HOXB4 (Homeobox B4)

Collectively, these findings delineate a HOXB4-SMO axis that drives BCa progression and suggest this pathway as a candidate target for patient stratification and therapeutic exploration. Future studies should validate these findings in larger multi-center cohorts and assess the therapeutic potential of SMO inhibition in preclinical BCa models.

In this process, hypermethylation of HOXB4 predicted early-stage LUAD and was associated with a poorer prognosis. Furthermore, HOXB4 regulated the EMT in LUAD cells through the RAP1 pathway, which in turn affected LUAD metastasis and invasion.

Notably, inhibitors of either HOXB4, RUNX1, or IGFBP3 could reverse the oncogenic activity mediated by circ_0044362. Collectively, our findings reveal the involvement of the circ_0044362/HOXB4 pathway in ovarian cancer progression and provide potential therapeutic strategies for ovarian cancer treatment.

The mRNA expression profile of human HTS samples showed significant changes compared to normal skin samples. TGF-β1, SMAD2, SMAD7, BAX, IGF2, COL1A1, COL1A2, MMPs, CDC14A, ITGB6, EGF, CDKN1C, CDKN2A, CTNNA3, HOXA3 and other related genes involved in biological processes, molecular functions, signaling pathways may be closely related to the occurrence and development of hypertrophic scars.

HOXB4 mediated the malignant phenotypes and modulated the immune evasion via METTL7B/TKT axis. The HOXB4/METTL7B cascade and its downstream changes might be novel targets for blocking hepatocellular carcinoma progression.

In conclusion, our study suggests that abnormal expression of self-renewal-related genes may be potential early biomarkers for benzene-induced hematotoxicity. This hematotoxicity may contribute to the acquisition of evolutionary advantages by leukemic precursor cells and accelerate malignant transformation.

Our findings highlight the strong effects of ASXL1 variants that supersede cell-type and even disease states. This is the first direct comparison of transcriptomic and methylation profiles driven by pathogenic variants in a chromatin modifier gene in distinct diseases. Similar to RASopathies, in which pathogenic variants in many genes lead to overlapping phenotypes that can be treated by inhibiting a common pathway, our data identifies common pathways for ASXL1 variants that can be targeted for both disease states. Comparative approaches of high-penetrance genetic variants across cell types and disease states can identify targetable pathways to treat multiple diseases. Finally, our work highlights the connections of epigenes, such as ASXL1, to an underlying stem-cell state in both early development and in malignancy.

We have developed a risk prediction model for pediatric R/R ALL utilizing the genes BAG2, EPHA4, FBXO9, SNX10, and WNK1. This model provides a scientific foundation for early identification of R/R ALL in children.

Specifically, our analysis implicated 2 stem cell-related transcription factors, HOXB4 and SALL4, in poor response to temozolomide in brain cancers. In addition, expression of SNRNP70 and its targets were implicated in cetuximab response by 3 different analyses, although the mechanism remains unclear...We also highlight the most promising of these results, which were supported by multiple analyses and by previous research. We report these findings as promising avenues for independent validation and further research into cancer treatments and patient response.

Interestingly, HOXB4 bound to the LINC00629 promoter and inhibited its transcription, indicating that LINC00629 is a transcriptional target of HOXB4. Collectively, these findings establish a direct role for LINC00629 in suppressing glucose metabolism, and HOXB4/LINC00629/c-Myc might serve as a potential biomarker and an effective therapeutic strategy for OC cancer treatment.

The 7 novel DMRs could be promising methylation biomarkers that merits further development as a noninvasive test for early detection of lung cancer.