Publications by authors named "R Chikarmane"
Article Synopsis
- Researchers are examining how prostate cancer cells alter their surrounding environment to promote growth, using both human tissues and a mouse model.
- They found that activation of the MYC signaling pathway is a common factor across different forms of human prostate cancer.
- The study shows that MYC-expressing cancer cells can reshape the tumor microenvironment, affecting various neighboring cell types and mirroring changes seen in human prostate cancer.
Article Synopsis
- - The study investigates how the microenvironment around prostate cancer tumors is significantly changed and how this affects the disease's development, utilizing single-cell RNA-sequencing and mouse models for research.
- - It was found that activation of the MYC signaling pathway in cancer cells is a major factor influencing these changes, indicating a common thread in the heterogeneity of prostate cancer across different patients.
- - The research also suggests that these cancer cells shape their environment by altering the states of surrounding non-cancerous cells, leading to changes associated with cancer progression, such as a switch from promoting immune responses to suppressing them.
Background: Evaluating the complex interplay of cell types in the tissue microenvironment is critical to understanding the origin and progression of diseases in the prostate and potential opportunities for intervention. Mouse models are an essential tool to investigate the molecular and cell-type-specific contributions of prostate disease at an organismal level. While there are well-documented differences in the extent, timing, and nature of disease development in various genetically engineered and exposure-based mouse models in different mouse strains and prostate lobes within each mouse strain, the underlying molecular phenotypic differences in cell types across mouse strains and prostate lobes are incompletely understood.
View Article and Find Full Text PDFResistance to AR signaling inhibitors (ARSis) in a subset of metastatic castration-resistant prostate cancers (mCRPCs) occurs with the emergence of AR- neuroendocrine prostate cancer (NEPC) coupled with mutations/deletions in PTEN, TP53, and RB1 and the overexpression of DNMTs, EZH2, and/or SOX2. To resolve whether the lack of AR is the driving factor for the emergence of the NE phenotype, molecular, cell, and tumor biology analyses were performed on 23 xenografts derived from patients with PC, recapitulating the full spectrum of genetic alterations proposed to drive NE differentiation. Additionally, phenotypic response to CRISPR/Cas9-mediated AR KO in AR+ CRPC cells was evaluated.
View Article and Find Full Text PDFRetinoic acid receptor beta (RARB) variants are heavily linked to pathologies of neural crest cell migration. The purpose of this report is to present a 23-month-old male with the previously described R387C RARB gain-of-function variant whose gastrointestinal issues and long-term constipation lead to the discovery of colonic hypoganglionosis. This case further delineates the pattern of malformation associated with RARB variants.
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