KAT6A amplifications are associated with shorter progression-free survival and overall survival in patients with endometrial serous carcinoma

Abstract

Somatic copy number alterations (CNA) are common in endometrial serous carcinoma (ESC). We used the Tumor Cancer Genome Atlas Pan Cancer dataset (TCGA Pan Can) to explore the impact of somatic CNA and gene expression levels (mRNA) of cancer-related genes in ESC. Results were correlated with clinico-pathologic parameters such as age of onset, disease stage, progression-free survival (PFS) and overall survival (OS) (n = 108). 1,449 genes with recurrent somatic CNA were identified, observed in 10% or more tumor samples. Somatic CNA and mRNA expression levels were highly correlated (r> = 0.6) for 383 genes. Among these, 45 genes were classified in the Tier 1 category of Cancer Genome Census-Catalogue of Somatic Mutations in Cancer. Eighteen of 45 Tier 1 genes had highly correlated somatic CNA and mRNA expression levels including ARNT,

KAT6A Acetylation of SMAD3 Regulates Myeloid‐Derived Suppressor Cell Recruitment, Metastasis, and Immunotherapy in Triple‐Negative Breast Cancer

“…[ 16 , 17 , 18 ] Increasing data demonstrate that KAT6A also regulates tumor progression. [ 10 , 14 ] KAT6A amplification and/or overexpression in luminal subtype breast cancers promoted tumor growth. [ 15 , 20 ] However, the mechanism by which KAT6A drives breast cancer progression is still elusive.…”

“…[ 9 , 10 , 11 , 12 ] While KAT6B is considered a tumor suppressor, [ 13 ] KAT6A exhibits a predominantly oncogenic function in a number of cancers, including leukemia, glioma, endometrial serous carcinoma, and breast cancer. [ 10 , 12 , 14 , 15 ] In acute myeloid leukemia, KAT6A undergoes changes including gene mutation and fusion with proteins resulting from chromosomal rearrangement. [ 16 , 17 , 18 , 19 ] Earlier studies showed that KAT6A is amplified and/or overexpressed in Luminal A, Luminal B, HER2 + , and TNBC/basal‐like subtype breast cancers, and its overexpression correlates with worse clinical outcome in ER + /HER2 − breast cancers.…”

KAT6A Acetylation of SMAD3 Regulates Myeloid‐Derived Suppressor Cell Recruitment, Metastasis, and Immunotherapy in Triple‐Negative Breast Cancer

“…[16][17][18] Increasing data demonstrate that KAT6A also regulates tumor progression. [10,14] KAT6A amplification and/or overexpression in luminal subtype breast cancers promoted tumor growth. [15,20] However, the mechanism by which KAT6A drives breast cancer progression is still elusive.…”

“…[9][10][11][12] While KAT6B is considered a tumor suppressor, [13] KAT6A exhibits a predominantly oncogenic function in a number of cancers, including leukemia, glioma, endometrial serous carcinoma, and breast cancer. [10,12,14,15] In acute myeloid leukemia, KAT6A undergoes changes including gene mutation and fusion with proteins resulting from chromosomal rearrangement. [16][17][18][19] Earlier studies showed that KAT6A is amplified and/or overexpressed in Luminal A, Luminal B, HER2 + , and TNBC/basal-like subtype breast cancers, and its overexpression correlates with worse clinical outcome in ER + /HER2 − breast cancers.…”

Expression of Enhancer-Binding Protein CEBPA mRNA and Protein in Ovarian Cancer and Its Relationship With Pathobiological Characteristics

“…According to our results, among ovarian cancer patients, the median survival time of patients with CEBPA high expression is shorter than that of patients with CEBPA low expression, and the overexpression of CEBPA level constitutes a factor of poor prognosis of ovarian cancer patients. This may be due to the obvious carcinogenic effect of CEBPA in ovarian cancer ( 25 ). Clinicians can consider measuring the expression level of CEBPA when treating patients with ovarian cancer, which is helpful to evaluate the prognosis of patients and improve their living standards.…”