Pleural Metastasis in Epithelioid Angiosarcoma - Cureus

Credit: Artur Plawgo / Getty Images / Science Photo Library The physical pressure that cancer cells encounter as tumors grow may do more than impede their movement. New research suggests that prolonged confinement can activate a molecular self-destruct mechanism in invasive cancer cells, potentially limiting their ability to spread to other parts of the body. The findings, published in Developmental Cell, reveal an unexpected connection between the mechanical forces within tumors and a form of programmed cell death called necroptosis. Researchers at the Chinese Academy of Sciences in Shanghai say the discovery could eventually lead to biomarkers for predicting metastatic risk and new approaches to preventing cancer spread.

Mitochondrial serine catabolic pathway (MSCP), also called serine, glycine, and one-carbon metabolism, is essential for cancer cells to produce amino acids, one-carbon units, and reducing equivalents. The pathway is frequently upregulated in tumors: serine hydroxymethyltransferase 2 (SHMT2) and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) are among the most overexpressed metabolic enzymes in human cancers, and their activity supports cancer cell proliferation, redox balance, and metastasis. Cancer cells rely on MSCP when the electron transport chain (ETC) is impaired, yet no effective therapy selectively targets this pathway. Fat mass and obesity-associated protein (FTO), an m⁶A demethylase, can be inhibited by 2-hydroxyglutarate (2-HG). FTO expression is associated with favorable prognosis and is downregulated in breast cancer, yet there is currently no effective way to reactivate FTO in cancer. Given these challenges, there is a need for in-depth research on therapies that safely reactivate respiration and target MSCP in metastatic breast cancer. Researchers at Stanford University School of Medicine, with collaborators at The Second Hospital of Jilin University and

Newswise — Mitochondrial serine catabolic pathway (MSCP), also called serine, glycine, and one-carbon metabolism, is essential for cancer cells to produce amino acids, one-carbon units, and reducing equivalents. The pathway is frequently upregulated in tumors: serine hydroxymethyltransferase 2 (SHMT2) and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) are among the most overexpressed metabolic enzymes in human cancers, and their activity supports cancer cell proliferation, redox balance, and metastasis. Cancer cells rely on MSCP when the electron transport chain (ETC) is impaired, yet no effective therapy selectively targets this pathway. Fat mass and obesity-associated protein (FTO), an m⁶A demethylase, can be inhibited by 2-hydroxyglutarate (2-HG). FTO expression is associated with favorable prognosis and is downregulated in breast cancer, yet there is currently no effective way to reactivate FTO in cancer. Given these challenges, there is a need for in-depth research on therapies that safely reactivate respiration and target MSCP in metastatic breast cancer.

Patients with asthma and chronic obstructive pulmonary disease (COPD) often receive systemic corticosteroids from multiple specialties, and that cumulative exposure is rarely tracked in 1 place. At the same time, the options for reducing reliance on oral steroids have grown, with approvals of dupilumab and mepolizumab for eosinophilic COPD and of depemokimab, a twice-yearly anti-interleukin (IL)-5 agent, for severe asthma.1-4 Clinicians outside pulmonology increasingly manage these patients when specialty access is limited. On October 6, 2026, Mollie Chartoff, FNP-BC, a nurse practitioner on the advanced COPD team at Vanderbilt Lung Institute in Nashville, Tennessee, moderated a virtual clinical forum for advanced practice providers on asthma and COPD. Participants included nurse practitioners and physician assistants in pulmonology, allergy and asthma, dermatology, oncology, and interventional pain practices in Tennessee, Texas, Missouri, and North Carolina. The discussion covered biomarkers, oral corticosteroid (OCS) exposure, biologic selection, and access barriers.

Treatment of pulmonary arterial hypertension (PAH) now spans 5 therapeutic pathways, and the options within them continue to expand. Recent developments include FDA approval of a once-daily single-tablet combination of macitentan and tadalafil, supported by the phase 3 A DUE trial, and a September 2026 European Respiratory Society (ERS) guideline update recommending add-on sotatercept for patients who remain at intermediate-low, intermediate-high, or high risk.1,2 How clinicians sequence oral, inhaled, parenteral, and injectable therapies in practice increasingly depends on risk assessment, payer requirements, and patient preference. In September 2026, Marc Simon, MD, MS, director of pulmonary vascular disease and the Pulmonary Hypertension Comprehensive Care Center at the University of California, San Francisco (UCSF), moderated a clinical forum in San Francisco. Participants included pulmonologists, advanced heart failure and critical care cardiologists, and a nurse practitioner from UCSF, Kaiser Permanente, and California Pacific Medical Center. The discussion covered initial combination therapy, risk reassessment, escalation beyond dual therapy, and long-term monitoring.