Liposomal nanomedicine represents a common and versatile carrier for the delivery of both lipophilic and hydrophilic drugs. However, the direct formulation of many chemotherapeutics into a liposomal system remains an...

Purpose Mismatch repair (MMR) deficiency plays a critical role in rectal cancer. This study aimed to explore the associations between genetic variations in seven MMR genes and adverse events (AEs) and survival of patients with rectal cancer treated with postoperative chemoradiotherapy (CRT). Materials and Methods Fifty single nucleotide polymorphisms in seven MMR ( MLH1, MLH3, MSH2, MSH3, MSH6, PMS1 and PMS2 ) genes were genotyped by Sequenom MassARRAY method in 365 patients with locally advanced rectal cancer receiving postoperative CRT. The associations between genotypes and AEs were measured by odds ratios and 95% confidence intervals (CIs) by unconditional logistic regression model. The associations between genetic variations and survival were computed by the hazard ratios and 95% CIs by Cox proportional regression model. Results The most common grade ≥ 2 AEs in those 365 patients, in decreasing order, were diarrhea (44.1%), leukopenia (29.6%), and dermatitis (18.9%). Except 38 cases missing, 61 patients (18.7%) died during the follow-up period. We found MSH3 rs12513549, rs33013 and rs6151627 significantly associated with the risk of grade ≥ 2 diarrhea. PMS1 rs1233255 had an impact on the occurrence of grade ≥2 dermatitis. Meanwhile, PMS1 rs4920657, rs5743030, and rs5743100 were associated with overall survival (OS) time of rectal cancer. Conclusion These results suggest that MSH3 and PMS1 polymorphisms may play important roles in AEs prediction and prognosis of rectal cancer patients receiving postoperative CRT, which can be potential genetic biomarkers for rectal cancer personalized treatment.

The systematic treatment of colorectal cancer (CRC) still has room for improvement.The efficacy of chemotherapy, that of anti-vascular therapy, and that of immunotherapy have been unsatisfactory. In recent years, nanomaterials have been used as carriers to improve the bioavailability of anticancer drugs. For the treatment of colorectal cancer, nanodrugs increase the possibility of more precise targeted delivery. However, the actual benefits may cover more aspects. Nanocarriers can produce synergistic effects with anticancer drugs, including the scavenging of reactive oxygen species and co-delivery of a variety of drugs. Currently, immunotherapy has very limited clinical applications in CRC. Modified nanocarriers can activate the immune microenvironment, which can be used for staging antigen recognition or the immune response. Cancer vaccines based on nanomaterials and modified immune checkpoint inhibitors have shown therapeutic potential in animal models. Considering the direct or indirect relationship between the intestinal microflora and CRC, a variety of nanodrugs that regulate microbial function have been explored as an anticancer strategy, and the special structure of microorganisms can also be used as a basis for improving the delivery of traditional nanoparticles (NPs). This review summarizes recent research performed on nanocarriers in in vivo and in vitro models and the synergistic anticancer effects of nanocarriers, focusing on the interaction between NPs and the body, resulting in enhanced efficacy and immune activation. Furthermore, this review describes the current trend of NPs used in the treatment of CRC.

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