Ask about this productRelated genes to: RAD54L Blocking Peptide
- Gene:
- RAD54L NIH gene
- Name:
- RAD54 like
- Previous symbol:
- -
- Synonyms:
- hHR54, hRAD54, RAD54A
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-04
- Date modifiied:
- 2017-08-08
Related products to: RAD54L Blocking Peptide
Related articles to: RAD54L Blocking Peptide
- Neoadjuvant therapy (NAT) is the standard treatment option for locally advanced breast cancer (BC). Noncoding RNAs are known to play a significant role in cancer development. However, the involvement of the circular RNA (circRNA)/long non-coding RNA (lncRNA)-(miRNA)-mRNA competitive endogenous RNA (ceRNA) network in the antitumor effects of NAT in BC remains unclear. - Source: PubMed
Publication date: 2026/01/17
Li DonghaiZhang ZhiyingChen YiboZhao XueyuHe KunyuanZhang Rui - To investigate the clinicopathological, imaging, and molecular characteristics of mammary Rosai-Dorfman disease (RDD). A retrospective analysis was performed on four cases of primary RDD in the breast diagnosed at the First Affiliated Hospital with Nanjing Medical University from January 2018 to September 2025. Clinical, histopathological, and immunohistochemical features were reviewed, next-generation sequencing (NGS) was conducted, and the findings were discussed in the context of relevant literature. Among the four cases, three were female and one was male, with ages of 54, 33, 67 and 62 years respectively. Ultrasound findings suggested inflammatory changes in one case, BI-RADS category 3 in one case, and BI-RADS category 4 in two cases. Microscopic examination revealed infiltration of lymphocytes, plasma cells, and histiocytes, with characteristic emperipolesis observed in some cases. Immunohistochemically, the lesional cells were positive for CD68, CD163, cyclin D1, S-100, and OCT2, and negative for Langerin and ALK. NGS performed in all four cases identified somatic mutations in homologous recombination repair-related genes-including RAD54L, RAD50, MRE11, and BRIP1-in three cases. One case showed somatic mutations in genes associated with signaling pathways and immune inflammation, such as AXIN2, FGF19, MYD88, NF2, and TSC2. RDD of the breast presents with non-specific clinical manifestations and radiologically misleading features. Its histopathological characteristics (especially the emperipolesis phenomenon) and typical immunohistochemical profile (CD68+, CD163+, cyclin D1+, S-100+, Langerin-, ALK-) may aid in differential diagnosis. The high frequency of DNA homologous recombination repair-related gene mutations in mammary RDD provides new insights into its pathogenesis and supports its classification as a clonal disease. - Source: PubMed
Huang Z DZhai B YXu CDing YZhang Z HWang C - We recently identified variants in 10 genes that are members of either the p53 pathway or Fanconi Anemia Complex (FAC), regulators of DNA repair (DNA damage response [DDR]) in 17 cases with pediatric acute-onset neuropsychiatric syndrome (PANS) or regression in autism spectrum disorder and other neurodevelopmental disorders (NDD). We aimed to identify additional cases with genetic vulnerabilities in DDR and related pathways. - Source: PubMed
Publication date: 2026/02/09
Vettiatil DhanyaSoorajkumar AnjanaDubin Robert APedrosa Erika MSchornagel AllanLambert John SCosta Isadora PinheiroMcDonald JosephSwagemakers Sigrid M Avan der Spek Peter JFrankovich JenniferCunningham Janet LLachman Herbert M - Androgen receptor pathway inhibitors (ARPIs), such as enzalutamide and abiraterone, are standard treatments for metastatic castration-resistant prostate cancer (mCRPC). However, a subset of patients display primary resistance, and most eventually acquire secondary resistance. This study aimed to define genomic features of ARPI resistance using longitudinal circulating tumor DNA (ctDNA) analysis. - Source: PubMed
Publication date: 2026/01/26
Valentín López José CYu ChenxiKnutson Todd PKobilka AnnaLyman JacquelineGuo SiyuanLuo BinMunro Sarah ALi YingmingHeer RakeshGaughan LukeMorris Michael JBeltran HimishaRyan Charles JAntonarakis Emmanuel SArmstrong Andrew JHalabi SusanDehm Scott M - Radiation resistance is the major cause of non-small cell lung cancer (NSCLC) treatment failure. Homologous recombination (HR), which mediates the repair of DNA double-strand breaks (DSB), is crucial for maintaining genomic integrity and enhancing survival in response to radiotherapy in NSCLC. However, the mechanisms of HR repair in radiation resistance remains unclear. In this study, we investigated the functional role of the transcription factor Spermatogenesis and oogenesis basic helix-loop-helix transcription factor 2 (SOHLH2) in NSCLC HR repair and radioresistance. Our research unveiled that the expression levels of SOHLH2 increased in NSCLC compared with adjacent non-tumor tissues. Elevated SOHLH2 expression promotes NSCLC cell proliferation and radiation resistance, while knocking down SOHLH2 has the opposite effect. Mechanistically, SOHLH2 transcriptionally activated the expression of RAD54L, thereby promoting HR repair and the survival of cancer cells in response to radiation. Notably, RAD54L overexpression was able to rescue the suppression of NSCLC HR repair and radioresistance induced by SOHLH2 knockdown. Therefore, SOHLH2-RAD54L axis may serve as a potential therapeutic target for overcoming radioresistance in NSCLC. - Source: PubMed
Publication date: 2026/01/14
Yang Jia-XueZhang Wei-HuaLei Jin-JuCheng ChunYu MengZhang PingSang Yi