AREG antibody - middle region (ARP30233_P050)
- Known as:
- AREG (anti-) - middle region (ARP30233_P050)
- Catalog number:
- arp30233_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- AREG antibody - middle region (ARP30233_P050)
Related genes to: AREG antibody - middle region (ARP30233_P050)
- Gene:
- AREG NIH gene
- Name:
- amphiregulin
- Previous symbol:
- SDGF, AREGB
- Synonyms:
- -
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2015-08-24
Related products to: AREG antibody - middle region (ARP30233_P050)
Related articles to: AREG antibody - middle region (ARP30233_P050)
- Colorectal cancer (CRC) remains a leading cause of cancer morbidity and mortality worldwide, with nearly one quarter of patients presenting with metastatic disease at diagnosis. The epidermal growth factor receptor (EGFR) plays a central role in CRC pathogenesis through activation of downstream //MAPK and PI3K/AKT/mTOR signaling pathways, and has become a major therapeutic target. Anti-EGFR monoclonal antibodies, cetuximab and panitumumab, have demonstrated survival benefit in selected patients, particularly those with left-sided, wild-type tumors. However, primary and acquired resistance limit their efficacy, underscoring the need for predictive biomarkers and novel strategies. This review synthesizes current knowledge of EGFR biology, therapeutic integration, and biomarker development, including and mutations, MSI status, amplification, EGFR ligands (AREG/EREG), consensus molecular subtypes, and liquid biopsy applications. We also discuss mechanisms of resistance such as pathway reactivation, receptor mutations, and epithelial-to-mesenchymal transition, alongside emerging approaches, including combination regimens, ctDNA-guided rechallenge, and genotype-specific inhibitors. Collectively, these insights highlight the evolving landscape of precision oncology in CRC and the importance of molecular stratification to optimize EGFR-targeted therapy and overcome resistance. - Source: PubMed
Publication date: 2026/04/03
Abbas NouraMourad MohamadSmaily HibaAl Mahmasani LayalShamseddine Ali - Dual-specificity phosphatase 5 (DUSP5) is a key regulator of the mitogen-activated protein kinase (MAPK) pathway, with established roles in various types of cancer. However, its function in esophageal squamous cell carcinoma (ESCC) remains unclear. This study combines single-cell transcriptomics with in vitro and in vivo models to investigate the role of DUSP5 in ESCC. Single-cell RNA sequencing revealed tumor-infiltrating myeloid populations, including apolipoprotein C-positive (APOC⁺) macrophages, which interact with tumor cells via the amphiregulin-epidermal growth factor receptor (AREG-EGFR) axis, activating MAPK/extracellular signal-regulated kinase (ERK) signaling to promote tumor growth and immune modulation. We identified a prognostic gene signature linked to these macrophages. DUSP5 expression was downregulated in ESCC tissues, and its overexpression inhibited cell proliferation, induced senescence and apoptosis, and suppressed migration and invasion. In mouse xenografts, overexpression of DUSP5 reduced tumor growth and metastasis. Mechanistically, DUSP5 inhibited ERK1/2 activation, and its tumor-suppressive effects were reversed by ERK1/2 activation. Moreover, ETS Like-1 protein (ELK1), an ERK1/2 downstream transcription factor, was identified as a negative regulator of DUSP5. In a carcinogen-induced model, DUSP5 knockout increased tumor burden, effects reversed by ERK1/2 inhibition. Our findings indicate that the DUSP5-ERK1/2-ELK1 signaling axis, modulated by tumor-infiltrating myeloid cells, contributes to ESCC progression and represents a promising source of biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/10
Huang XuXu WenyiYou RunzeKuang JunjieZhu KaiLi JunLi JingzhangErtas Yavuz NuriMa QiuhongTian MaojinLin Miao - Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by type 2 (T2) inflammation with elevated IL-5 and IL-13. Although group 2 innate lymphoid cells (ILC2s) drive T2 inflammation, their subset diversity and clinical relevance in nasal polyps (NPs) remain unclear. - Source: PubMed
Publication date: 2026/04/07
Kidoguchi MasanoriIwasaki NaruhitoPoposki Julie AOgasawara NorikoOka AikoKlingler Aiko ISuh LydiaAgrwal AditiBai JunqinStevens Whitney WPeters Anju TGrammer Leslie CWelch Kevin CSmith Stephanie SJohnson MicahRadwan AmrConley David BSchleimer Robert PKern Robert CTan Bruce KOkano MitsuhiroFujieda ShigeharuKato Atsushi - This study evaluated the carcinogenic potential of inhaled micro-polystyrene (mPS) and nano-polystyrene (nPS) using a murine exposure model. Repeated inhalation of environmentally relevant doses for up to 12 weeks resulted in marked pulmonary toxicity, most prominently in the mPS group. mPS exposure led to greater reductions in lung volume, impaired exercise capacity, and stronger induction of EGFR expression. Transcriptomic profiling further identified AREG and MAP3K13 as key mediators, indicating activation of EGFR-dependent MAPK signalling. Overall, these findings demonstrate that polystyrene (PS) particles exert size-dependent toxic effects, with mPS showing greater pathogenicity than nPS, and provide evidence linking airborne MP exposure to molecular pathways relevant to lung carcinogenesis. - Source: PubMed
Publication date: 2026/03/27
Shanmugiah JoycieKim SeungyounJeong HyejuKong JoonseogLee Seung-SookKang Do KyunKim Jin Su - When cultured with Wnt, R-spondin, EGF, Noggin, myofibroblast conditioned medium and Matrigel, crypts from normal mouse colon mucosa form crypt-producing organoids and can be passaged every seven days. Under the same culture and passage conditions, crypts isolated from colon adenomas derived from Apc mice typically grow as spheroidal cysts and do not produce crypts. The adenoma organoids require EGF, but not Wnt, R-spondin or Noggin for continuous passaging. However, when mouse colon adenoma spheroids are grown for more than 10 days in the presence of EGF, crypt formation occurs. EGF, EREG, β-cellulin, Neuregulin-1 or AREG are sufficient for initiating crypt formation, however, neuregulin-1 is more potent than the other EGF-family members. EGFR and ErbB2 inhibitors both prevent crypt formation in these adenoma cultures. Either EGFR:ErbB2 or ErbB3:ErbB2 signaling is sufficient to initiate adenoma crypt budding and elongation. ErbB2 inhibitors may provide a therapeutic avenue for ablating colon adenomas. - Source: PubMed
Publication date: 2026/03/31
Tan Chin WeeZhu RuiyanKane Serena RAu MichelleZhang XiaoyuHirokawa YumikoFaux Maree CBurgess Antony W