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Anti-BRCA2 antibody produced in rabbit

RRID:AB_10602692

Antibody ID

AB_10602692

Target Antigen

BRCA2 antibody produced in rabbit human

Vendor

Sigma-Aldrich

Cat Num

HPA026815

Proper Citation

(Sigma-Aldrich Cat# HPA026815, RRID:AB_10602692)

Reference

PMID:28092266

Clonality

polyclonal antibody

Host Organism

rabbit

Comments

Vendor recommendations: Immunohistochemistry; Other; indirect immunofluorescence: suitable, protein array: suitable, immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable

Publications that use this research resource

TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24- cancer cells.

  • Pal D
  • Elife
  • 2017 Jan 16

Literature context: PA026815 (RRID:AB_10602692)


Abstract:

Many lines of evidence have indicated that both genetic and non-genetic determinants can contribute to intra-tumor heterogeneity and influence cancer outcomes. Among the best described sub-population of cancer cells generated by non-genetic mechanisms are cells characterized by a CD44+/CD24- cell surface marker profile. Here, we report that human CD44+/CD24- cancer cells are genetically highly unstable because of intrinsic defects in their DNA-repair capabilities. In fact, in CD44+/CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduce the expression of genes that are crucial in coordinating DNA damage repair mechanisms. Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are characterized by increased accumulation of DNA copy number alterations, greater genetic diversity and improved adaptability to drug treatment. Together, these data suggest that the transition into a CD44+/CD24- cell state can promote intra-tumor genetic heterogeneity, spur tumor evolution and increase tumor fitness.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA045508()