Platinum-resistant recurrent epithelial ovarian cancer carries a bleak prognosis, with single-agent chemotherapy yielding response rates below 20% and median progression-free survival barely reaching 4 months; the A-Plus phase II trial therefore tested a chemotherapy-free, all-oral regimen combining albumin-bound paclitaxel and the multi-kinase inhibitor anlotinib in 44 heavily pre-treated women. Between January 2021 and March 2023, patients aged 32-70 years received nab-paclitaxel 260 mg m⁻² intravenously on day 1 plus anlotinib 12 mg orally once daily on days 1-14 of each 21-day cycle until progression or intolerable toxicity. Eligibility required documented platinum resistance, ECOG performance status 0-1, measurable or evaluable disease by RECIST 1.1 or Rustin criteria, and adequate organ function; prior anti-angiogenic therapy or PARP inhibitors was allowed, reflecting real-world refractory populations.

Advanced biliary tract cancer represents one of the most challenging gastrointestinal malignancies in China, with increasing incidence and extremely poor prognosis due to late-stage diagnosis and limited treatment options. The integration of precision medicine approaches has transformed the therapeutic landscape by enabling personalized treatment strategies based on molecular profiling, tumor characteristics, and patient-specific factors. Recent developments encompass novel chemotherapy combinations, targeted therapies for specific genetic alterations, immunotherapy approaches, and emerging biomarkers that guide treatment selection and predict therapeutic responses.

The Warburg effect describes how cancer cells switch from oxidative phosphorylation to glycolysis even in oxygen-rich conditions, producing massive amounts of lactate that accumulate in the tumor microenvironment. This metabolic reprogramming creates an acidic milieu that suppresses immune function while fueling tumor growth and metastasis. Beyond serving as a waste product, lactate functions as a powerful signaling molecule that reshapes immune responses through multiple mechanisms, including direct receptor binding, transporter-mediated cellular reprogramming, and post-translational protein modifications known as lactylation.

Kyoto, Japan -- Aged and frail people often suffer a decline in tissue reserve capacity during aging. This reserve, called resilience, helps the body maintain homeostasis through various defense, compensation, modulation, and repair responses. When resilience is impaired, elderly people tend to experience a gradual waning of their daily activity and an increase in multimorbidity, or dealing with multiple chronic illnesses.

One major cause of resilience decline is an increase in senescent cells that have stopped dividing. The human body has a natural mechanism for eliminating these cells called senolysis, but as we age this 'clearing' mechanism becomes less efficient.

Senescent cells exert harmful effects through the senescence-associated secretory phenotype, or SASP: the release of pro-inflammatory molecules that can adversely affect surrounding cells. This leads to chronic inflammation and age-related diseases, partly explaining why elderly people suffer impaired resilience. Yet how metabolic resilience is involved in survival capacity and SASP has remained unclear.

A new study published today in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in  patients with an aggressive subtype of triple-negative breast cancer.

Gastric (stomach) cancer remains one of the most common and deadly cancers in East Asia, including Korea. Yet despite its high prevalence, it has received far less molecular attention than colorectal cancer, which is more common in Western countries. As a result, many of today’s models of gastric cancer biology are still based on assumptions borrowed from colorectal cancer research — often with limited success when applied to patients.

One of the biggest unanswered questions has concerned the very first steps of gastric cancer development: how do early cancer cells survive and grow when they should not?

Under normal conditions, cells lining the stomach cannot grow independently. They rely on constant signals from their surrounding tissue — known as the microenvironment — to tell them when to divide, when to rest, and when to die. Losing this dependence is one of the defining features of cancer. But in gastric cancer, researchers have long struggled to explain how this transition occurs.

This problem has been tackled by a joint international research team led by Dr. LEE Ji-Hyun, Dr. KOO Bon-Kyoung, and Dr. LEE Heetak at the Center for Genome Engineering within the Institute for Basic Science (IBS), in partnership with the laboratories of Prof. CHEONG Jae-Ho and Prof. KIM Hyunki (Yonsei University College of Medicine) and Prof. Daniel E. STANGE (TU Dresden / University Hospital Carl Gustav Carus). The team has identified a previously unknown mechanism that allows early gastric cancer cells to become self-sufficient. The findings provide a new framework for understanding how stomach cancer begins — and point to potential new targets for treatment.

BUFFALO, NY — December 23, 2025 — A new research paper was published in Volume 12 of Oncoscience on October 14, 2025, titled “Bridging clinical insight and laboratory model in high-grade serous ovarian carcinoma (HGSOC) using DNA sequencing-based profiling of TP53.”