Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer, representing approximately 75-85% of all cases. Often considered preventable, primary liver cancer ranks as the sixth most frequently diagnosed cancer and the third leading cause of cancer deaths worldwide. Through a multi-institutional effort, researchers have identified activated ATF6α as a driver of HCC that suppresses immune defenses, predicts response to immune checkpoint therapy, and represents a potential target for intervention.
Chemotherapy is often seen solely as a tumor-targeting treatment, yet new evidence reveals a paradox: the tissue injury it causes can reprogram the body’s defenses, influencing the risk of metastasis. Researchers from the University of Lausanne and collaborators reported that chemotherapy reshapes the gut-immune axis by inducing microbiota-derived indole-3-propionic acid, which reprograms myelopoiesis to curb monocyte-driven immunosuppression and metastasis in colorectal cancer.
Chemotherapy is often seen solely as a tumor-targeting treatment, yet new evidence reveals a paradox: the tissue injury it causes can reprogram the body’s defenses, influencing the risk of metastasis. Researchers from the University of Lausanne and collaborators reported that chemotherapy reshapes the gut-immune axis by inducing microbiota-derived indole-3-propionic acid (IPA), which reprograms myelopoiesis to curb monocyte-driven immunosuppression and metastasis in colorectal cancer (CRC).
For decades, scientists have searched for a mechanistic link between viral infection and multiple sclerosis (MS). Insights from three studies recently published in Cell bring that connection into sharper focus. By tracing how the immune system responds to Epstein-Barr virus (EBV) – and how those responses can misfire against the brain – researchers are beginning to uncover a compelling biological explanation for MS.
Over the course of the year, and continuing into the latest scientific meetings, an extraordinary breadth of new antibody-drug conjugate (ADC) designs was reported, with innovations spanning targets, linkers, payloads, conjugation chemistries and overall architectures. Once defined by a simple “one target, one payload” model, the field is lately expanding into a more versatile and diverse therapeutic space.
Over the course of the year, and continuing into the latest scientific meetings, an extraordinary breadth of new antibody-drug conjugate (ADC) designs was reported, with innovations spanning targets, linkers, payloads, conjugation chemistries and overall architectures. Once defined by a simple “one target, one payload” model, the field is lately expanding into a more versatile and diverse therapeutic space.
Fat tissue balances energy by storing lipids during times of abundance and mobilizing them when needed, yet sustained metabolic stress demands mechanisms that limit excessive lipid loss. Researchers at the University of California San Diego (UCSD) report that stress-induced fat breakdown triggers a neutrophil response in visceral adipose tissue that feeds back to restrain lipolysis and preserve lipid reserves.
Fat tissue balances energy by storing lipids during times of abundance and mobilizing them when needed, yet sustained metabolic stress demands mechanisms that limit excessive lipid loss. Researchers at the University of California San Diego (UCSD) report that stress-induced fat breakdown triggers a neutrophil response in visceral adipose tissue that feeds back to restrain lipolysis and preserve lipid reserves.
NIH researchers report that in severe influenza, survival improves at late stages only when antivirals are combined with therapies that repair lung damage or limit harmful T-cell responses, explaining why anti-inflammatory treatments alone are often ineffective.
NIH researchers report that in severe influenza, survival improves at late stages only when antivirals are combined with therapies that repair lung damage or limit harmful T-cell responses, explaining why anti-inflammatory treatments alone are often ineffective.