Current status of pharmacological treatment of colorectal cancer

Akhtar, Reyhan; Chandel, Shammy; Sarotra, Pooja; Medhi, Bikash

doi:10.4251/wjgo.v6.i6.177

Cited by 41 publications

(33 citation statements)

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“…1 B) is an important component of FOLFIRI and FOLFIRINOX chemotherapy regimen which are used as first line treatment against colorectal and advanced pancreatic cancer [1, 2]. It has also shown clinical activity against other types of cancers such as lung, ovarian, cervical, gastric, refractory lymphoma and leukemia etc.…”

Section: Introductionmentioning

confidence: 99%

Development and validation of an UPLC–MS/MS method for the quantification of irinotecan, SN-38 and SN-38 glucuronide in plasma, urine, feces, liver and kidney: Application to a pharmacokinetic study of irinotecan in rats

Basu

Zhang

Yin

et al. 2016

Journal of Chromatography B

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The objective of this research is to develop and validate a sensitive and reproducible UPLC-MS/MS method to quantify irinotecan, its active metabolite SN-38 and SN-38 glucuronide (phase II metabolite of SN-38) simultaneously in different bio-matrices (plasma, urine, feces), tissues (liver and kidney) and to use the method to investigate its pharmacokinetic behavior in rats. Irinotecan, SN-38 and SN-38 glucuronide has been resolved and separated by C18 column using acetonitrile and 0.1% formic acid in water used as the mobile phases. Triple quadruple mass spectrometer using multiple reaction monitoring (MRM) with positive scan mode were employed to perform mass analysis. The results showed that the linear response range of irinotecan and SN-38 in plasma, feces, liver and kidney is 4.88 –10000 nM, 39 – 5000 nM, 48.8 –6250 nM and 48.8 – 6250 nM, respectively (R2 > 0.99). In case of SN-38 glucuronide, the standard curves were linear in the concentration range of 6.25 – 2000 nM, 4.88 – 1250 nM, 9.8 – 1250 nM and 9.8 – 1250 nM in plasma, feces, liver and kidney homogenates, respectively. The lower limit of detection (LLOD) of irinotecan, SN-38 and SN-38 glucuronide was determined to be less than 25 nM in all bio-matrices as well as tissue homogenates. Recoveries of irinotecan, SN-38 and SN-38 glucuronide at three different concentrations (low, medium and high) were not less than 85% at three different concentrations in plasma and feces. The percentage matrix factors in different bio-matrices and tissues were within 20%. The UPLC-MS/MS method was validated with intra-day and inter-day precision of less than 15% in plasma, feces, liver and kidney. Owing to the high sensitivity of this method, only 20 µl of plasma, urine and homogenates of liver, kidney and feces is needed. The validated method has been successfully employed for pharmacokinetic evaluation of irinotecan in male wistar rats to quantify irinotecan, SN-38 and SN-38 glucuronide in plasma, feces, and urine samples.

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Section: Introductionmentioning

confidence: 99%

Development and validation of an UPLC–MS/MS method for the quantification of irinotecan, SN-38 and SN-38 glucuronide in plasma, urine, feces, liver and kidney: Application to a pharmacokinetic study of irinotecan in rats

Basu

Zhang

Yin

et al. 2016

Journal of Chromatography B

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“…The exact mechanism responsible for CRC development is unknown (Akhtar et al, 2014;Fujii and Sato, 2014). Despite the use of multimodel treatment strategies, including surgery, perioperative chemotherapy, radiotherapy, and targeted therapy, CRC is still the second leading cause of cancer-related death in Western countries (Weitz et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Serum level of endothelial cell-specific molecule-1 and prognosis of colorectal cancer

Jiang¹,

Fu²,

Chen³

2015

Genet. Mol. Res.

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ABSTRACT. We evaluated the clinical significance and explored the prognostic value of serum endothelial cell-specific molecule-1 (ESM-1) expression in colorectal cancer (CRC) in a Chinese population. Serum samples were obtained from 89 CRC patients undergoing surgical treatment and 90 healthy volunteers (control group). ESM-1 levels in serum samples from CRC patients and controls were measured using a sandwich enzyme-linked immunosorbent assay. Overall survival was analyzed by the log-rank test, and survival curves were plotted according to the Kaplan-Meier method. Univariate Cox regression was performed on each clinical covariate to examine its influence on patient survival. Final multivariate models were based on step-wise addition. Serum ESM-1 expression levels were significantly higher in patients with CRC (66.81 ± 22.97 pg/mL) than in healthy volunteers (31.50 ± 16.81 pg/mL, P = 0.012). Expression levels of ESM-1 in CRC patients were significantly correlated with histological differentiation (P = 0.004), TNM stage (P = 0.007), depth of tumor invasion (P = 0.02), and lymph node metastasis (P = 0.001). Kaplan-Meier survival curves revealed that the overall survival was significantly lower in patients with high ESM-1 levels than in those with low levels (29.43 vs 61.20%, P = 0.0166). Multivariate analysis confirmed that the hazard risk of 5520 H. Jiang et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 5519-5526 (2015) death was significantly higher in patients with high serum ESM-1 expression compared with low expression (hazard risk = 4.09, 95% confidence interval: 2.27-10.88, P < 0.001). Detection of ESM-1 levels in the serum may serve as a tumor biomarker for assessing prognosis in CRC.

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“…Irinotecan is clinically used together with cetuximab, fluorouracil, and leucovorin for first-line chemotherapy of colorectal cancer [1]. Irinotecan is metabolized into SN-38 by carboxylesterase 1 and 2 [2].…”

Section: Introductionmentioning

confidence: 99%

Irinotecan Induces Cell Cycle Arrest, but Not Apoptosis or Necrosis, in Caco-2 and CW2 Colorectal Cancer Cell Lines

Kaku¹,

Tsuchiya²,

Kanno³

et al. 2015

Pharmacology

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Irinotecan, a topoisomerase I inhibitor, is clinically used as an anticancer drug. The present study investigated the anticancer effect of irinotecan on p53-negative Caco-2 and p53-positive CW2 human colorectal cancer cell lines. Cell viability for both Caco-2 and CW2 cells was little affected by treatment with irinotecan at concentrations ranging from 0.3 to 30 μmol/l for 24-48 h. Irinotecan did not increase the number of TUNEL-positive cells and did not affect the population of propidium iodide (PI)-positive and annexin V-negative cells, corresponding to primary necrosis, or that of PI-positive and annexin-positive cells, corresponding to late apoptosis/secondary necrosis, in either of the two cell lines. In the cell cycle analysis, irinotecan significantly increased the proportions at the S and G₂/M phases of cell cycling in parallel with a decreased population at the G₁ phase in both cell lines. Irinotecan significantly inhibited tumor growth in mice inoculated with CW2 cells. Taken together, these results indicate that irinotecan induces cell cycle arrest, but not apoptosis or necrosis, both in Caco-2 and CW2 cells, leading to suppression of cell proliferation.

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Current status of pharmacological treatment of colorectal cancer

Cited by 41 publications

References 0 publications

Development and validation of an UPLC–MS/MS method for the quantification of irinotecan, SN-38 and SN-38 glucuronide in plasma, urine, feces, liver and kidney: Application to a pharmacokinetic study of irinotecan in rats

Development and validation of an UPLC–MS/MS method for the quantification of irinotecan, SN-38 and SN-38 glucuronide in plasma, urine, feces, liver and kidney: Application to a pharmacokinetic study of irinotecan in rats

Serum level of endothelial cell-specific molecule-1 and prognosis of colorectal cancer

Irinotecan Induces Cell Cycle Arrest, but Not Apoptosis or Necrosis, in Caco-2 and CW2 Colorectal Cancer Cell Lines

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