Random Records

Paper: Tumor suppressor RecQL5 controls recombination induced by DNA crosslinking agents doi: 10.1016/j.bbamcr.2014.01.005. Epub 2014 Jan 10 It is a little bit complicated to imagine how RecQL5 repairs the damage from interstrand crosslink (ICL) agent, like in this case cisplatin and mitomycin C. RecQ-family; DNA helicase (denature DNA duplex) - maintenance genome stability Focus on RecQL5 - RecQL5 - tumor suppressor - interact with Rad51- displace Rad51-ssDNA Gap; Precise role of RecQL5 is elusive. Results; 1.RecQL5 is involved in DNA interstrand crosslink (cisplatin, mitomycin C) repair. 2.Phenotype of RecQL5 KO resembled to FA gene KO cells 3.RecQL5 is involved in FANCD1 (BRCA2)-dependent ICL repair 4. Disappear of Rad51-foci delayed in REQL5KO cells after MMC treatment 5. Rad54 delayed Rad51-ssDNA in HR, compare to RecQL5 6.RecQL5 sensitivity to CDDP, and delayed Rad51-ssDNA detachment. 7.RecQL5 and Rad54 have a different effect on Rad51-ssDNA detachment. 8.Su

I have read the news and view in the nature which summarizes two articles demonstrating the tumor cells, esp. lung adenocarcinomas (advanced and aggressive stage) divided and gave rise to two cell populations. ( doi :10.1038/nature22494) 1. tumour cells - actively dividing cells 2. supporting cell or so called "niche cell" - which provide the microenvironment to support the growth of the tumour cells Picture indicates the tumour cell divides and gives rise to two subpopulations (a). Within the tumour tissue, there are two cell subpopulations, one support the growth of tumour by which it secretes the growth factor that can stimulate the tumour cell growth (b). Question remains; supporting cell can secrete and promote the cancer growth in the other cancer type besides the its own neighbouring cells