HMBOX1 (Homeobox Containing 1)

In vivo tumor‑bearing experiments also verified the function of the HMBOX1/PTPN1/AKT1 pathway in HCC development. Taken together, the present findings revealed a new HMBOX1/PTPN1/AKT1 axis that inhibits tumor progression and provides new candidate therapy targets for HCC.

Moreover, PLB also inhibited tumor formation in a xenograft transplantation model via PI3K/Akt/mTOR signaling. Collectively, our results suggested that HMBOX1 played a key role in PLB-induced inhibition of HCC growth through PI3K/Akt/mTOR signaling pathway.

Induction chemotherapy (cytarabine and idarubicin) initially achieved remission, but subsequent relapses led to the use of venetoclax and 5-azacytidine, which again resulted in remission. This is the first report that molecularly characterizes the HMBOX1::JAK2 fusion in a de novo AML patient. The identification of this novel alteration adds to the growing and heterogeneous molecular landscape of AML and suggests a potential new avenue for targeted therapy.

Future research must bridge mechanistic insights with clinical innovation. By harmonizing pathophysiological understanding with precision medicine approaches, this synthesis underscores the potential to transform SIMD management from supportive care to targeted functional recovery.

Continued efforts should focus on identifying optimal treatment strategies for this high-risk group of patients.

The family of ALK-rearranged mesenchymal neoplasms is expanding and ensartinib could be a potential treatment option for patients with HMBOX1::ALK. Repeated biopsy and NGS detection are critical to guide treatment selection at disease progression.

Maybe there are some differences in the malignant diagnostic criteria and molecular genetic characteristics between visceral derived glomus tumors and soft tissue derived tumors of the same kind, such as limbs and skin. More data accumulation is needed.

Furthermore, we confirm that HMBOX1 expression positively correlates with HACE1 expression and inversely correlates with autophagy levels in clinical colorectal cancer tissues. Our findings suggest that HMBOX1 downregulation drives 5-FU resistance through autophagy enhancement in colorectal cancer, highlighting HMBOX1 as a potential target for improving chemosensitivity and patient prognosis.Abbreviation: 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; ATG: autophagy related; CASP3: caspase 3; C-CASP3: cleaved caspase 3; C-PARP: cleaved PARP; CCK8: cell counting kit-8; ChIP: chromatin immunoprecipitation; CHX: cycloheximide; CNV: copy number variation; co-IP: co-immunoprecipitation; COAD: colorectal adenocarcinoma; CQ: chloroquine; CRC: colorectal cancer; CR: complete response; FHC: fetal human colon; GEO: Gene Expression Omnibus; HACE1: HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1; HMBOX1: homeobox containing 1; IHC: immunohistochemistry; LC-MS/MS: liquid chromatography-tandem mass spectrometry; mIHC: multiplexed immunohistochemistry; MUT: mutant; NC: negative control; OS: overall survival; PBS: phosphate-buffered saline; PD: progressive disease; PFA: paraformaldehyde; PFS: progression-free survival; PR: partial response; qPCR: quantitative polymerase chain reaction; RAPA: rapamycin; SD: stable disease; TCGA: The Cancer Genome Atlas; TEM: transmission electron microscopy; TF: translation factor; USP22: ubiquitin specific peptidase 22; WT: wild type.

Knockdown of METTL3 or HMBOX1 attenuated the oncogenic effects of circCD44 overexpression both in vitro and in vivo. These findings suggest that circCD44 promotes ESCC progression by facilitating HMBOX1 mRNA m6A modification and protein expression through METTL3 binding, providing insights into the molecular mechanisms underlying ESCC pathogenesis.

Infantile high-grade glioma should be regarded as a unique tumor entity and a multidisciplinary approach is paramount in improving survival for this group of patients.

HMBOX1 expression was positively correlated with the expression of VEGF, elaborating that HMBOX1 probably promoted the growth of LSCC cells by affecting VEGF. HMBOX1 might contribute to the development of LSCC.

Our cases predominately occurred in older children and mainly exhibited epithelioid to round cell morphology, as opposed to spindle cell morphology. We also show that tumors in a deep location with higher-grade features follow a more aggressive clinical course.