Mouse Hoxa10 (Center)
- Known as:
- Mouse Hoxa10 (Center)
- Catalog number:
- AP19374c-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Mouse Hoxa10 (Center)
Related genes to: Mouse Hoxa10 (Center)
- Gene:
- HOXA10 NIH gene
- Name:
- homeobox A10
- Previous symbol:
- HOX1H, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
Related products to: Mouse Hoxa10 (Center)
Related articles to: Mouse Hoxa10 (Center)
- Homeobox (HOX) genes are essential regulators of embryonic development and cellular differentiation under physiological conditions. Among this gene family, HOXA10 has emerged as a pivotal factor in gastrointestinal (GI) cancers, influencing tumor growth, metastasis, disease progression, and resistance to therapy. HOXA10 functions as a transcription factor and plays key roles not only in embryogenesis but also in immunomodulation. HOXA10 and its transcriptional targets play a crucial role in cancer development, promoting cell growth, invasion, migration, metastasis, and resistance to cell death. Recent studies have explored the influence of HOXA10 on the tumor immune microenvironment, particularly its role in modulating immune cell recruitment and signaling pathways that enable tumor immune evasion. Our recent research identified a HOXA10-regulated five-gene signature that distinguishes long-term from short-term survivors of pancreatic cancer, with HOXA10 expression correlating with increased regulatory T cell (T) infiltration. HOXA10 impacts genes and pathways involving macrophages, Tregs, and other immune cells, potentially creating an immunosuppressive niche that promotes metastasis and diminishes the effectiveness of immunotherapies. In this review, we examine the diverse functions of HOXA10 in GI cancers, offering a comprehensive comparison with other HOX family proteins to elucidate their overlapping and distinct roles in malignancy. Our goal is to provide a thorough overview of how HOXA10 contributes to tumor development and its microenvironment. We highlight its critical role in facilitating cancer progression and metastasis, supported by data from cell lines, patient tumor samples, and clinical studies. Recognizing existing gaps in the understanding of HOXA10's role in cancer, we also explore potential strategies to target this gene, with an emphasis on synergistic approaches that combine HOXA10 inhibition and immunotherapy. Ultimately, these insights aim to identify vulnerabilities within GI cancers that could be exploited through novel therapeutic agents and combination treatments, paving the way for improved clinical outcomes. - Source: PubMed
Publication date: 2026/05/08
Kisling Sophia GShah AshuJohnson EstherAlsafwani Zahraa WRaman VenuBatra Surinder K - MLL-rearranged acute myeloid leukemia (AML) is a high-risk hematological malignancy driven by aberrant epigenetic regulation. MLL fusion proteins recruit the DOT1L methyltransferase, causing dysregulated histone H3K79 methylation and sustained leukemogenic gene expression (HOXA10, MLLT10), while BCL-2 overexpression contributes to apoptosis resistance. This study evaluated the synergistic efficacy of combining the DOT1L inhibitor EPZ004777 with the BCL-2 inhibitor ABT-737. THP-1 cells were treated with EPZ004777 and ABT-737 alone or in combination. Cell proliferation, apoptosis, H3K79 methylation, target gene expression, and PI3K/AKT signaling were assessed. An in vivo xenograft mouse model (C-NKG mice) validated therapeutic effects. Combined treatment exhibited potent synergistic cytotoxicity. Dual inhibition reduced H3K79 di- and tri-methylation, downregulated HOXA10 and MLLT10, and blocked PI3K/AKT phosphorylation. In vivo, combination therapy prolonged survival, restored bone marrow function, and alleviated organ infiltration. These findings demonstrate that dual targeting of DOT1L and BCL-2 exerts synergistic anti-leukemic activity via PI3K/AKT suppression in MLL-rearranged AML, providing a pharmacological rationale for this innovative combination strategy. - Source: PubMed
Publication date: 2026/05/04
Zuo YabeiGeng LiGuo YujieZhao DaitianchangQi NannanWang YanZhang JingyuNiu Zhiyun - : Endometrial polyps are common in women presenting with subfertility, yet uncertainty persists regarding which lesions warrant removal and how best to integrate hysteroscopic management with contemporary fertility treatment pathways. This narrative review synthesizes current evidence on pathophysiological mechanisms, diagnostic approaches, fertility outcomes, and practical clinical management for women under 40 years of age. : PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library were searched for English-language human studies published between January 2005 and December 2025. From 2352 records identified, 83 studies were included after screening of 1517 unique records (7 randomized controlled trials, 12 systematic reviews/meta-analyses, 14 prospective cohort studies, 31 retrospective cohort studies, 5 case-control and other study designs, 11 narrative reviews and supporting evidence studies, 1 clinical guideline, and 2 targeted 2025 additions). This structured narrative review employed a systematic search strategy to ensure comprehensive coverage, with evidence synthesized thematically in accordance with the SANRA guidelines. No formal risk-of-bias assessment or pre-registered protocol was used. : Across treatment modalities, hysteroscopic polypectomy was consistently associated with improved fertility outcomes. The landmark Pérez-Medina randomized trial reported a relative risk of 2.1 (95% CI 1.5-2.9) for pregnancy after polypectomy before intrauterine insemination. For IVF/ICSI, reported clinical pregnancy rates after polypectomy range from 53-72% and live birth rates from 43-66%. Proposed mechanisms include mechanical interference, chronic inflammation with cytokine dysregulation, altered endometrial receptivity (including dysregulation of HOXA10/HOXA11), and impaired decidualization. Current evidence supports hysteroscopic polypectomy as an effective intervention to improve fertility outcomes in subfertile women with endometrial polyps, particularly prior to intrauterine insemination. For IVF/ICSI, polypectomy of documented polyps appears beneficial, though evidence quality is moderate and heterogeneity exists across studies. It is critical to distinguish routine screening hysteroscopy before IVF from targeted polypectomy when a polyp has been documented. Contemporary guidance (including the 2024 SOGC guideline) favors polypectomy for symptomatic polyps and those that meet specific clinical criteria; for small asymptomatic polyps (<10 mm), individualized decision-making is appropriate, given limited direct evidence and the potential for spontaneous regression. Future research should clarify molecular predictors of polyp-associated infertility, optimal timing relative to fertility treatment, and long-term reproductive outcomes. - Source: PubMed
Publication date: 2026/04/03
Goc GoksuBirge Ozer - Endometriosis (EMs) affects approximately 10% of reproductive-age women worldwide, yet its pathogenesis remains incompletely understood. Abnormal cell differentiation and somatic mutations in the ectopic endometrial microenvironment play critical roles in disease progression and treatment response heterogeneity. This study is aimed at elucidating the molecular mechanisms underlying ectopic endometrial cell differentiation using machine learning (ML) approaches and single-cell RNA sequencing (scRNA-seq), and identifying novel prognostic biomarkers and therapeutic targets, with particular attention to mutation-driven transcriptional alterations. - Source: PubMed
Publication date: 2026/04/23
Zhang HuipengLuo Yuli - Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor originating in the nasopharynx. Ubiquitin-specific peptidase 31 (USP31) exerts a tumor-promoting role in diverse cancers, but the function of USP31 in NPC is unclear. - Source: PubMed
Publication date: 2026/04/14
Liu JunSu ShengtianLu WenjingGuo Ping