SAA1
- Known as:
- SAA1
- Catalog number:
- 000386A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SAA1
Related genes to: SAA1
- Gene:
- SAA1 NIH gene
- Name:
- serum amyloid A1
- Previous symbol:
- SAA
- Synonyms:
- PIG4, TP53I4
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-01-18
- Date modifiied:
- 2015-09-09
Related products to: SAA1
Related articles to: SAA1
- Disruption of cation homeostasis is increasingly recognized as a driver of breast cancer (BC) progression, yet a clinically actionable gene signature that quantifies this disturbance has been lacking. This study aims to systematically explore the value of cation homeostasis-related genes in the prognosis assessment of BC through bioinformatics analysis, construct and validate a prognostic model based on these genes, and integrate immune mechanism and drug sensitivity analyses to provide novel biomarkers and potential therapeutic targets for precise prognosis evaluation and individualized treatment of BC. - Source: PubMed
Publication date: 2026/04/29
Xu MingxingYe ZhihaoHong WeiminZhu LiquanHe ChaoqiYang ZhuotaoHu JunsiQian DaMeng XuliRen Zhuozhuo - Myelodysplastic neoplasms (MDS) are clonal hematopoietic disorders defined by ineffective hematopoiesis, cytopenias, and variable risk of progression to acute myeloid leukemia. Although genomic and epigenomic studies have provided insight into disease pathogenesis, reliable biomarkers for diagnosis and prognosis remain limited. Proteomics offers an important advantage because it reflects the functional protein state and captures post-translational modifications, making it highly relevant for risk assessment and therapy guidance. Recent studies have identified several groups of candidate biomarkers. Kinases and signal transduction proteins such as CAMK1D, PRKCZ, KIT, MAST4, PAK6, PTK7, and NTRK1 are dysregulated in MDS and associated with poor outcomes, immune evasion, and aberrant stem cell signaling. Oncofetal proteins like IGF2BP3 and signaling regulators such as RBP4 further highlight proteomic signatures linked to chemoresistance and subtype specificity. In the transplant setting, immune regulators including CSK, FGR, CRTAM, GP1BA, UBE2N, and STAT1 may serve as predictors of graft rejection and relapse. Cytoskeletal and extracellular matrix proteins such as CEP55, Talin-1, Kindlin-3, Vinculin, THBS1, LRG1, SPARC, SAA1, Clusterin, and PRDM16 underscore the role of bone marrow microenvironmental remodeling and adhesion defects in disease progression. Finally, metabolic enzymes such as LDHA reflect altered energy metabolism and correlate with more aggressive disease biology. Collectively, these proteomic candidates illustrate the complex interplay of signaling, immune regulation, bone microenvironment, and metabolism in MDS. Their validation in clinical cohorts could enable early detection, refined risk stratification, and new therapeutic avenues, positioning proteomics as a central tool in the future management of MDS. - Source: PubMed
Novak RuđerMandac Smoljanović IngaGrgurević Lovorka - High-grade serous ovarian cancer (HGSOC) is a lethal malignancy characterized by profound intratumoral heterogeneity and immune evasion. While previous research has identified four molecular subtypes of HGSOC, defining their spatial distribution across anatomical sites could help identify functional mediators of progression and immune evasion. In this study, we performed single-cell and spatial transcriptomic sequencing on 66 anatomically paired samples across five sites from eight patients and conducted an integrated analysis on the generated datasets. Five distinct gene programs with specific spatial distributions and functional roles were identified: GP1 (differentiated-invasive), GP2 (differentiated-proliferative), GP3 (immunoreactive), GP4 (mesenchymal), and GP5 (proliferative). Interestingly, molecular subtypes exhibited dynamic spatial transitions that promote HGSOC progression. The differentiated-proliferative subtype dominated tumor cores while the differentiated-invasive subtype localized to the invasive front driven by SDC4-expressing epithelial cells (c40) that were functionally validated to promote migration/invasion. Concurrently, immune evasion operated through distinct mechanisms. Differentiated-invasive and immunoreactive subtypes co-localization established immunosuppression via the TNFα-SAA1/2-APOE signaling axis that recruits immunosuppressive myeloid cells across primary and metastatic sites, while fibroblast-derived collagen barriers were constructed at the interfaces between mesenchymal and immunoreactive subtypes in omental metastases along with dysregulated chemokines to exclude immune infiltration. This spatially resolved atlas directly links subtype spatial transitions to tumor progression and subtype co-localization to immune evasion, providing a mechanistic framework for targeting spatially organized tumor-immune interactions in HGSOC. - Source: PubMed
Publication date: 2026/05/27
Zhang YueleiYang BinHou XinMing WenxuanJin XinChen GangChen DijunZhang Wenwei - Serum amyloid A1 (SAA1) is closely associated with malignant progression and unfavorable prognosis in multiple cancers. However, the specific cellular sources and mechanisms of SAA1 within the breast cancer tumor microenvironment (TME) remain incompletely understood. This study aims to investigate the SAA1 expression in the breast cancer and to elucidate its functional roles in tumor progression. - Source: PubMed
Publication date: 2026/04/28
Lin JialiHuang XiaozhiPan LiuxianLi MingliLei LanghuanYang XingShi WeiDing YanpingJiang ZiqiongLi WeiLiang Qiuyu - Patients with advanced high-grade serous ovarian carcinoma (HGSOC) often experience extremely poor prognoses due to extensive peritoneal metastases, yet the underlying driving mechanisms remain unclear. This study reveals that serum amyloid A1 (SAA1) is markedly upregulated in late-stage HGSOC and is closely associated with poor prognosis and distant metastasis. These findings were validated through both single-cell RNA sequencing and clinical specimen analyses. Surprisingly, SAA1 does not directly promote tumour cell proliferation or migration. Instead, it reshapes the immunosuppressive tumour microenvironment by activating FPR2 tumour-associated macrophages (TAMs). Mechanistically, the SAA1-FPR2 signalling axis triggers the JAK2/STAT3 pathway in macrophages, enhancing the transcription and secretion of CXCL1. This, in turn, induces epithelial-mesenchymal transition (EMT) in tumour cells and endows them with greater metastatic potential. Animal models further confirmed that SAA1 knockdown, macrophage depletion, or CXCL1 blockade all significantly suppressed peritoneal dissemination. Collectively, this study identifies a novel SAA1-TAM-CXCL1 immune-inflammatory signalling axis, elucidates its critical role in ovarian cancer metastasis, and provides a robust theoretical foundation for the development of innovative anti-metastatic therapeutic strategies. KEY POINTS: A distinct SAA1-enriched tumour cell subset with metastasis-associated features is identified in ovarian cancer. Tumour-derived SAA1 reprograms TAM through FPR2-mediated JAK2-STAT3 signalling to induce an immunosuppressive phenotype. The SAA1-TAM-CXCL1 axis facilitates metastatic progression in ovarian cancer. - Source: PubMed
Zhou XuanMeng HuangyangChang QianjingRen JingjingWen MeichenZhang LinCheng Wenjun