Apoptosis and chemo‐resistance in colorectal cancer

Prabhudesai, Shirish G.; Rekhraj, S.; Roberts, Gretta; Darzi, Ara; Ziprin, Paul

doi:10.1002/jso.20785

Cited by 42 publications

(25 citation statements)

References 109 publications

(104 reference statements)

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“…Abnormalities in the pathways that control apoptosis may result in intrinsic or acquired resistance to therapy [83]. These abnormalities may arise either in the extrinsic apoptosis pathway which is triggered by the membrane-embedded death receptors [84, 85] or more commonly the intrinsic pathway, where the interplay of proapoptotic and antiapoptotic members of the BCL-2 family results in the release of mitochondrial contents (and subsequent apoptosis) following DNA damage, chemotherapy, or cellular stress [86–88].…”

Section: Nononcogene Targets For Mtasmentioning

confidence: 99%

How Many Diseases Are Colorectal Cancer?

Greystoke

Mullamitha

2012

Gastroenterology Research and Practice

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The development of personalised therapy and mechanism-targeted agents in oncology mandates the identification of the patient populations most likely to benefit from therapy. This paper discusses the increasing evidence as to the heterogeneity of the group of diseases called colorectal cancer. Differences in the aetiology and epidemiology of proximal and distal cancers are reflected in different clinical behaviour, histopathology, and molecular characteristics of these tumours. This may impact response both to standard cytotoxic therapies and mechanism-targeted agents. This disease heterogeneity leads to challenges in the design of clinical trials to assess novel therapies in the treatment of “colorectal cancer.”

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Section: Nononcogene Targets For Mtasmentioning

confidence: 99%

How Many Diseases Are Colorectal Cancer?

Greystoke

Mullamitha

2012

Gastroenterology Research and Practice

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“…The regulation of apoptosis is a crucial step for either intestinal renewal after injuries [13] or tumour growth [14]. The antiapoptotic effect of the GH-IGF1 system might be counterbalanced by IGFBP-3, which has anti proliferating and pro apoptotic actions [15].…”

Section: Introductionmentioning

confidence: 99%

Reduced colonic apoptosis in mice overexpressing bovine growth hormone occurs through changes in several kinase pathways

Bogazzi¹,

Ultimieri²,

Raggi³

et al. 2009

Growth Hormone & IGF Research

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“…20 Therefore, in the current study, we evaluated EGFR, phosphorylated extracellular signal-regulated protein kinase (pERK), receptor for hyaluronic acid-mediated motility (RHAMM), and phosphorylated protein kinase B (pAKT) for their prognostic effects in primary tumor and lymph nodes. 21 Proteins involved in cell cycle regulation, apoptosis, or proliferation (p21, p16, B-cell lymphoma 2 [Bcl-2], Ki67, apoptotic protease activating factor 1 [APAF-1], and mammalian sterile 20-like kinase 1 [MST1]) can have a major effect on patient response to chemotherapeutic agents 22 ; whereas proteins like Raf kinase inhibitor protein (RKIP), vascular endothelial growth factor (VEGF), ephrin type-B receptor 2 (EphB2), matrix metalloproteinase 7 (MMP7), laminin5c2 (lam5c2), mucin 1 (MUC1), and caudalrelated homeobox 2 (CDX2) are linked to angiogenesis, lymph node positivity, or distant metastasis. [23][24][25][26][27] To account for possible heterogeneity in tumor protein expression, multiple-punch tissue microarrays (TMAs) were used.…”

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confidence: 99%

Expression of p16 in lymph node metastases of adjuvantly treated stage III colorectal cancer patients identifies poor prognostic subgroups

Karamitopoulou

Zlobec

Koumarianou

et al. 2010

Cancer

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BACKGROUND:The objective of identifying protein biomarkers for patients with stage III and IV colorectal cancer is to improve risk stratification and, thus, to identify patients in the postoperative setting who may benefit from more targeted treatment. The objective of the current study was to determine the prognostic value of 19 protein markers assessed in primary tumors and matched lymph node (LN) metastases from patients with stage III and IV colorectal cancer. METHODS: Matched primary tumors and LN metastases from 82 patients with stage III and IV colorectal cancer were mounted onto a multiple-punch tissue microarray and were stained for 19 protein markers involved in tumor progression (b-catenin, E-cadherin, epidermal growth factor receptor, phosphorylated extracellular signal-regulated kinase [pERK], receptor for hyaluronic acid-mediated motility, phosphorylated protein kinase B, p21, p16, B-cell lymphoma 2, Ki67, apoptotic protease activating factor 1, mammalian sterile 20-like kinase 1, Raf kinase inhibitor protein, vascular endothelial growth factor, ephrin type-B receptor 2, matrix metalloproteinase 7, laminin5c2, mucin 1 [MUC1], and caudal-related homeobox 2). The prognostic effects of biomarkers in both primary tumor and positive LNs were assessed. RESULTS: MUC1, pERK and p16 in LN (P ¼ .002, P ¼ .014, and P ¼ .002, respectively) had independent prognostic value. In patients with stage III disease who received adjuvant treatment, negative p16 expression was associated with highly unfavorable outcomes overall (hazard ratio [HR], 0.26; 95% confidence interval [CI], 0.1-0.6; P ¼ .005) when the analysis was stratified by pathologic tumor classification (HR, 0.25; 95% CI, 0.1-0.7; P ¼ .005), age (HR, 0.23; 95% CI, 0.1-0.6; P ¼ .004), and LN ratio (HR, 0.26; 95% CI, 0.1-0.7; P ¼ .007); and, in multivariate analysis, it was associated with performance status and the receipt of folic acid treatment (HR, 0.29; 95% CI, 0.09-0.89; P ¼ .03). CONCLUSIONS: The loss of p16 in LN metastases contributed to adverse outcomes in adjuvantly treated patients with stage III colorectal cancer independent of pathologic tumor classification, age, LN ratio, performance status, or folic acid treatment. The current results support the investigation of p16 as a prognostic and potential predictive biomarker for future randomized trials of patients with stage III colorectal cancer. Cancer 2010;116:4474-86.

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Apoptosis and chemo‐resistance in colorectal cancer

Cited by 42 publications

References 109 publications

How Many Diseases Are Colorectal Cancer?

How Many Diseases Are Colorectal Cancer?

Reduced colonic apoptosis in mice overexpressing bovine growth hormone occurs through changes in several kinase pathways

Expression of p16 in lymph node metastases of adjuvantly treated stage III colorectal cancer patients identifies poor prognostic subgroups

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