ArticleBritish journal of cancer2000
Sensitivity to CPT-11 of xenografted human colorectal cancers as a function of microsatellite instability and p53 status.
Article in British journal of cancer, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 71 citations in OpenAlex.
- Lack of Bax expression is associated with irinotecan-based treatment activity in advanced colorectal cancer patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013Trial
- Microsatellite instability predicts improved response to adjuvant therapy with irinotecan, fluorouracil, and leucovorin in stage III colon cancer: Cancer and Leukemia Group B Protocol 89803.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009Trial
- Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer.The New England journal of medicine · 2003Trial
- Association of Microsatellite Instability and Gene Expression Profile in Colorectal Carcinoma and Potential Implications for Therapy.Medicina (Kaunas, Lithuania) · 2024Article
- Artesunate alleviates 5-fluorouracil-induced intestinal damage by suppressing cellular senescence and enhances its antitumor activity.Discover oncology · 2023Article
- Tumour immune microenvironment biomarkers predicting cytotoxic chemotherapy efficacy in colorectal cancer.Journal of clinical pathology · 2021Review
- Glutamate receptor, ionotropic, N‑methyl D‑aspartate‑associated protein 1 promotes colorectal cancer cell proliferation and metastasis, and is negatively regulated by miR‑296‑3p.Molecular medicine reports · 2021Article
- Review
- Genomic Alterations and Their Implications on Survival in Nonmetastatic Colorectal Cancer: Status Quo and Future Perspectives.Cancers · 2020Review
- Synergistic Anti-Tumor Effect of mTOR Inhibitors with Irinotecan on Colon Cancer Cells.Cancers · 2019Article
- In Vitro and in Vivo antitumor activity and the mechanism of siphonodictyal B in human colon cancer cells.Cancer medicine · 2019Article
- Prognostic implications of mismatch repair deficiency in patients with nonmetastatic colorectal and endometrial cancer.ESMO open · 2019Article
- Role of Deficient Mismatch Repair in the Personalized Management of Colorectal Cancer.International journal of environmental research and public health · 2016Review
- Implications of mismatch repair-deficient status on management of early stage colorectal cancer.Journal of gastrointestinal oncology · 2015Review
- Review
- RFPL4A increases the G1 population and decreases sensitivity to chemotherapy in human colorectal cancer cells.The Journal of biological chemistry · 2015Article
- Prognostic and predictive biomarkers: tools in personalized oncology.Molecular diagnosis & therapy · 2014Review
- γ-Glutamyl hydrolase modulation and folate influence chemosensitivity of cancer cells to 5-fluorouracil and methotrexate.British journal of cancer · 2013Article
- Epigenetic and genetic features of 24 colon cancer cell lines.Oncogenesis · 2013Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biological parameters influencing the response of human colorectal cancers (CRCs) to CPT-11, a topoisomerase 1 (top1) inhibitor, were investigated using a panel of nine CRCs xenografted into nude mice. CRC xenografts differed in their p53 status (wt or muf) and in their microsatellite instability phenotype (MSI+ when altered). Five CRC xenografts were established from clinical samples. All five had a functional p53, two were MSI+ and three were MSI-. Tumour-bearing nude mice were treated intraperitonealy (i.p.) with CPT-11. At 10 mg kg(-1) of CPT-11, four injections at 4-day intervals, four of the five xenografts responded to CPT-11 (growth delay of up to 10 days); the non-responder tumour was MSI-. At 40 mg kg(-1) of CPT-11, six injections at 4-day intervals, the five CRCs displayed variable but marked responses with complete regressions. In order to assess the role of p53 status in CPT-11 response, four CRC lines were used. HT29 cell line was MSI-/Ala273-mutp53, its subclone HT29A3 being transfected by wtp53. LoVo cell line was MSI+/wtp53, its subclone X17LoVo dominantly expressed Ala273-mutp53 after transfection. LoVo tumours (MSI+/mutp53) were more sensitive than X17LoVo (MSI+/mutp53. HT 29 tumours (MSI-Imutp53), were refractory to CPT-11 while HT29A3 tumours (MSI-/wtp53) were sensitive, showing that wtp53 improves the drug-response in these MSI- tumours. Levels of mRNA expression of top1, fasR, TP53 and mdr1 were semi-quantified by reverse transcription polymerase chain reaction. None of these parameters correlated with CPT-11 response. Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.