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Journal ArticleDOI

Tracing the cellular origin of cancer

Cédric Blanpain
- 01 Feb 2013 - 
- Vol. 15, Iss: 2, pp 126-134
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TLDR
This review explores how mouse genetic lineage-tracing experiments that allow the expression of oncogenes and/or the deletion of tumour suppressor genes in defined cell lineages have been instrumental in defining the cellular origin of different solid tumours in mouse models for various human cancers.
Abstract
Although many genes that lead to different types of cancer when mutated have been identified, the cells that initiate tumour formation following accumulation of these mutations have, until recently, remained elusive. This review explores how mouse genetic lineage-tracing experiments that allow the expression of oncogenes and/or the deletion of tumour suppressor genes in defined cell lineages have been instrumental in defining the cellular origin of different solid tumours in mouse models for various human cancers.

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Citations
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In vitro and in vivo antitumor activity of a novel carbonyl ruthenium compound, the ct-[RuCl(CO)(dppb)(bipy)]PF-6[dppb=1,4-bis(diphenylphosphine)butane and bipy=2,2'-bipyridine]

TL;DR: The results showed that ct-[RuCl(CO)(dppb)(bipy)]PF6 was cytotoxic against all tumor cell lines tested and was more effective against tumor cells compared to the normal cell line, indicating selectivity, especially in B16F10 cells.
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Telomerase: The Devil Inside.

TL;DR: The recent findings that telomerase reverse transcriptase (TERT) promoter mutations represent the most common non-coding mutations in human cancer have flared up the long-standing discussion whether cancer originates from telomersase positive stem cells or telomerases reactivation is a final step in cellular transformation.
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How do K - RAS -activated cells evade cellular defense mechanisms?

TL;DR: Evidence is summarized suggesting that K-RAS-activated cells do not evade cellular defense mechanisms per se; instead, cells with K- RAS mutations are selected only if they occur in cells in which defense mechanism is abrogated.
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Lipopolysaccharide promotes tumorigenicity of hepatic progenitor cells by promoting proliferation and blocking normal differentiation.

TL;DR: It is concluded that LPS may promote aberrant proliferation of mouse hepatic progenitor cells and restrict their normal differentiation, and long-term exposure of mHPCs to LPS increased the risk of tumour formation.
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Transcriptional memory of cells of origin overrides β‐catenin requirement of MLL cancer stem cells

TL;DR: It is shown that transcriptional memory from cells of origin predicts AML patient survival and allows β‐catenin‐independent transformation in MLL‐CSCs derived from hematopoietic stem cell (HSC)‐enriched LSK population but not myeloid–granulocyte progenitors.
References
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Journal ArticleDOI

Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
Journal ArticleDOI

Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008.

TL;DR: The results for 20 world regions are presented, summarizing the global patterns for the eight most common cancers, and striking differences in the patterns of cancer from region to region are observed.
Journal ArticleDOI

Lessons from Hereditary Colorectal Cancer

TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
Journal ArticleDOI

Identification of stem cells in small intestine and colon by marker gene Lgr5

TL;DR: The expression pattern of Lgr5 suggests that it marks stem cells in multiple adult tissues and cancers, suggesting that it represents the stem cell of the small intestine and colon.
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Trending Questions (1)
Cancer is traced from when?

The paper does not explicitly mention when cancer is traced from. The paper discusses the cellular origin of cancer and how mouse genetic lineage-tracing experiments have helped in identifying the cells that initiate tumor formation.