Genetic polymorphisms in cytochrome P450 and clinical outcomes of FOLFIRI chemotherapy in patients with metastatic colorectal cancer

Dong, Ningning; Meng, Fandong; Wu, Yongdong; Wang, Mingyu; Cui, Yongchun; Zhang, Shutian

doi:10.1007/s13277-015-3492-1

Cited by 5 publications

(5 citation statements)

References 34 publications

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“…21 Some SNPs are in connection with increasing risk 24 Increasing GWAS have brought new hope to identify susceptibility loci of CRC in the past decade. 21 Some SNPs are in connection with increasing risk 24 Increasing GWAS have brought new hope to identify susceptibility loci of CRC in the past decade.…”

Section: Discussionmentioning

confidence: 99%

“…21 Some SNPs are in connection with increasing risk of developing CRC, 22,23 some SNPs appear to lower the metastatic risk of CRC and others have been associated with the efficacy of various treatments for CRC. 24 Increasing GWAS have brought new hope to identify susceptibility loci of CRC in the past decade. Several previous large-scale meta-analysis studies of GWAS on colorectal cancer identified novel CRC risk loci at 14q22 (BMP4), 16q22 (CDH1), 19q13 (RHPN2), and 20p12, 25 genetic loci at 1q41, 3q26 (MYNN), 12q13 (ATF1/DIP2B), and 20q13 (LAMA5), 26 6p21 (CDKN1A), 11q13 (POLD3), and Xp22 (SHROOM2), 27 and 5q31, 12p13 (CCND2), and 20p12 (HAO1/PLCB1).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous SNPs have been reported to be associated with CRC . Some SNPs are in connection with increasing risk of developing CRC, some SNPs appear to lower the metastatic risk of CRC and others have been associated with the efficacy of various treatments for CRC …”

Section: Discussionmentioning

confidence: 99%

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HSPB1 rs2070804 polymorphism is associated with the depth of primary tumor

Hung

Huang

Hsu

et al. 2019

J of Cellular Biochemistry

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Background Colorectal cancer (CRC) is the third most common cancer in the world. Genome‐wide association studies are a powerful method to analyze the status of single‐nucleotide polymorphisms (SNPs) in specific genes. Heat shock proteins (HSPs) were found to be involved in the cancer progression and chemoresistance. However, there is still no further study about polymorphisms of HSP beta‐1 (HSPB1) in colorectal cancer. We proposed the SNP of HSPB1 may be correlated with the progression and metastasis in colon cancer. Methods We recruited 379 colorectal cancer patients and categorized as four stages following the UICC TNM system. Then, we selected tagging SNPs of HSPB1 by 10% minimum allelic frequency in Han Chinese population from the HapMap database and analyze with the Chi‐square test. Results We demonstrated the association of HSPB1 genetic polymorphisms rs2070804 with tumor depth with colorectal cancer. But, there is a lack of association between HSPB1 genetic polymorphisms and colorectal cancer invasion, recurrence or metastasis. Conclusions The polymorphisms of HSPB1 seemed to change the tumor behavior of colorectal cancer. HSPB1 rs2070804 polymorphism is associated with the depth of the primary tumor. But, there is no further correlation with other to the clinical parameters such as cancer invasiveness, local recurrence, or distant metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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HSPB1 rs2070804 polymorphism is associated with the depth of primary tumor

Hung

Huang

Hsu

et al. 2019

J of Cellular Biochemistry

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“…Using RCT data alone resulted in the conditional variance 0.0089 (95% CrI: 0.0000, 0.11), while the addition of cRWE gave a conditional variance of 0.010 (95% CrI: 0.0002, 0.051). Thus, the addition of cRWE reduced 40 Matsumoto 2007 41 Catalano 2009 42 Fuse 2008 43 Suenaga 2008 44 Fuse 2007 45 Hochster 2003 46 Yoshino 2007 47 Bendell uncertainty by 54% in terms of the CrI width. The addition of sRWE to RCTs and cRWE further improved precision of the intercept, slope, and conditional variance estimates.…”

Section: Dandh Modelmentioning

confidence: 99%

Using Bayesian Evidence Synthesis Methods to Incorporate Real-World Evidence in Surrogate Endpoint Evaluation

et al. 2023

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Objective Traditionally, validation of surrogate endpoints has been carried out using randomized controlled trial (RCT) data. However, RCT data may be too limited to validate surrogate endpoints. In this article, we sought to improve the validation of surrogate endpoints with the inclusion of real-world evidence (RWE). Methods We use data from comparative RWE (cRWE) and single-arm RWE (sRWE) to supplement RCT evidence for the evaluation of progression-free survival (PFS) as a surrogate endpoint to overall survival (OS) in metastatic colorectal cancer (mCRC). Treatment effect estimates from RCTs, cRWE, and matched sRWE, comparing antiangiogenic treatments with chemotherapy, were used to inform surrogacy patterns and predictions of the treatment effect on OS from the treatment effect on PFS. Results Seven RCTs, 4 cRWE studies, and 2 matched sRWE studies were identified. The addition of RWE to RCTs reduced the uncertainty around the estimates of the parameters for the surrogate relationship. The addition of RWE to RCTs also improved the accuracy and precision of predictions of the treatment effect on OS obtained using data on the observed effect on PFS. Conclusion The addition of RWE to RCT data improved the precision of the parameters describing the surrogate relationship between treatment effects on PFS and OS and the predicted clinical benefit of antiangiogenic therapies in mCRC. Highlights Regulatory agencies increasingly rely on surrogate endpoints when making licensing decisions, and for the decisions to be robust, surrogate endpoints need to be validated. In the era of precision medicine, when surrogacy patterns may depend on the drug’s mechanism of action and trials of targeted therapies may be small, data from randomized controlled trials may be limited. Real-world evidence (RWE) is increasingly used at different stages of the drug development process. When used to enhance the evidence base for surrogate endpoint evaluation, RWE can improve inferences about the strength of surrogate relationships and the precision of predicted treatment effect on the final clinical outcome based on the observed effect on the surrogate endpoint in a new trial. Careful selection of RWE is needed to reduce risk of bias.

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“…The presence of CYP3A5 has been demonstrated in normal colon (3,17,18), colon adenoma (19), and CRC (20). The CYP3A5*3 polymorphism, which can lead to reduced enzyme activity, has been associated with significantly longer progression-free survival in patients with metastatic CRC (21).…”

Section: Introductionmentioning

confidence: 99%

Tumor response to irinotecan is associated with CYP3A5 expression in colorectal cancer

et al. 2019

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Recently, a tumor-autonomous cytochrome P450 (CYP)-3A5-mediated resistance to cancer therapy has been demonstrated in pancreatic ductal adenocarcinoma. Expression of CYP3A5, which is involved in the degradation of irinotecan, has also been reported in colorectal cancer (CRC). The aim of the present study was to analyze CYP3A5 expression in the normal colon, colon adenoma, CRC and normal tissues, as well as to examine whether CYP3A5 expression in CRC has an impact on tumor response to irinotecan treatment. Immunohistochemistry was used to assess 85 tissue samples from 65 patients with CRC, along with 15 samples of normal colon and 45 samples of colon adenoma (including tubular, tubulovillous, and sessile serrated adenomas), and a tissue microarray (TMA) comprised of 26 different normal tissue types. Expression of CYP3A5 was evaluated with a semi-quantitative score. Tumor response to irinotecan therapy was assessed according to the Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 guidelines. In normal tissues, CYP3A5 was expressed in epithelial cells of the colon, gallbladder, kidney, liver, small intestine, stomach, thyroid gland and tonsil, as well as in nerves. Expression in colon mucosa was heterogeneous, with only weak staining in the minority of specimens. CYP3A5 exhibited markedly higher expression in adenomas compared with normal colon tissues. A statistically significant inverse correlation was identified between CYP3A5 expression in CRC tissues and tumor response to irinotecan therapy. Irinotecan treatment itself did not alter CYP3A5 expression in CRC tissues. As CYP3A5 is involved in the degradation of irinotecan, the significantly higher intratumoral expression of CYP3A5 in patients with CRC who do not respond to irinotecan-based chemotherapy may indicate a causal role of CYP3A5 in tumor resistance.

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Genetic polymorphisms in cytochrome P450 and clinical outcomes of FOLFIRI chemotherapy in patients with metastatic colorectal cancer

Cited by 5 publications

References 34 publications

HSPB1 rs2070804 polymorphism is associated with the depth of primary tumor

HSPB1 rs2070804 polymorphism is associated with the depth of primary tumor

Using Bayesian Evidence Synthesis Methods to Incorporate Real-World Evidence in Surrogate Endpoint Evaluation

Tumor response to irinotecan is associated with CYP3A5 expression in colorectal cancer

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