Results 21 to 30 of about 239,737 (256)
Structural insights for selective disruption of Beclin 1 binding to Bcl-2
Communications Biology, 2023 Stimulation of autophagy could provide powerful therapies for multiple diseases, including cancer and neurodegeneration. An attractive drug target for this purpose is Bcl-2, which inhibits autophagy by binding to the Beclin 1 BH3-domain.
Yun-Zu Pan +4 more
doaj +1 more source
Neoplasia: An International Journal for Oncology Research, 2007 Head, neck squamous cell carcinomas (HNSCCs) are frequently characterized by chemotherapy, radiation resistance, by overexpression of Bcl-XL, an antiapoptotic member of the Bcl-2 protein family. In this report, we examined whether cell-permeable peptides
Rongxiu Li +5 more
doaj +1 more source
Cancer Biology & Therapy, 2004 Commentary to: Expression of Inducible Bcl-XS in Myeloid Leukemia: Compensatory Upregulation of Bcl-XL and Bcl-2 Prevents Apoptosis and Chemosensitization Frank Tacke, Frank C. Marini, III, Shourong Zhao, Teresa McQueen, Marina Konopleva, Peter P.
Jan, Schmidt-Mende, Boris, Zhivotovsky
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Differential dependence on Beclin 1 for the regulation of pro-survival autophagy by Bcl-2 and Bcl-xL in HCT116 colorectal cancer cells. [PDF]
PLoS ONE, 2010 Autophagy is described to be involved in homeostasis, development and disease, both as a survival and a death process. Its involvement in cell death proceeds from interrelationships with the apoptotic pathway.
Muriel Priault +5 more
doaj +1 more source
Molecular Oncology, EarlyView.Dimethyl fumarate (DMF) reduces growth of HPV‐positive cervical cancer spheroids and induces ferroptosis in cervical cancer cells via blocking SLC7A11/Glutathione (GSH) axis. Combination of subcytotoxic doses of DMF and cisplatin (CDDP) further suppresses spheroid growth and drives cell death in 2D culture models.
Carolina Punziano +6 more
wiley +1 more source
The p53–Bcl-2 connection [PDF]
Cell Death & Differentiation, 2006 The tumor suppressor p53 and the proto-oncogene Bcl-2 were two of the earliest identified cancer genes. Mutant p53 proteins were first discovered in transformed murine cell lines,1,2 whereas Bcl-2 translocations were first identified in human follicular lymphoma.3,4,5 Despite this shared cancer relevance, they were initially thought to have little else
M T, Hemann, S W, Lowe
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Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer
Molecular Oncology, EarlyView.Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas +16 more
wiley +1 more source
FEBS Open Bio, EarlyView.Chemotherapy side effects significantly impact cancer survivors' quality of life. Using protein levels in blood samples from breast cancer patients before and after 12 weeks of taxane treatment, we detected treatment‐dependent changes in calcium signaling and aging pathways associated with cancer recurrence.
Saira Munshani +6 more
wiley +1 more source
Combinatorial BCL2/BCL2L1 expression predicts clinical response to ruxolitinib in myelofibrosis
Biomarker ResearchMyelofibrosis is characterized by aberrant JAK/STAT signaling, with approved therapy including the JAK inhibitor ruxolitinib. Preclinical evidence implicates BCL-2 family proteins in MF pathogenesis and therapeutic response.
Giacomo Coltro +6 more
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Molecular Cancer, 2022 Background Chronic lymphocytic leukemia (CLL) results in increased susceptibility to infections. T cell dysfunction is not associated with CLL in all patients; therefore, it is important to identify CLL patients with T cell defects.
Lu Liu +13 more
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