X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

NMuMG

RRID:CVCL_0075

Organism

Mus musculus

Comments

Breed/subspecies: Namru.

Proper Citation

ECACC Cat# 94081121, RRID:CVCL_0075

Reference

PMID:4366196

Category

Spontaneously immortalized cell line

Sex

Female

Vendor

ECACC

Cat Num

94081121

Cross References

BTO; BTO:0004183 CLO; CLO_0008186 CLDB; cl3719 ATCC; CRL-1636 BCRC; 60087 ECACC; 94081121 IZSLER; BS CL 188

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

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.