Results 251 to 260 of about 8,011,267 (345)

Endometrial Stromal Nodule Showing Intense Positivity for ^|^alpha;-SMA

open access: bronze, 2000
Yoshiki Ohta   +3 more
openalex   +2 more sources

Interplay of integrins and selectins in metastasis

open access: yesMolecular Oncology, EarlyView.
Here we review the role of integrins and their interplay with selectins in metastasis. The efficacy of integrin‐targeted therapies may be reduced in tumors where metastasis relies heavily on selectins. In certain tumors, integrins and selectins exhibit a synergistic interaction during intraperitoneal dissemination.
Diana Maltseva   +2 more
wiley   +1 more source

Detection of a de novo mutation in a family with SMA Type I: The importance of dosage testing

open access: bronze, 2000
Jean McGowan‐Jordan   +6 more
openalex   +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

Efficacy of Mitochondrial Transfer in Healing Toxin-Induced Damage to Neuromuscular Junction, an Empirical Study. [PDF]

open access: yesSynapse
Deschenes MR   +7 more
europepmc   +1 more source

Study on the Improvement of Cu-SMA System Performance.

open access: bronze, 2000
Yoshikazu Suzuki   +2 more
openalex   +2 more sources

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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