Study focuses on resistance to androgen receptor-targeted therapy in advanced prostate cancer
Peer-Reviewed Publication
Updates every hour. Last Updated: 30-Apr-2025 15:08 ET (30-Apr-2025 19:08 GMT/UTC)
In an effort to find new treatments for castrate-resistant prostate cancer, a TTUHSC research team led by Srinivas Nandana, Ph.D., and Manisha Tripathi, Ph.D., recently completed a study focused on uncovering the molecular and signaling mechanisms that drive the progression of advanced prostate cancer. Their study (“A TBX2-Driven Signaling Switch from Androgen Receptor to Glucocorticoid Receptor Confers Therapeutic Resistance in Prostate Cancer”), published by Oncogene, emphasized overcoming resistance to androgen receptor signaling inhibitors.
Molecular biologist Yali Dou, PhD, holder of the Marion and Harry Keiper Chair in Cancer Research and professor of medicine and cancer biology at the Keck School of Medicine of USC, has been elected a fellow of the American Association for the Advancement of Science (AAAS). She is one of seven USC faculty members in the 2025 cohort of new fellows. Dou, the associate director for basic research at USC Norris Comprehensive Cancer Center, is a recognized leader in the study of epigenetics, the mechanisms that enable the singular instructions in DNA to be expressed as myriad cell and tissue types. She has made major contributions to the fundamental understanding of a family of enzymes that plays a vital role in fetal development by altering the coiled chromatin, which packages DNA to fit in the chromosomes of a cell’s nucleus, so that genes are activated. Because mutations of the founding member of this family of enzymes can also spur leukemia, they are known as mixed-lineage leukemia proteins, or MLL. MLL enzymes are among the most frequently mutated genes in cancer.
Cancer remains a leading cause of death globally, with lung cancer being particularly lethal. Despite advancements in diagnostics and therapies, the five-year survival rates for advanced tumors have seen minimal improvement, largely due to therapeutic resistance. This resistance can be genetic or nongenetic, with the latter being less understood but increasingly recognized for its role in treatment failure. Non-genetic resistance is associated with resistant cancer cells that have innate or acquired drug resistance traits. These cells are often found in heterogeneous tumors and include cancer stem-like cells (CSCs), cells undergoing epithelial-to-mesenchymal transition (EMT), partial EMT cells, and drug-tolerant persisters (DTPs). NOTCH signaling plays a crucial role in tumorigenesis and therapeutic resistance, with its activation linked to drug resistance in various cancers.
Using cutting-edge spatial and genetic tools, Singapore scientists have uncovered two gastric cancer tumour subgroups, characterising their unique cellular states, immune responses and interactions with their surroundings. Their discoveries can potentially revolutionise stomach cancer therapy by unveiling new targets for precision diagnostics and treatment.
The mechanism of anticancer activity of a pigment OR3 from Streptomyces coelicolor is explored in in vitro and in vivo metastatic breast cancer models.
Background: Recent evidence suggests that postoperative adjuvant radiotherapy (PORT) may enhance survival outcomes in patients with pN2 non-small cell lung cancer (NSCLC), particularly when evaluating through examined lymph nodes (ELNs) and lymph node ratio (LNR). This study aims to explore the impact of ELNs and LNR on the efficacy of postoperative radiotherapy in pN2 stage NSCLC patients through a multicenter retrospective cohort analysis, providing valuable insights for clinical treatment decisions.
Methods: Data were meticulously extracted from the Surveillance, Epidemiology, and End Results (SEER) 17 registry spanning 2015 to 2019. The study specifically targeted pN2 stage NSCLC patients who underwent surgical intervention and lymph node biopsy, involving an analysis of 1,875 patients while excluding those with incomplete data. The impact of PORT on overall survival (OS) was assessed, stratified by ELNs and LNR. Statistical analyses employed X-tile software to categorize LNR into three distinct groups, and Cox proportional hazard models were utilized to evaluate the influence of various factors on OS.
Results: The Cox proportional hazards model revealed a significant survival advantage associated with PORT, demonstrating a 22% higher mortality rate in the non-PORT group [hazard ratio (HR) =1.22, 95% confidence interval (CI): 1.02–1.46, P=0.03] and up to 31% higher in the fully adjusted model (HR =1.31, 95% CI: 1.09–1.58, P=0.004). PORT notably improved survival in patients with ELNs <10, particularly when LNR ≤0.2 (HR =4.15, P=0.03) and LNR ≥0.53 (HR =1.83, P=0.01). Kaplan-Meier survival curves corroborated these findings.
Conclusions: Our findings indicate that the number of ELNs and the LNR could serve as valuable criteria for selecting pN2 NSCLC patients who may benefit from PORT. PORT has been linked to improved survival outcomes in pN2 stage NSCLC, with a particular emphasis on its efficacy in patients with ELNs <10 and an LNR of ≤0.2.
Keywords: Postoperative adjuvant radiotherapy (PORT); examined lymph nodes (ELNs); lymph node ratio (LNR); non-small cell lung cancer (NSCLC); Surveillance, Epidemiology, and End Results (SEER)
The University of Texas MD Anderson Cancer Center today announced that Jeffrey E. Lee, M.D., an internationally regarded leader in the field of oncology, has been appointed chief medical executive (CME) effective April 1. Prior to his appointment, Lee served as CME ad interim, demonstrating strength as a leader committed to advancing the institution’s efforts in research, patient care, prevention and education. Assuming the role of CME is the culmination of Lee’s 34-year tenure at the institution, where he has made substantial contributions in the field of oncology and served in multiple leadership roles
A tiny magnetic robot which can take 3D scans from deep within the body, that could revolutionise early cancer detection, has been developed by researchers.
The team, led by engineers from the University of Leeds, say this is the first time it has been possible to generate high-resolution three-dimensional ultrasound images taken from a probe deep inside the gastrointestinal tract, or gut.
New Haven, Conn. — Mutations in BRCA2 — a gene known to repair damaged DNA and suppress tumor formation — can predict an individuals’ predisposition to develop breast cancer, ovarian, prostate, pancreatic, and other epithelial tumors.
A new study led by scientists at Yale School of Medicine and New York University (NYU) Grossman School of Medicine unveils a previously unknown protective mechanism employed by the gene — and how an existing class of drugs used to treat cancer might be improved.
The study was published March 26 in the journal Nature.