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With disruption of DNA repair pathways pertinent to the timeline of cancer, thorough evaluation of mutations relevant to DNA repair proteins is crucial within cancer research. One such mutation includes S815L PMS2 - a mutation that results in significant decrease of DNA repair function by PMS2 protein. While mutation of PMS2 is associated with significantly increased colorectal and endometrial cancer risk, much work is left to do to establish the functional effects of the S815L PMS2 mutation in ovarian cancer progression. In this article, researchers contribute to this essential area of research by uncovering the tumor-progressive effects of the S815L PMS2 mutation in the context of ovarian cancer cell lines.

In this study, we performed orthotopic auto-transplantation of fresh ovarian tissues by transplanting unilateral half ovarian tissue to the contralateral ovary in the ICR (Institute of Cancer Research) strain of outbred, heterogeneous mice to determine if the transplanted tissue could be functional. We found that the freshly transplanted mouse ovarian tissue survived and functional, as histochemical and immunofluorescence assays have shown that not only both follicles at different developing stages and corpus luteum are available, but the morphology of them are properly maintained within the transplanted tissue.

Inefficient penetration of cancer drugs into the interior of the three-dimensional (3D) tumor tissue limits drugs' delivery. The authors hypothesized that the addition of phospholipase A2 (PLA2) would increase the permeability of the drug doxorubicin for efficient drug penetration. They found that 1 mM PLA2 had the highest permeability. Increased efficiency in drug delivery would allow lower concentrations of drugs to be used, minimizing damage to normal cells.