08.2018
https://doi.org/10.21541/apjes.403727

Abstract

Tümör içi genomik heterojenlik kanserlerde sıkça karşılaşılan bir durumdur. Normal şartlarda her bir hücrede her bir genin iki kopyası vardır ve bazı istisnalar dışında organizmanın farklı hücreleri aynı DNA dizisini taşır. Kanser hücrelerinde ise gerek mutasyonlar sonucu gerekse de DNA silinmeleri ve eklenmeleri sonucu bu düzenli yapı karmaşık ve heterojen bir yapıya dönüşür. Bu genetik heterojenliğin sebebi ve tümör oluşumundaki rolü, genetik veri üretebilme teknolojilerindeki gelişmeler ışığında son zamanlarda çokça çalışılan önemli bir problemdir. Aynı tümörden elde edilmiş yüksek çözünürlüklü homojen numuneler, heterojenliği anlamak için yapılan çalışmalarda büyük önem arz etmektedir. Gerek kanser dokusuna erişimdeki zorluklar, gerekse de finansal limitler böyle yüksek çözünürlüklü veri setlerinin elde edilmesi önünde engel oluşturmaktadır. Glioblastoma multiforme teşhis sonrası ortalama yaşam süresi yaklaşık on beş ay olan, en sık görülen ve en agresif beyin tümörüdür. Bu çalışmada bir glioblastoma hastasından alınan detaylı homojen ve heterojen numuneler kullanılarak elde edilmiş yüksek çözünürlüklü bir veri seti incelenip, yapılan analizler sunulacaktır.

References

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  • [18] N. J. Szerlip et al., "Intratumoral heterogeneity of receptor tyrosine kinases EGFR and PDGFRA amplification in glioblastoma defines subpopulations with distinct growth factor response," Proceedings of the National Academy of Sciences, vol. 109, no. 8, pp. 3041-3046, 2012.
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  • [22] K. Harada, T. Nishizaki, S. Ozaki, H. Kubota, H. Ito, and K. Sasaki, "Intratumoral cytogenetic heterogeneity detected by comparative genomic hybridization and laser scanning cytometry in human gliomas," Cancer research, vol. 58, no. 20, pp. 4694-4700, 1998.
  • [23] S. L. Carter et al., "Absolute quantification of somatic DNA alterations in human cancer," Nature biotechnology, vol. 30, no. 5, pp. 413-421, 2012.
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  • [25] N. Andor, J. V. Harness, S. Mueller, H. W. Mewes, and C. Petritsch, "EXPANDS: expanding ploidy and allele frequency on nested subpopulations," Bioinformatics, vol. 30, no. 1, pp. 50-60, 2014.
  • [26] L. Ding et al., "Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing," (in eng), Nature, vol. 481, no. 7382, pp. 506-10, Jan 2012.
  • [27] M. Baysan et al., "Detailed longitudinal sampling of glioma stem cells in situ reveals Chr7 gain and Chr10 loss as repeated events in primary tumor formation and recurrence," International journal of cancer, vol. 141, no. 10, pp. 2002-2013, 2017.
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Year 2018, Volume: 6 Issue: 2, 63 - 71, 03.08.2018
https://doi.org/10.21541/apjes.403727

Abstract

References

  • 5. Referanslar[1] M. Baysan et al., "G-Cimp Status Prediction Of Glioblastoma Samples Using mRNA Expression Data," PloS ONE, vol. 7, no. 11, p. e47839, 2012.
  • [2] B. E. Johnson et al., "Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma," Science, vol. 343, no. 6167, pp. 189-193, 2014.
  • [3] T. M. Brown and E. Fee, "Rudolf Carl Virchow: medical scientist, social reformer, role model," American Journal of Public Health, vol. 96, no. 12, p. 2104, 2006.
  • [4] S. Makino, "Further evidence favoring the concept of the stem cell in ascites tumors of rats," Annals of the New York Academy of Sciences, vol. 63, no. 5, pp. 818-830, 1956.
  • [5] G. H. Heppner and B. E. Miller, "Tumor heterogeneity: biological implications and therapeutic consequences," Cancer and Metastasis Reviews, vol. 2, no. 1, pp. 5-23, 1983.
  • [6] I. J. Fidler and M. L. Kripke, "Metastasis results from preexisting variant cells within a malignant tumor," Science, vol. 197, no. 4306, pp. 893-895, 1977.
  • [7] I. J. Fidler, "Tumor heterogeneity and the biology of cancer invasion and metastasis," Cancer research, vol. 38, no. 9, pp. 2651-2660, 1978.
  • [8] N. Navin et al., "Tumour evolution inferred by single-cell sequencing," Nature, vol. 472, no. 7341, pp. 90-94, 2011.
  • [9] M. Gerlinger et al., "Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing," Nature genetics, vol. 46, no. 3, pp. 225-233, 2014.
  • [10] J. Zhang et al., "Intratumor heterogeneity in localized lung adenocarcinomas delineated by multiregion sequencing," Science, vol. 346, no. 6206, pp. 256-259, 2014.
  • [11] L. H. Mengelbier et al., "Intratumoral genome diversity parallels progression and predicts outcome in pediatric cancer," Nat Commun, vol. 6, p. 6125, 2015.
  • [12] N. McGranahan and C. Swanton, "Biological and Therapeutic Impact of Intratumor Heterogeneity in Cancer Evolution," Cancer cell, vol. 27, no. 1, pp. 15-26, 2015.
  • [13] D. R. Johnson and B. P. O’Neill, "Glioblastoma survival in the United States before and during the temozolomide era," Journal of neuro-oncology, vol. 107, no. 2, pp. 359-364, 2012.
  • [14] D. R. Johnson, H. E. Leeper, and J. H. Uhm, "Glioblastoma survival in the United States improved after Food and Drug Administration approval of bevacizumab: A population‐based analysis," Cancer, vol. 119, no. 19, pp. 3489-3495, 2013.
  • [15] P. Y. Wen and S. Kesari, "Malignant gliomas in adults," New England Journal of Medicine, vol. 359, no. 5, pp. 492-507, 2008.
  • [16] V. Jung et al., "Evidence of focal genetic microheterogeneity in glioblastoma multiforme by area-specific CGH on microdissected tumor cells," Journal of Neuropathology & Experimental Neurology, vol. 58, no. 9, pp. 993-999, 1999.
  • [17] M. Snuderl et al., "Mosaic amplification of multiple receptor tyrosine kinase genes in glioblastoma," Cancer cell, vol. 20, no. 6, pp. 810-817, 2011.
  • [18] N. J. Szerlip et al., "Intratumoral heterogeneity of receptor tyrosine kinases EGFR and PDGFRA amplification in glioblastoma defines subpopulations with distinct growth factor response," Proceedings of the National Academy of Sciences, vol. 109, no. 8, pp. 3041-3046, 2012.
  • [19] A. Sottoriva et al., "Intratumor heterogeneity in human glioblastoma reflects cancer evolutionary dynamics," Proceedings of the National Academy of Sciences, vol. 110, no. 10, pp. 4009-4014, 2013.
  • [20] A. P. Patel et al., "Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma," Science, vol. 344, no. 6190, pp. 1396-1401, 2014.
  • [21] A. L. Vital et al., "Intratumoral patterns of clonal evolution in gliomas," Neurogenetics, vol. 11, no. 2, pp. 227-239, 2010.
  • [22] K. Harada, T. Nishizaki, S. Ozaki, H. Kubota, H. Ito, and K. Sasaki, "Intratumoral cytogenetic heterogeneity detected by comparative genomic hybridization and laser scanning cytometry in human gliomas," Cancer research, vol. 58, no. 20, pp. 4694-4700, 1998.
  • [23] S. L. Carter et al., "Absolute quantification of somatic DNA alterations in human cancer," Nature biotechnology, vol. 30, no. 5, pp. 413-421, 2012.
  • [24] A. Roth et al., "PyClone: statistical inference of clonal population structure in cancer," Nature methods, vol. 11, no. 4, pp. 396-398, 2014.
  • [25] N. Andor, J. V. Harness, S. Mueller, H. W. Mewes, and C. Petritsch, "EXPANDS: expanding ploidy and allele frequency on nested subpopulations," Bioinformatics, vol. 30, no. 1, pp. 50-60, 2014.
  • [26] L. Ding et al., "Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing," (in eng), Nature, vol. 481, no. 7382, pp. 506-10, Jan 2012.
  • [27] M. Baysan et al., "Detailed longitudinal sampling of glioma stem cells in situ reveals Chr7 gain and Chr10 loss as repeated events in primary tumor formation and recurrence," International journal of cancer, vol. 141, no. 10, pp. 2002-2013, 2017.
  • [28] T. I. Zack et al., "Pan-cancer patterns of somatic copy number alteration," Nature genetics, vol. 45, no. 10, pp. 1134-1140, 2013.
There are 28 citations in total.

Details

Primary Language Turkish
Subjects Engineering
Journal Section Articles
Authors

Mehmet Baysan 0000-0001-7359-2965

Publication Date August 3, 2018
Submission Date March 9, 2018
Published in Issue Year 2018 Volume: 6 Issue: 2

Cite

IEEE M. Baysan, “Homojen Glioblastoma Örneklerinin Yüksek Çözünürlüklü Genetik Teknolojiler ile Analizi”, APJES, vol. 6, no. 2, pp. 63–71, 2018, doi: 10.21541/apjes.403727.