Background: Previous studies have documented pain as an important concern for quality of life (QoL) and one of the most challenging manifestations for cancer patients. Thus, cancer pain management (CPM) plays a key role in treating pain related to cancer. The aim of this systematic review was to investigate CPM, with an emphasis on personalized medicine, and introduce new pharmacogenomics-based procedures for detecting and treating cancer pain patients. Methods: This study systematically reviewed PubMed from 1990 to 2023 using keywords such as cancer, pain, and personalized medicine. A total of 597 publications were found, and after multiple filtering processes, 75 papers were included. In silico analyses were performed using the GeneCards, STRING-MODEL, miRTargetLink2, and PharmGKB databases. Results: The results reveal that recent reports have mainly focused on personalized medicine strategies for CPM, and pharmacogenomics-based data are rapidly being introduced. The literature review of the 75 highly relevant publications, combined with the bioinformatics results, identified a list of 57 evidence-based genes as the primary gene list for further personalized medicine approaches. The most frequently mentioned genes were CYP2D6, COMT, and OPRM1. Moreover, among the 127 variants identified through both the literature review and data mining in the PharmGKB database, 21 variants remain as potential candidates for whole-exome sequencing (WES) analysis. Interestingly, hsa-miR-34a-5p and hsa-miR-146a-5p were suggested as putative circulating biomarkers for cancer pain prognosis and diagnosis. Conclusions: In conclusion, this study highlights personalized medicine as the most promising strategy in CPM, utilizing pharmacogenomics-based approaches to alleviate cancer pain.

Background: Gastric cancer is a complicated malignancy whose aetiology is not well characterized. Single nucleotide polymorphisms (SNPs), some located within microRNA genes, are linked with gastric cancer. We hypothesized a link between SNP rs2620381 (A > C) in miR-627 and gastric cancer. Material and methods: We recruited 280 healthy controls and 240 gastric cancer patients. Genotyping was conducted by allele-specific polymerase chain reaction. In addition, in silico analyses were carried out via databases and web tools including miRBase, dbSNP, RNAfold, MiRNASNP V2.0, miRWalk V2.0, miRTarBase, and miRmap. Results: Any C genotype in rs2620381 was linked to gastric cancer: CC vs. AA: OR/95% CI 2.67 (1.17–6.09), p = 0.01, CC+AC vs. AA: OR/95% CI 1.66 (1.12–2.46), p = 0.01, CC vs. AC+AA: OR/95% CI 2.44 (1.07–5.54), p = 0.03. The minor allele C of miR-627 was linked with gastric cancer compared with A allele (OR/95%CI 1.88 (1.30–2.73), p = 0.0008). There were no links between age, sex, tumour type, distant metastasis, and tumour stages and the miR-627 polymorphism in gastric cancer patients. Conclusion: Presence of the C SNP in miR-627 rs2620381 in linked with gastric cancer, and may be important in pathogenesis.

Background: Although miR-410 acts as a cancer inducer in colorectal cancer, there is limited data on the clinical implications of miR-410 expression levels in patients. We hypothesized a link between miR-410 expression and its potential clinical values in patients with colorectal cancer. Material and methods: 120 colorectal cancer tissue specimens and 120 adjacent non-tumour tissues were obtained. Quantification of miR-410 expression levels was determined by, quantitative RT-PCR. Expression was analysed by clinical features. Results: miR-410 was up-regulated in malignant tissues compared with corresponding normal tissues (P < 0.01), with TNM stage and lymph node metastasis (P = 0.03, P = 0.004, respectively), and with worse overall survival (P = 0.002). Multivariate survival analysis identified it as an independent risk factor for outcome (P = 0.021, HR = 2.19; 95% CI = 1.12–4.25). Conclusion: Compared to normal non-cancerous tissues, miR-410 was overexpressed in tumour tissues and is independently associated with the unfavourable outcome. Levels of MiR-410 might a useful laboratory tool in managing and predicting the prognosis of colorectal cancer.

Waldenstrom macroglobulinemia (WM) is a non-Hodgkin B-cell lymphoma, characterized by bone marrow infiltration with plasma cells and lymphocytes. The tumor microenvironment (TME) plays an important role in mediating WM cell biology, but the effects of macrophages on WM biology remains unclear. Here, we investigated the effects of macrophages on WM growth and survival and identified a novel role for transcription factor GLI3 in macrophage polarization. We found that co-culture of M0 and M2 macrophages promoted WM cell growth and survival, and co-culture WM cells with M0 macrophages induced M2-like phenotypes. Interestingly, GLI3 expression was induced in M2 macrophages (not M1), leading us to perform analysis of macrophages from mice lacking Gli3 in myeloid cells (M-Gli3^−/− mice). A subset of differentially expressed genes implicated a role for GLI3 in macrophage polarization. Macrophages from M-Gli3^−/− mice did not induce WM cell proliferation and reduced survival compared to M2 macrophages from WT mice. In addition, in vitro polarization of M0 macrophages from M-Gli3^−/− was not able to induce M2 markers such as CD163, despite inducing iNos expression (M1 marker). Taken together, these results suggest a role for M2 macrophages in promoting WM cell growth and identify GLI3 as a modulator of macrophage polarization.