Results 101 to 110 of about 463,429 (352)

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

open access: yesMolecular Oncology, EarlyView.
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee   +8 more
wiley   +1 more source

JAK inhibitors: a new choice for diabetes mellitus?

open access: yesDiabetology & Metabolic Syndrome
Altered tyrosine kinase signaling is associated with a variety of diseases. Tyrosine kinases can be classified into two groups: receptor type and nonreceptor type. Nonreceptor-type tyrosine kinases are subdivided into Janus kinases (JAKs), focal adhesion
Mengjun Zhou, Qi Shen, Bo Li
doaj   +1 more source

Outcome of 82 chronic myeloid leukemia patients treated with nilotinib or dasatinib after failure of two prior tyrosine kinase inhibitors

open access: yesHaematologica, 2013
There have been few reports of a response to dasatinib or nilotinib after failure of two prior sequential tyrosine kinase inhibitors. We report the outcome of 82 chronic phase patients who received nilotinib or dasatinib as third-line alternative ...
Antonella Russo Rossi   +19 more
doaj   +1 more source

Role of growth factors in the pathogenesis of tissue fibrosis in systemic sclerosis. [PDF]

open access: yes, 2010
The most severe clinical and pathologic manifestations of systemic sclerosis (SSc) are the result of a fibrotic process characterized by the excessive and often progressive deposition of collagen and other connective tissue macromolecules in skin and ...
Castro, Susan V.   +2 more
core   +2 more sources

Tumor mutational burden as a determinant of metastatic dissemination patterns

open access: yesMolecular Oncology, EarlyView.
This study performed a comprehensive analysis of genomic data to elucidate whether metastasis in certain organs share genetic characteristics regardless of cancer type. No robust mutational patterns were identified across different metastatic locations and cancer types.
Eduardo Candeal   +4 more
wiley   +1 more source

Severe adverse effects associated with tyrosine kinase inhibitors therapy in chronic myeloid leukaemia – case reports and literature review

open access: yesZdravniški Vestnik, 2011
Background: Chronic myeloid leukaemia is a clonal myeloproliferative disorder of myeloid progenitor cells. The availability of moleculartargeted therapy with tyrosine kinase inhibitors has changed the course and treatment for patients with chronic ...
Frosina Krstanovska   +4 more
doaj  

Somatic variants in epigenetic modifiers can predict failure of response to imatinib but not to second-generation tyrosine kinase inhibitors

open access: yesHaematologica, 2019
There are no validated molecular biomarkers to identify newly-diagnosed individuals with chronic-phase chronic myeloid leukemia likely to respond poorly to imatinib and who might benefit from first-line treatment with a more potent second-generation ...
Georgios Nteliopoulos   +15 more
doaj   +1 more source

LBA58 Sintilimab with or without IBI305 plus chemotherapy in patients with EGFR mutated non-squamous non-small cell lung cancer (EGFRm nsqNSCLC) who progressed on EGFR tyrosine-kinase inhibitors (TKIs) therapy: Second interim analysis of phase III ORIENT-31 study [PDF]

open access: bronze, 2022
Shaoming Lu   +19 more
openalex   +1 more source

Overcoming myelosuppression due to synthetic lethal toxicity for FLT3-targeted acute myeloid leukemia therapy. [PDF]

open access: yes, 2014
Activating mutations in FLT3 confer poor prognosis for individuals with acute myeloid leukemia (AML). Clinically active investigational FLT3 inhibitors can achieve complete remissions but their utility has been hampered by acquired resistance and ...
He, Bai-Liang   +9 more
core  

Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer

open access: yesMolecular Oncology, EarlyView.
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta   +10 more
wiley   +1 more source

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