Apoptosis and chemotherapy resistance
References (67)
- et al.
An evolutionary perspective on apoptosis
Cell
(1994) - et al.
Anchorage dependence, integrins, and apoptosis
Cell
(1994) - et al.
Integrin α4β3 antagonists promote tumor regression by inducing apoptosis of angiogenic blood vessels
Cell
(1994) - et al.
Oncogenes and cell death
Curr Opin Genet Dev
(1994) - et al.
Bcl-2 and Bcl-x: regulator switches for lymphoid death and survival
Immunology
(1994) - et al.
Bad, a heterodimeric partner for bcl-x1 and bcl-2, displaces bax and promotes cell death
Cell
(1995) Apoptosis in cancer therapy: crossing the threshold
Cell
(1994)- et al.
DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by Bcl-2
Cell
(1994) - et al.
Bcl-2 oncoprotein blocks chemotherapyinduced apoptosis in a human leukemia cell line
Blood
(1993) Cell death: a new classification separating apoptosis from necrosis
Social controls on cell survival and cell death
Nature
Disruption of epithelial cell-matrix interactions induces apoptosis
J Cell Biol
Requirement of basement membrane for suppression of programmed cell death in mammary epithelium
J Cell Sci
Apoptosis regulated by a death factor and its receptor: fas ligand and fas
Phil Trans R Soc Lond (B)
Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells
Nature
Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death
Nature
Bcl-2 and the regulation of programmed cell death
J Cell Biol
BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax
Nature
Bcl-2 heterodimerizes in vivo with a conserved homolog, bax, that accelerates programmed cell death
Cell
Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak
Nature
Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K
Nature
Induction of apoptosis by the Bcl-2 homologue Bak
Nature
Interactions among members of the Bcl-2 protein family analyzed with a yeast two-hybrid system
Differential expression of bcl-2 in intestinal epithelia
J Cell Sci
Cell cycle and cancer
J Natl Cancer Inst
Drug-target interactions: only the first step in the commitment to a programmed cell death
Br J Cancer
Apoptosis induced by anticancer drugs
Cancer Metast Rev
Apoptosis and cancer chemotherapy
Apoptosis and cancer chemotherapy
Response of intestinal cells of differing topographical and hierarchical status to ten cytotoxic drugs and five sources of radiation
Br J Cancer
An electron-microscope study of the mode of cell death induced by cancer-chemotherapeutic agents in populations of proliferating normal and neoplastic cells
J Pathol
BCL-2 expression delays drug-induced apoptosis but does not increase clonogenic survival after drug treatment in HeLa cells
Cancer Res
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2016, Pharmacological ResearchCitation Excerpt :This was confirmed by display of 200 bp internucleosomal DNA ladder when DNA extracted from SRJ09-treated HCT-116 cells was resolved in agarose gel electrophoresis. The ability of SRJ09 to induce apoptosis is considered as a good therapeutic end point for an anticancer agent [49]. This indicates that SRJ09 is unlikely to be a DNA damaging agent, as p53 appears to be a universal signaling molecule in response to DNA damage triggered by a variety of stimuli [50].
The role of mitochondrial electron transport in tumorigenesis and metastasis
2014, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :Experiments in our laboratory with B16ρo melanoma, 4T1ρo breast carcinoma and other mtDNA-depleted tumor cells show reduced ROS production, anchorage-dependent survival, delayed tumor growth and failure to form lung tumors in vivo [7] (see Fig. 3). Genes such as Bcl-2 and mutant TP53 that are important in tumorigenicity [131] and anchorage independence [132] through mitochondrial mechanisms [133], are not differentially expressed between wild type and ρo cells [134]. A variety of anaplerotic pathways are activated in respiration-deficient cells to maintain the synthesis of α-ketoglutarate, a precursor to glutamate and glutamine (Fig. 1), thus preventing amino acid starvation [135].
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