Largest genomic study of veterans with metastatic prostate cancer reveals critical insights for precision medicine
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Updates every hour. Last Updated: 11-Jul-2025 15:10 ET (11-Jul-2025 19:10 GMT/UTC)
A research team from Sun Yat-sen University Sixth Affiliated Hospital has made a groundbreaking discovery in colorectal cancer (CRC) research, identifying a long noncoding RNA (lncRNA) named ESSENCE (EGF Signal Sensing CAD's Effect; ENST00000415336) as a critical regulator of tumor progression. The study reveals that ESSENCE stabilizes a key metabolic enzyme, CAD (carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase), to promote cancer growth and suppress ferroptosis. The findings also propose a novel combination therapy targeting ESSENCE-high tumors, offering new hope for precision treatment.
Albert Einstein College of Medicine has appointed Britta Will, Ph.D., associate professor of oncology, of medicine and of cell biology, and the Diane and Arthur B. Belfer Scholar in Cancer Research, as the permanent director of the Ruth L. and David S. Gottesman Institute for Stem Cell Research and Regenerative Medicine.
With mitochondrial DNA (mtDNA) base editing tools, this study controlled the nuclear background to investigate the causal effect of mtDNA mutations. Co-existence of wild-type and mutant mtDNA (heteroplasmy) in MT-ND5 was introduced. Enhanced oncogenic potential was confirmed with in vitro and in vivo assays. They reported compromised mitochondrial respiration and increased glycolytic activity, often termed as the Warburg effect following the mutations. By tracking cellular phenotypes during the MT-ND5 heteroplasmy decay, they reasoned that the increased glycolytic activity was to rescue NAD+ depreciation. Increased ROS level, genome instability, altered NAD+ epigenetics are the likely factors drove oncogenesis post MT-ND5 mutations.
A study published today in the Journal of Cancer Survivorship found that cancer survivors receiving high-cost immunotherapy treatments were more likely to face financial hardship, leading to increased instances of being unable to afford care and taking fewer medications due to cost.
The research, focusing on Medicare-enrolled patients, investigated the financial challenges faced by cancer survivors, particularly those receiving expensive immunotherapies.
“Although it’s well-known that many cancer patients experience financial hardship due to healthcare costs, there’s not much research available that specifically assesses the financial strain linked to immunotherapy treatments, particularly among Medicare enrollees,” said the study’s senior author Cathy Bradley, PhD, Dean of the Colorado School of Public Health on the University of Colorado Anschutz Medical Campus. “As more therapies are developed and the cost of drugs continues to increase, it’s important to determine if patients, even those who are insured, can afford out-of-pocket costs or if these costs are becoming a barrier to access life-saving treatment.”
Initial results from a clinical trial reveal the potential of an anti-osteoporosis drug for its possible application in breast cancer: although it does not reduce the proliferation of cancer cells, it does stimulate the anti-tumour immune response.
Immunotherapy is the strategy that is driving cancer treatment forward, but the response is relatively low in luminal type B breast cancer. This latest finding opens an avenue of clinical interest.
This advance, led by researchers and oncologists at ICO, IBIDELL and the CNIO, is a direct result of the synergy between basic science, clinical research and patient involvement.Metastatic cancer remains a major cause of death. MT1-MMP is a key enzyme facilitating cancer cells' invasion and spread. Researchers from Yunnan University have made a surprising discovery: the VPS35/Retromer complex regulates MT1-MMP levels through a dual mechanism, both stabilizing the MT1-MMP protein and increasing its transcription via the STAT3 pathway. This leads to increased MT1-MMP levels and accelerates melanoma metastasis. The findings offer a potential new therapeutic target for preventing or treating metastatic cancer.
Scientists have uncovered a key driver of triple-negative breast cancer (TNBC) progression—a metabolic enzyme called LPCAT1—and developed a targeted nanoparticle therapy to block it. By silencing LPCAT1, the treatment disrupts cancer cell energy production and halts tumor growth and lung metastasis in TNBC, the most aggressive breast cancer subtype. This breakthrough offers a promising new strategy for treating advanced TNBC, which currently has limited therapeutic options.
Researchers from the Stem Cells and Cancer team at the Josep Carreras Leukaemia Research Institute and the Hospital del Mar Research Institute have developed a method to confidently produce blood cell precursors from stem cells in mice, by activating a set of seven key genes in the laboratory. The team, led by Dr. Anna Bigas, takes a step forward towards the production of precursor cells able to restore the bone marrow of blood cancer patients, in a successful example of regenerative medicine.