Results 41 to 50 of about 51,266 (223)

KMT2A degradation is observed in decitabine‐responsive acute lymphoblastic leukemia cells

open access: yesMolecular Oncology, EarlyView.
We demonstrate that decitabine (DEC) not only degrades the DNA methyltransferase DNMT1 but also the leukemic driver lysine methyltransferase KMT2A likely due to structural similarity of the DNA‐binding CXXC domains. DEC influences KMT2A downstream processes and synergizes with menin inhibitor revumenib (REV) to decrease leukemic cell proliferation, and
Luisa Brock   +10 more
wiley   +1 more source

Polyfunctional CD8+CD226+RUNX2hi effector T cells are diminished in advanced stages of chronic lymphocytic leukemia

open access: yesMolecular Oncology, EarlyView.
CD226+CD8+ T cells express elevated levels of RUNX2, exhibit higher proliferation capacity, cytokines and cytolytic molecules expression, and migratory capacity. In contrast, CD226−CD8+ T cells display an exhausted phenotype associated with the increased expression of co‐inhibitory receptors and impaired effector functions.
Maryam Rezaeifar   +4 more
wiley   +1 more source

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

open access: yesMolecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy   +12 more
wiley   +1 more source

Drug therapy in headache [PDF]

open access: yesClinical Medicine, 2015
All physicians will encounter patients with headaches. Primary headache disorders are common, and often disabling. This paper reviews the principles of drug therapy in headache in adults, focusing on the three commonest disorders presenting in both primary and secondary care: tension-type headache, migraine and cluster headache.
openaire   +3 more sources

Integration of single‐cell and bulk RNA‐sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer

open access: yesMolecular Oncology, EarlyView.
Prostate cancer is a leading malignancy with significant clinical heterogeneity in men. An 11‐gene signature derived from dysregulated epithelial cell markers effectively predicted biochemical recurrence‐free survival in patients who underwent radical surgery or radiotherapy.
Zhuofan Mou, Lorna W. Harries
wiley   +1 more source

Drug Therapy

open access: yesThe American Journal of the Medical Sciences, 1963
Mode of access: Internet.
openaire   +1 more source

Clinical significance of stratifying prostate cancer patients through specific circulating genes

open access: yesMolecular Oncology, EarlyView.
We tested a specific panel of genes representative of luminal, neuroendocrine and stem‐like cells in the blood of prostate cancer patients, showing predictive value from diagnosis to late stages of disease. This approach allows monitoring of treatment responses and outcomes at specific time points in trajectories.
Seta Derderian   +12 more
wiley   +1 more source

Designing the statistically optimal drug for cancer therapy [PDF]

open access: yesarXiv, 2013
Cancer and healthy cells have distinct distributions of molecular properties and thus respond differently to drugs. Cancer drugs ideally kill cancer cells while limiting harm to healthy cells. However, the inherent variance among cells in both cancer and healthy cell populations increases the difficulty of selective drug action.
arxiv  

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

open access: yesMolecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita   +1 more
wiley   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

open access: yesMolecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi   +5 more
wiley   +1 more source

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