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Mesenchymal stem cells(MSCs) play a role in tumor formation by differentiating into cancer associated fibroblasts (CAFs) which enable metastasis of tumors. The process of conversion of MSCs into CAFs is not clear. In this study, authors tested the hypothesis that cancers cells secrete soluble factors that induce differentiation by culturing bone marrow mesenchymal stem cells in media conditioned by a breast cancer cell line.

Authors emphasize the challenges of manual tumor segmentation and the potential of deep learning models to enhance accuracy by automatically analyzing MRI scans.

This paper hypothesized that the tumor microenvironment mediates cancer’s response to oxidative stress by delivering extracellular vesicles to cancer cells. Breast and lung cancer cells were treated with EVs, reavealing that EVs extracted from oxidatively stressed adipocytes increased the cell proliferation of breast cancer cells. These findings present a novel way that the TME influences cancer progression.

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.

Glioblastoma Multiforme (GBM) is the most malignant brain tumor with the highest fraction of genome alterations (FGA), manifesting poor disease-free status (DFS) and overall survival (OS). We explored The Cancer Genome Atlas (TCGA) and cBioportal public dataset- Firehose legacy GBM to study DNA repair genes Activating Signal Cointegrator 1 Complex Subunit 3 (ASCC3) and Alpha-Ketoglutarate-Dependent Dioxygenase AlkB Homolog 3 (ALKBH3). To test our hypothesis that these genes have correlations with FGA and can better determine prognosis and survival, we sorted the dataset to arrive at 254 patients. Analyzing using RStudio, both ASCC3 and ALKBH3 demonstrated hypomethylation in 82.3% and 61.8% of patients, respectively. Interestingly, low mRNA expression was observed in both these genes. We further conducted correlation tests between both methylation and mRNA expression of these genes with FGA. ASCC3 was found to be negatively correlated, while ALKBH3 was found to be positively correlated, potentially indicating contrasting dysregulation of these two genes. Prognostic analysis showed the following: ASCC3 hypomethylation is significant with DFS and high ASCC3 mRNA expression to be significant with OS, demonstrating ASCC3’s potential as disease prediction marker.

Tertiary lymphoid structures (TLS) are lymph node-like structures that form at sites of inflammation, and their presence in cancer patients is predictive of a better clinical outcome. One significant obstacle to TLS formation is reduced immune cell infiltration into the tumor microenvironment (TME). Recent studies have shown that vasculature normalizing (VN) agents may override this defect to improve tissue perfusion and increased immune cell entry into the TME. However, their effects on immune cell and tumor cell phenotype remain understudied. Here the authors investigate whether treating tumor cells with VN would reduce their immunosuppressive phenotype and promote production of chemokine that recruit immune cells and foster TLS formation.

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 article the authors created an interaction map of proteins involved in colorectal cancer to look for driver vs. non-driver genes. That is they wanted to see if they could determine what genes are more likely to drive the development and progression in colorectal cancer and which are present in altered states but not necessarily driving disease progression.

The authors looked at biomarkers in glioblastoma patients they hypothesized to be correlated with survival rate. Ultimately they did not find hMSH2 or hMSH6, genes involved in mismatch repair, to be significantly associated with outcomes related to increased survival.

The authors found that treatment with AS20 suppressed phorbol 12-myristate 13-acetate (PMA) and 5-flurouracil (5-FU) induction of COX2 expression. We also observed AS20 treated cells showed DNA fragmentation in HeLa cells.