Background: We investigated the frequency of c-MYC amplification in esophageal squamous cell carcinoma (ESCC), including both stage I to II and III to IVa disease, and evaluated the correlation of c-MYC amplification with clinicopathologic variables and outcome.
Methods: In 259 ESCCs resected at Zhongshan Hospital, Fudan University, from January 2007 to November 2010, c-MYC amplification was analyzed by using tissue microarray, with fluorescence in situ hybridization assay.
Results: c-MYC gene amplification was found in 43.2% (112 of 259) of patients with ESCC. Significant differences were found between c-MYC amplification and patient age (p = 0.009) and lymph node metastasis (p = 0.046). The median follow-up period was 33 months (range: 4 to 102 months). A survival difference was found between patients with different c-MYC status. Among 112 patients with c-MYC amplification, a significantly poorer prognosis was observed, with a median disease-free survival (DFS) and overall survival (OS) of 24.0 and 31.0 months compared with 48.0 and 48.0 months, respectively, for patients without c-MYC amplification (p = 0.011 and 0.018). On univariate and multivariate analysis, site, clinical stage, lymph node metastasis, adjuvant therapy, and c-MYC amplification were associated with DFS and OS. When patients were divided into stage I to II and stage III to IV subgroups, c-MYC amplification tended to associate with poorer survival but without statistical difference (p > 0.05).
Conclusions: c-MYC amplification was associated with age and lymph node metastasis and was an independent poor-prognostic factor for DFS and OS in the full cohort of patients with ESCC.
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http://dx.doi.org/10.1016/j.athoracsur.2018.07.077 | DOI Listing |
Clin Epigenetics
December 2024
Univ. Grenoble Alpes, Inserm, CNRS, Institute for Advanced Biosciences, Grenoble, France.
Background: MYC-driven lymphomas are a subset of B-cell lymphomas characterized by genetic alterations that dysregulate the expression of the MYC oncogene. When overexpressed, typically through chromosomal translocations, amplifications, or other mechanisms, MYC can drive uncontrolled cell growth and contribute to cancer development. MYC-driven lymphomas are described as aggressive entities which require intensive treatment approaches and can be associated with poor prognosis.
View Article and Find Full Text PDFAppl Immunohistochem Mol Morphol
January 2025
Surgery, Security Forces Hospital.
Introduction: In addition to mutations in KIT and PDGFRA, many other genetic alterations have been described in gastrointestinal stromal tumors (GISTs), including amplifications of C-MYC and EGFR, which are often associated with increased protein expression. The main of this study was to investigate the prognostic significance of C-MYC and EGFR expression in GISTs using immunohistochemistry (IHC).
Methods: We collected all GIST cases over a 16-year period.
Transl Oncol
January 2025
Research Institute of Pharmaceutical Science, Department of Pharmacy, Seoul National University, College of Pharmacy, Seoul, South Korea; R&D Center, ABION Inc., Seoul 08394, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Seoul National University, Graduate School of Convergence Science and Technology, Seoul, South Korea; Bio-MAX/N-Bio, Seoul National University, Seoul, South Korea. Electronic address:
MYC amplification is disproportionally elevated in triple-negative breast cancer (TNBC) compared to other subtypes of breast cancer. Indeed, MYC has long been considered an undruggable oncogene using conventional drug design strategies or small molecules. We hypothesized that targeting MYC using asymmetric siRNA (asiRNA) alone or in combination with chemotherapeutic agents or indirectly via BRD4 and RRM2, may curb its oncogenic behavior.
View Article and Find Full Text PDFBMC Gastroenterol
December 2024
Human Genetics Unit, Indian Statistical Institute, 203, B. T. Road, Kolkata, 700108, India.
Background And Introduction: Two and half percent of the Indian population suffer from gallbladder cancer (GBC). The primary factors that lead GBC are associated with mutation of several protooncogenes such as EGFR, ERBB2, Myc, and CCND1 along with dysregulation of several tumor suppressor genes such as SMAD4 and CDKN2A. Bacterial infection caused by S.
View Article and Find Full Text PDFJ Oral Pathol Med
November 2024
Human and Medical Genetics Laboratory, Federal University of Jataí, Jataí, Goiás, Brazil.
Background: Lip exposure to carcinogens lead to several disorders, such as actinic cheilitis (AC) and lower lip squamous cell carcinoma (LLSCC). Although several studies have described important pathways in lip carcinogenesis, the comprehension of association of target genes in this process and their association with tumor microenvironment still need to be better understood.
Methods: Tissue samples of 30 AC and 17 LLSCC cases were included for histopathological analysis, immunohistochemical expression of CD4, CD8, and PD-L1, and fluorescence in situ hybridization for AURKA, AURKB, TP53, PTEN, CCND1, and MYC.
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