OncoCell Presents Noninvasive Blood-Based Assay for Prostate Cancer

OncoCell Announces Late-Breaking Poster Presentation at AACR 2019 on a Noninvasive Blood-Based Assay for Prostate Cancer Prognosis

ATLANTA--(BUSINESS WIRE)--Apr 1, 2019--OncoCell MDx, a company developing novel noninvasive diagnostic and prognostic tests, will present results from a feasibility study of a new prostate cancer prognostic assay in a late-breaking poster session at the American Association of Cancer Research (AACR) Annual Meeting tomorrow. The study demonstrates that the blood-based immunogenomics RNA expression assay provides a prognostic summary comparable to that of prostate biopsy.

OncoCell’s Subtraction-Normalized Expression of Phagocytes (SNEP) based platform, invented by Professor Amin Kassis, while at Harvard Medical School, uses a proprietary algorithm to interrogate changes in gene expression of two immune cell types consequent to prostate cancer including phagocytic (CD14) and non-phagocytic (CD2) cells, filters out intrinsic genomic variation not related to the disease, and identifies and validates prostate cancer-specific signatures. A study of blood samples from 713 prostate cancer patients showed the platform provides a prognostic summary including tumor Gleason grade distribution, size/volume and heterogeneity that is comparable to prostate biopsy information, and that it stratifies patients with aggressive disease that need life-saving treatment from those with indolent disease.

READ MORE …

Insights into how prostate cancers become resistant, and new potential targets (original article)

Increased Serine and One-Carbon Pathway Metabolism by PKCλ/ι Deficiency Promotes Neuroendocrine Prostate Cancer

Increasingly effective therapies targeting the androgen receptor have paradoxically promoted the incidence of neuroendocrine prostate cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which there is no effective therapy. Here we report that protein kinase C (PKC)λ/ι is downregulated in de novo and during therapy-induced NEPC, which results in the upregulation of serine biosynthesis through an mTORC1/ATF4-driven pathway. This metabolic reprogramming supports cell proliferation and increases intracellular S-adenosyl methionine (SAM) levels to feed epigenetic changes that favor the development of NEPC characteristics. Altogether, we have uncovered a metabolic vulnerability triggered by PKCλ/ι deficiency in NEPC, which offers potentially actionable targets to prevent therapy resistance in PCa.

READ MORE …