ABCB1 3435C>T

In summary, our findings prove that the host's genotypes might modify the risk of developing Peri-ES, contribute to a better understanding of the inter-individual difference in efficacy, and facilitate the development of individualized approaches to GvHD prophylaxis.

MTHFR 677C>T and ABCB1 3435 C>T predicted the risk of delayed MTX clearance during HD-MTX treatment in children with ALL. Serum L-phenylalanine levels were significantly elevated after HD-MTX treatment in children with the MTHFR 677C>T mutation gene.

Conclusions The homozygous mutant TT genotypes (C1236T and C3435T) and heterozygous CT genotypes (C1236T) showed significant association to chemo-induced toxicity (hematological toxicity, nausea, vomiting, alopecia) in patients underwent anthracycline and taxane. Hence, these SNPs could serve as predictive markers to mitigate chemotherapy's adverse effects and optimize treatment to reduce the grade of toxicity and improves patients quality of life.

A wide interindividual variability in therapeutic response to cyclin-dependent kinases 4 and 6 inhibitors (CDKis) palbociclib, ribociclib and abemaciclib, among patients with HR+/HER2- metastatic breast cancer has been reported. Homozygous carriers of the ABCB1 T-T-T(A) haplotype tended to have a higher mean ribociclib C (934.0 ng/mL vs. 752.0 ng/mL and 668.0 ng/mL). Regardless preliminary, these findings offer promising insights into the role of pharmacogenetic markers in CDKis safety profiles, potentially contributing to address the interindividual variability in CDKis responses.

Addition of ABCG2 inhibitors for patients without ABCG2 34G>A should be studied further, to prevent new CNS metastases during osimertinib treatment. No funding was received for this trial.

The ABCB1 2677G>T/A polymorphism may influence tolerance to abemaciclib in breast cancer patients by affecting the pharmacokinetics of the agent and its active metabolites.

Table: 27P Conclusions In EGFRm+ NSCLC patients treated with OSI, the SNPs ABCG2 421C>A, ABCB1 3435C>T and ABCG2 34G>A can impact CNS-DFS, and not CNS-PFS. Genotyping these patients may guide monitoring strategies aimed at early detection of brain metastases.

Moreover, the advent of second generation TKIs, namely nilotinib and dasatinib, have largely increased the number of CML patients achieving deep and sustained molecular responses. Finally, we found ABCG2 rs2231142 GG genotype to be associated with a decrease risk of MR3 loss. In conclusion, MDR-transporters SNPs may significantly affect the achievement and loss of molecular response in CML patients treated with nilotinib.