Therefore, the early detection of hypomagnesaemia is essential and should be factored into the design of large-scale, controlled studies in the future. Conclusion

Although our retrospective analysis was based on a small sample size, we found that Cmab, as a second-line therapy in patients with long-term L-OHP exposure, may exacerbate residual L -OHP-induced neurotoxicity by inducing hypomagnesaemia. Therefore, we recommend serially Inhibitors,research,lifescience,medical evaluating serum magnesium levels and neurotoxicity when initiating Cmab treatment after L-OHP therapy. Footnotes No potential conflict of interest.
5-Fluorouracil (5-FU) remains the most commonly used chemotherapeutic agent for the treatment of colorectal cancers (CRCs). Nevertheless, more than 40 years of 5-FU usage has not see more yielded responses greater than 35-40% (1)-(5), neither has it decreased the rates of recurrence (6),(7). Therefore, novel strategies are required to predict response

Inhibitors,research,lifescience,medical to treatment. Although several molecular markers have prognostic value for CRCs (8)-(15) their predictive value in assessing treatment response remains controversial(7),(16)-(18). In addition to selecting the best chemotherapeutic tools, a new challenge is to identify genetic and/or molecular markers that can be used as Inhibitors,research,lifescience,medical predictors of response to treatment. As demonstrated for cultured cells, p53-dependent apoptosis modulates the cytotoxic effect of chemotherapeutic agents; cells with functional p53 or wild-type p53 (wt-p53) are more sensitive, and cells with mutated or lack of p53 are more resistant (19),(20). Lenz et al demonstrated a better rate of response to 5-FU for patients whose tumors were wild-type for p53 than those Inhibitors,research,lifescience,medical whose tumors had overexpressed or mutated p53 (21). In contrast, Allegra et al found that overexpressed p53 correlated with a better response to treatment (22),(23), and Elsaleh et al (24) could not find any relationship between p53 status and 5-FU response or survival of patients with Inhibitors,research,lifescience,medical colon or rectal tumors. Thus, data relating to the predictive value of p53 in CRCs is contradictory and inconclusive. Apoptosis is a complex process that proceeds

through two pathways. The extrinsic pathway is based on cell surface receptors and cytoplasmic proteins. The intrinsic pathway occurs in the mitochondria, where the balance of pro-and anti-apoptotic proteins is largely regulated by the members of the Bcl-2 family. p53 has been from described as a main modulator of apoptosis in both pathways (25). The anti-tumor activity of 5-FU has been related to its capacity to induce apoptosis by damaging the DNA and/or by altering the expression profiles of pro- and anti-apoptotic molecules (26)-(28). Chemo-resistance may depend on the function and relationship between pro-and anti-apoptotic proteins (29),(30). The balance between anti-apoptotic (e.g., Bcl-2) and pro-apoptotic proteins (e.g., Bax) in a cell determines its susceptibility to apoptosis after 5-FU treatment(31).