SATB2 (SATB Homeobox 2)

In CSC-enriched cells, SATB2 inhibition was associated with increased sensitivity to cisplatin and pemetrexed, concomitant with reduced OCT4 and SOX2 expression. Collectively, these findings support SATB2 as a candidate therapeutic target in MPM and suggest that SATB2 suppression may enhance chemotherapy response when combined with standard agents.

Importantly, pharmacological inhibition of USP10 by Wu-5 effectively suppresses tumor growth. These findings highlight the antagonistic roles of USP10 and DTX3L in the regulation of GBM malignancy and propose USP10 as a potential therapeutic target.

The patient underwent transhepatic arterial chemotherapy with epirubicin 30mg/m² and cisplatin 40mg/m², succeeded by 3 cycles of MAP regimen chemotherapy (methotrexate, doxorubicin, cisplatin) in conjunction with sorafenib-targeted therapy, achieving a recurrence-free survival (RFS) of 21 months. The literature analysis and our case report point to TP53 mutations and aberrant SATB2 expression as possible genetic markers that could close the diagnostic gap for this uncommon and frequently misdiagnosed illness. Preliminary findings indicate that multimodal therapies-surgery, chemotherapy, and targeted therapy-hold promise for improving patient survival despite PHO's high malignancy and poor prognosis.

We propose that the initial IHC panel should include TRPS1, CK7 and CK20. In TRPS1-negative cases, additional immunostains should be performed: CDX2 and SATB2 for colonic; p63, GATA3 and uroplakin II/III for urothelial; and PSA and NKX3.1 for prostatic secondary EMPD.

SATB2 expression can be reliably used in the differential diagnosis of primary endometrial endometrioid and serous carcinomas as well as primary endocervical adenocarcinomas because nearly all of these tumors are SATB2-negative. SATB2 positivity in endometrial carcinomas is almost always restricted to morules within endometrioid adenocarcinomas.

Loss of SATB2 staining in CRC is associated with inferior survival outcomes and adverse clinicopathologic features.

Immunophenotyping demonstrated TTF-1 nuclear positivity in the metastatic tumor alongside a classic colorectal profile: cytokeratin 7 (CK7) negativity, cytokeratin 20 (CK20) positivity, strong caudal-type homeobox transcription factor 2 (CDX2) and special AT-rich sequence-binding protein 2 (SATB2) nuclear expression, and absence of Napsin A. The patient underwent surgical resection of the primary sigmoid colon tumor and received 16 cycles of capecitabine plus bevacizumab chemotherapy. We discuss how the comprehensive immunohistochemical panel and genetic findings confirmed the colorectal origin of the lung lesions, emphasizing that combined marker profiles (TTF-1 +/CK7 -/CK20 +/CDX2 +/SATB2 +/Napsin A -) are more consistent with metastatic colorectal adenocarcinoma rather than an enteric-type adenocarcinoma of the lung, primary. The report reviews relevant literature and underscores the importance of correlating clinical history with pathology to avoid misdiagnosis.

Furthermore, the inhibitory effect of the PI3K/AKT inhibitor on PI3K and p-AKT protein expression was counterbalanced by upregulating SATB2. In conclusion, SATB2 promotes fracture healing in humeral fracture rats by stimulating the proliferation and differentiation of osteoblasts, which is related to the activation of PI3K/AKT signaling pathway.

As verified by antibody array chip analysis, Coala cells express Snail, Pdx-1, FoxA2, and E-cadherin. Our cell line represents a new, well characterized in vitro research tool for cancer research and will be available to researchers in the field via biorepository centers.

Early recognition and surgical intervention are crucial given the aggressive nature and rapid progression of ATC. Emerging biomarkers like SATB2 may enhance diagnostic sensitivity, especially in challenging morphological variants.

Understanding its precise mechanisms in these contexts can pave the way for future advancements in therapeutic strategies. This review highlights the current state of knowledge on the roles of SATB2 and discusses its structural characteristics, biological functions, and potential implications in tumor development.

Chromosomal instability is a hallmark of osteosarcoma and is characterized by heterogeneous and extensive genetic complexity. Various numerical and structural genomic rearrangements have been described in cancer cells. However, there is little consistent genetic change to understand the etiopathogenesis of this aggressive tumor.