Results 301 to 310 of about 16,801,423 (422)

Targeting the AKT/mTOR pathway attenuates the metastatic potential of colorectal carcinoma circulating tumor cells in a murine xenotransplantation model

open access: yesMolecular Oncology, EarlyView.
Dual targeting of AKT and mTOR using MK2206 and RAD001 reduces tumor burden in an intracardiac colon cancer circulating tumor cell xenotransplantation model. Analysis of AKT isoform‐specific knockdowns in CTC‐MCC‐41 reveals differentially regulated proteins and phospho‐proteins by liquid chromatography coupled mass spectrometry. Circulating tumor cells
Daniel J. Smit   +19 more
wiley   +1 more source

Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry

open access: yesMolecular Oncology, EarlyView.
Elevated expression of transcriptional regulator inhibitor of DNA binding 1 (ID1) promoted cancer cell‐mediated vasculogenic mimicry (VM) through regulation of pro‐angiogenic and pro‐cancerous genes (e.g. VE‐cadherin (CDH5), TIE2, MMP9, DKK1). Higher ID1 expression also increased metastases to the lung and the liver.
Emma J. Thompson   +11 more
wiley   +1 more source

Microglial reprogramming: a potential new frontier in enhancing immunotherapy for melanoma brain metastasis

open access: yesMolecular Oncology, EarlyView.
Microglia act as tumor suppressors during brain metastasis colonization but shift to a tumor‐promoting role after melanoma brain metastases form. NF‐κB/RelA signaling emerges as a key driver of this phenotypic shift. Targeting this pathway reprograms microglia into a pro‐inflammatory state, enhancing antitumor immunity and immune checkpoint inhibitor ...
Noam Savion‐Gaiger   +2 more
wiley   +1 more source

Quarterly progress report [PDF]

open access: green, 1947
K. Pierce, Leo Goldberg
openalex  

MET and NF2 alterations confer primary and early resistance to first‐line alectinib treatment in ALK‐positive non‐small‐cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu   +11 more
wiley   +1 more source

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