KRT7 expression

ATL-I acts by inhibiting the expression of KRT7, which can greatly inhibit the formation of CRC transplantation tumors in nude mice. ATL-I can impede the malignant biological process and glycolysis of CRC cells by inhibiting KRT7 expression in vitro and in vivo.

KRT17 was not associated with tumor site, grade, or stage. In summary, K17 is a sensitive and specific marker of neoplastic upper tract urothelium, and its potential use in routine diagnostics should be explored in larger studies.

This morphologic variant has a striking similarity with biphasic renal neoplasms, especially with mixed epithelial and stromal tumors and angiomyolipoma with epithelial cysts. This report describes a novel renal solitary fibrous tumor subtype within this differential and underscores clinical and pathological distinctions of biphasic renal neoplasms.

The silenced KRT17 remarkably downregulated the expression of cyclinD1, Cyclin Dependent Kinase 1 (CDK1), CDK2, Phospho-Focal Adhesion Kinase (p-FAK), p-Src, and p-ERK proteins in the PC cells. Generally, an essential signaling cascade of miRNA-485-5p/KRT17/FAK/Src/ERK influences the biological functions of PC cells.

Notably, low KRT17TB can specifically identify those patients with a poor prognosis among colorectal cancer patients with low TB and high T-lymphocyte infiltration. KRT17 can be employed as a new indicator for distinguishing different immunological TBs.

KRT7 as a biomarker potentiated the prediction of bladder cancer prognosis and the immune microenvironment.

Potential pitfalls seen in a subset of cases included misleading radiologic and cystoscopic findings, replacement of the overlying urothelial mucosa by tumor mimicking precursor lesions, focal GATA3 and/or p63 positivity, and areas of squamous differentiation in tumors of endometrioid histology. A combination of clinical history, certain morphologic features, and proper selection of immunohistochemical stains is key for the correct diagnosis of secondary gynecologic adenocarcinomas involving the urinary bladder.

In a cohort of patients with colorectal cancer receiving pembrolizumab, high KRT17 expression was found within the tumors of responders. Collectively, we elucidated a critical role of KRT17 in CRC to prevent immune escape. These findings present new insights into potential therapeutic strategies and effective markers of immunotherapy reactivity against pMMR tumors.

KRT7 is correlated with immune infiltration and paclitaxel resistance in OC patients. Therefore, clinicians could use KRT7 as a prognostic marker and a target in the development of new drugs.

Additionally, KRT7-AS sensitized cancer cells to the anti-cancer drug cisplatin, consequently enhancing cancer cell apoptosis...Collectively, KRT7-AS functions as a new tumor suppressor and an apoptosis enhancer in lung and breast cancers, and we unraveled that the RXRα-KRT7-AS-PTEN signaling axis controls carcinogenesis and apoptosis. Our findings highlight a tumor suppressive role of endogenous KRT7-AS in cancers and an important effect the RXRα-KRT7-AS-PTEN axis on control of cancer cell tumorigenesis and apoptosis, and offer a new platform for developing novel therapeutics against cancers.

This case demonstrates a rare presentation of a well-differentiated neuroendocrine tumor (NET) of an unclear primary site with extensive metastasis to the bone that initially presented with hypercalcemia of unclear cause.CaseWe report a case of a 76-year-old-female with a history of depression and hypertension who was initially admitted for evaluation of hypercalcemia with a corrected calcium of 11.9, low normal PTH of 14.2, and PTHrP of 18, treated with zoledronic acid who presented again 3 months later with a 30lb weight loss for 2 months and bright red blood per rectum for one day...Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*

Furthermore, the rescue assay verified that TP63 could facilitate KRT17 expression to activate the AKT signaling pathway, which in turn stimulated TC cell invasion and migration, and induced EMT. All these results verified that TP63 facilitates TC malignant progression by promoting KRT17 expression and inducing EMT.