Empowering Self-Management for Chronic Low Back Pain: A Human-Centered Design Study of Spanish- and Cantonese-Preferring Patients in the United States.

Introduction: Chronic low back pain (cLBP) is a leading cause of disability with disproportionately high impacts on marginalized populations, including non-English-preferring patients. These patients face significant barriers to accessing care and adhering to self-management strategies due to language barriers, socioeconomic challenges, and cultural differences. Despite the emphasis on self-management for cLBP, limited research has focused on understanding the specific needs and preferences of Spanish- and Cantonese-preferring patients.

Analysis of Common Exercise Modalities in Improving Athletic Performance in Older Adults: A Narrative Review.

Exercise leads to robust cardiovascular, musculoskeletal, and psychological benefits that improve quality of life and longevity for older adults, but accompanying improvements in athletic parameters are less well explored. The aim of this review is to summarize some of the most common exercise modalities, namely, Pilates, martial arts (tai chi, Japanese-style karate, hard martial arts), locomotion (brisk walking/jogging and running), Masters sports, resistance training, and high-intensity interval training, in improving athletic performance for older adults. Regular participation in these activities can have robust yet unique impacts on physical performance that prolong exercise participation.

The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer.

Background: The discovery of functionally relevant KRAS effectors in lung and pancreatic ductal adenocarcinoma (LUAD and PDAC) may yield novel molecular targets or mechanisms amenable to inhibition strategies. Phospholipids availability has been appreciated as a mechanism to modulate KRAS oncogenic potential. Thus, phospholipid transporters may play a functional role in KRAS-driven oncogenesis.

FOSL1 promotes cholangiocarcinoma via transcriptional effectors that could be therapeutically targeted.

Background & Aims: Cholangiocarcinoma (CCA) is a neoplasia of the biliary tract driven by genetic, epigenetic and transcriptional mechanisms. Herein, we investigated the role of the transcription factor FOSL1, as well as its downstream transcriptional effectors, in the development and progression of CCA.

Methods: FOSL1 was investigated in human CCA clinical samples.

The Mir181ab1 cluster promotes KRAS-driven oncogenesis and progression in lung and pancreas.

Few therapies are currently available for patients with KRAS-driven cancers, highlighting the need to identify new molecular targets that modulate central downstream effector pathways. Here we found that the microRNA (miRNA) cluster including miR181ab1 is a key modulator of KRAS-driven oncogenesis. Ablation of Mir181ab1 in genetically engineered mouse models of Kras-driven lung and pancreatic cancer was deleterious to tumor initiation and progression.

Genetic Mouse Models as In Vivo Tools for Cholangiocarcinoma Research.

Cholangiocarcinoma (CCA) is a genetically and histologically complex disease with a highly dismal prognosis. A deeper understanding of the underlying cellular and molecular mechanisms of human CCA will increase our current knowledge of the disease and expedite the eventual development of novel therapeutic strategies for this fatal cancer. This endeavor is effectively supported by genetic mouse models, which serve as sophisticated tools to systematically investigate CCA pathobiology and treatment response.

Inhibitor of Differentiation-1 Sustains Mutant -Driven Progression, Maintenance, and Metastasis of Lung Adenocarcinoma via Regulation of a FOSL1 Network.

Because of the refractory nature of mutant lung adenocarcinoma (LUAD) to current therapies, identification of new molecular targets is essential. Genes with a prognostic role in mutant LUAD have proven to be potential molecular targets for therapeutic development. Here we determine the clinical, functional, and mechanistic role of inhibitor of differentiation-1 (Id1) in mutant LUAD.

All for one and FOSL1 for all: FOSL1 at the crossroads of lung and pancreatic cancer driven by mutant KRAS.

() remains refractory to current therapies. We devised an integrative cross-tumor approach to expose common core elements up-regulated in mutant KRAS cancers that could provide new treatment opportunities. This approach identified () as a clinically and functionally relevant gene in mutant -driven lung and pancreatic cancers, and unveiled downstream transcriptional targets amenable to pharmacological inhibition.

An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.

KRAS mutated tumours represent a large fraction of human cancers, but the vast majority remains refractory to current clinical therapies. Thus, a deeper understanding of the molecular mechanisms triggered by KRAS oncogene may yield alternative therapeutic strategies. Here we report the identification of a common transcriptional signature across mutant KRAS cancers of distinct tissue origin that includes the transcription factor FOSL1.