Death and anti-death: tumour resistance to apoptosis

By F. Igney, P. Krammer. Nature Reviews. Cancer, 2002

628 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/edeb4ce54557c9c33ecc7fa8d06bd18fe57e1670

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Citations in the corpus

Calreticulin exposure dictates the immunogenicity of cancer cell death (2007, neutral): “It has long been hypothesized that apoptotic cell death is poorly immunogenic (or even tolerogenic) whereas necrotic cell death is truly immunogeni”
The mystery of BCL2 family: Bcl-2 proteins and apoptosis: an update (2015, neutral): “Two main mechanistic pathways of apoptosis have been reported: extrinsic or death receptor pathway and intrinsic or mitochondrial pathway (Igney and Krammer 2002).”
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014, critical): “Along similar lines, apoptosis was misconceived as an immunologically silent, if not tolerogenic, cell death modality.(61,62) It is now clear that PCD does not always manifest with an apoptotic morphotype and does not necessarily fail to induce inflammatory or immune responses.”
Cell Death Pathways in Photodynamic Therapy of Cancer (2011, background): “essential feature of cancer development thus, modulation of the key elements of apoptosis signaling may directly influence therapy-induced tumor-cell death [26,27].”
Anti-apoptosis and cell survival: a review. (2011, neutral): “to the up-regulation of a number of anti-apoptotic genes such as Bcl-2 and cFLIP [157,158].”
DNA damage-induced apoptosis (2004, neutral): “Consequences of cell survival after DNA damage Loss of apoptosis undoubtedly plays a major role in tumorigenesis (Igney and Krammer, 2002).”
Apoptosis and melanoma chemoresistance (2003, positive): “The identification of Bcl-2 as an oncogene that prevented apoptosis served as a catalyst for one of the most prolific areas of research in molecular oncology that revealed apoptosis as a critical tumor control mechanism (Lowe and Lin, 2000; Igney and Krammer, 2002; Johnstone et al., 2002).”
Radiation-induced cell death mechanisms (2010, neutral): “Furthermore, tumors that retain a functional p53 pathway still frequently lose the basic apoptotic mechanisms and acquire resistance to apoptosis [ 5 ].”
Caspase-dependent immunogenicity of doxorubicin-induced tumor cell death (2005, background): “In biochemical terms, apoptosis is frequently accompanied by the activation of a specific subset of cysteine kinases, the caspases (4).”
Apoptosis: A Review of Programmed Cell Death (2007, neutral): “This is one example of the “cross-talk” between the death-receptor (extrinsic) pathway and the mitochondrial (intrinsic) pathway (Igney and Krammer, 2002).”
Death-receptor O-glycosylation controls tumor-cell sensitivity to the proapoptotic ligand Apo2L/TRAIL (2007, neutral): “Further stimulation is mediated by engagement of the intrinsic (mitochondrial) apoptosis pathway through caspase-8-dependent activation of the proapoptotic Bcl-2 family protein Bi”
Tumor cell metabolism: cancer's Achilles' heel. (2008, neutral): “HIF-1a activation also causes the expression of the met proto-oncogene and of TWIST, both of which favor EMT (Pennacchietti et al., 2003; Yang et al., 2008), and induces two proteins that play a cardinal role in metastasis, the chemokine receptor CXCR4 (Igney and Krammer, 2002) and lysyl oxidase (LO”