Journal of Blood & Lymph

Malignant Rhabdoid Tumor (MRT) is a quite rare malignant pediatric disease that occurs primarily in infants and young children. Although most patients with MRT are treated with the intensive multimodal treatment, the results are unsatisfied and there is no established standard of care for MRT. Therefore, there is a great need for more effective treatment(s) for MRT. Recently, we have demonstrated that RUNX1 silencing and “CROX (Cluster Regulation of RUNX)” strategy using our novel RUNX inhibitor (Chb-M') strongly reduce MRT cell proliferation rate via the augmentation of p53-mediated apoptotic pathway in vitro and in vivo. In this mini-review, we describe the molecular characteristics of our RUNX inhibitor, DNA-alkylating Pyrrole-Imidazole (PI) polyamides, and its anti-tumor effects on a variety of cancers including MRT. Finally, we discuss the precise molecular mechanisms behind p53-mediated apoptosis induced by RUNX inhibition in MRT cells.

Background: Age-related differences in Multiple Myeloma (MM) are studied in clinical and genomic context, however, transcriptome changes have not yet been determined. The aim of this study is to identify the genes that are expressed differently in young and old patient groups and to examine the relationship of these genes with biological pathways and the drugs that can be used.

Methods: The MMRF CoMMpass cohort RNA-Seq data (n=634) was used to analyze differentially expressed genes between young and old patients. GO term and KEGG gene-set enrichment analysis were conducted using R packages. Drug-gene interactions were detected using DGIdb.

Results: Globally, 523 genes (366 upregulated, 157 downregulated) were differentially expressed (p<0.05) in young patients. Totally 220 GO terms, mostly related to immune regulation pathways were enriched. “Cytokine-cytokine receptor interaction” gene-set was enriched in KEGG GSEA. Among the highest expression difference, genes involved in immune regulation (FCGR1A, FCER1G, TLR2), known proto-oncogenic genes (BCL2, FGR) and genes under investigation for association with various cancers (RGL4, MT-RNR1, ETS2, ENPP3, FUT7, NTNG2, PRAM1) were identified. Drugs associated with the pathways affected by these genes were identified.

Conclusion: Further investigation of differentially expressed genes in young patients may shed light on new treatment options.

Despite having a basic grasp of laser wavelengths and dose ranges, there was no consensus on whether continuous mode or pulsing mode should be used, which is more dependable, and what determinants should be used to support the parameters of a pulsating laser. The molecular and cellular mechanisms of cold laser treatment have been investigated. The many types of pulsed lasers available have been described as the factors that influence the creation of their pulses. Investigations that were dissolved by continuous and/or pulsed laser modes were evaluated in vivo and in vitro. The laser therapy pulse repetition rates were matched. Several notable confirmations have shown that pulse mode has different effects on wound healing and damaged tissue than continuous mode. To completely assess the performance of cold laser treatment in cutaneous wounds healing, measurable clinical research that associates cellular effects in addition to biological processes is required. More research is needed to confirm these findings for a variety of wound types and treatments in a variety of settings, including pulsating mode structures. Future research should concentrate on well-controlled studies that rationally determine laser types and therapy parameters.