Results 131 to 140 of about 7,167,330 (247)

Assessment of uncertainty quantification in universal differential equations. [PDF]

open access: yesPhilos Trans A Math Phys Eng Sci
Schmid N   +3 more
europepmc   +1 more source

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

Modeling of Biological Intelligence for SCM System Optimization [PDF]

open access: gold, 2011
Shengyong Chen   +3 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

Computational modelling of CAR T-cell therapy: from cellular kinetics to patient-level predictions. [PDF]

open access: yesEBioMedicine
Murias-Closas A   +4 more
europepmc   +1 more source

GemCell: A generic platform for modeling multi-cellular biological systems

open access: bronze, 2007
Hila Amir-Kroll   +3 more
openalex   +1 more source

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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