Objective: Stimulated mesenchymal stem cells (MSCs) have capacity of differentiation in many cell types. It is being used in degenerative diseases treatment protocols. We evaluated the collagen V (COL V) and collagen XI (COL XI) influence in the differentiation of rabbits adipose tissue-derived MSCs in a chondrocyte-like cell phenotype. Method: MSCs isolated of New Zealand rabbits adiposetissue were maintained in culture by 4 weeks. COLV, COLXI and COLV/XI (10 μg/ml) were added to culture during 72 h. The cells aggregates were stained with Toluidine blue, Alcian blue and Picrosirius. Chondrocyte-like phenotype was confirmed by immunofluorescence to CD34, vimentin and collagens I, II and III. Results: MSCs stimulated with COLV expressed proteoglicans and collagen, when compared with COLXI and COLV/ XI and control. In the presence of COLV, MSCs was capable to increase collagen II expression confirming its chondrocyte-like cell phenotype. In contrast, MSCs cultured with COLXI and COLV/XI express collagen I and III. Conclusion: The data suggest that COLV may facilitate the differentiation of rabbit adipose tissue-derived stem cells into a chondrocyte-like phenotype. Further studies are urged in order to evaluate the influence of COLV in the ability of chondrocytes to remodel osteoarthritic joint surface at ultra structural and molecular levels. Objective: XRCC1 is essential for DNA base excision repair, single strand break repair and nucleotide excision repair. Method: We evaluated XRCC1 immunohistochemically in early stage breast (n=2046), ovarian (n=157), gastric (n= 140), colorectal (n=250) and pancreaticobiliary cancers (n= 240). Pre-clinically, we evaluated a panel of XRCC1 deficient and proficient Chinese hamster ovary and human cancer cell lines. Double strand break repair (DSB) inhibitors targeting ATM (KU55933), DNA-PKcs (NU7441) and ATR (NU6027) were evaluated for synthetic lethality and cisplatin alone or in combination with DSB inhibitors for chemopotentiation. Results: In breast cancer, XRCC1 loss (16 %) was associated with a 2-fold increase in risk of death and metastasis (p< 0.0001). In ovarian cancer, XRCC1 positive tumours (44 %) were more resistant to platinum chemotherapy (p=0.0001). XRCC1 positivity conferred a 2 fold increase of risk of death (p=0.002) and independently associated with poor survival (p= 0.002). Pre-clinically, KU55933, NU7441 and NU6027 were synthetically lethal in XRCC1 deficient compared to proficient cells as evidenced by DSB accumulation, G2/M cell cycle arrest and apoptosis. XRCC1 deficient cells were hypersensitive to cisplatin which was enhanced by DSB repair inhibitors compared to in proficient cells. Conclusion: Conclusions: XRCC1 deficiency in human tumours may be suitable for synthetic lethality application and exploited for cisplatin chemotherapy potentiation.