Aneuploidy in Cancer: Seq-ing Answers to Old Questions

被引：62

作者：

Knouse, Kristin A. ^{[1
,2
]}

Davoli, Teresa ^{[3
,4
]}

Elledge, Stephen J. ^{[3
,4
]}

Amon, Angelika ^{[1
]}

机构：

[1] MIT, Dept Biol, Howard Hughes Med Inst, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA

[2] Harvard Med Sch, Div Hlth Sci & Technol, Boston, MA 02115 USA

[3] Harvard Med Sch, Howard Hughes Med Inst, Dept Genet, Boston, MA 02115 USA

[4] Brigham & Womens Hosp, Div Genet, 75 Francis St, Boston, MA 02115 USA

来源：

ANNUAL REVIEW OF CANCER BIOLOGY, VOL 1 | 2017年 / 1卷

关键词：

chromosome missegregation; karyotype; copy number alterations; cancer genomics; SPINDLE-ASSEMBLY CHECKPOINT; CYTOMETRIC DNA ANALYSIS; ACUTE MYELOID-LEUKEMIA; HEAT-SHOCK FACTOR-1; BREAST-CANCER; CHROMOSOME MISSEGREGATION; S-PHASE; BARRETTS-ESOPHAGUS; CLONAL EVOLUTION; PROGNOSTIC VALUE;

D O I：

10.1146/annurev-cancerbio-042616-072231

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Aneuploidy, the state of having gained or lost chromosomes, is a hallmark of cancer. Approximately 90% of tumors have gained or lost at least one chromosome. In spite of aneuploidy occurring as frequently as, if not more often than, disruption of the p53 pathway, whether and how aneuploidy influences tumorigenesis is still poorly understood. Here, we take advantage of large-scale tumor sequencing efforts to assess karyotypic alterations across many cancer types and review recent sequencing studies that show how karyotypes change in space and time. We further summarize findings that describe the effects of aneuploidy on untransformed cells, the mechanisms by which aneuploidy could drive tumorigenesis, and the potential to target aneuploidy for cancer therapy.

引用

页码：335 / 354

页数：20

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