Results 191 to 200 of about 2,387,864 (261)

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

Cough syrup buyers get referred but not tested: private pharmacy-based tuberculosis surveillance pilot in Jaipur, India. [PDF]

open access: yesPublic Health Action
Gupta K   +13 more
europepmc   +1 more source

Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk

open access: yesMolecular Oncology, EarlyView.
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley   +1 more source

Overcoming the last mile: practical strategies for leprosy elimination in Pakistan. [PDF]

open access: yesBMJ Glob Health
Fastenau A   +8 more
europepmc   +1 more source

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

open access: yesMolecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad   +2 more
wiley   +1 more source

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