LMX1A as a Prognostic Marker in Ovarian Mucinous Cystadenocarcinoma (Retracted article. See vol. 138, pg. 167, 2012)
ABSTRACT This study aimed to evaluate the relationship of LMX1A and osteopontin (OPN) expression with clinicopathologic parameters for the 4 most common ovarian surface epithelial carcinomas. Both biomarkers were investigated immunohistochemically using tissue microarrays of 249 specimens including 91 serous cystadenocarcinomas, 56 mucinous cystadenocarcinomas, 64 endometrioid adenocarcinomas, 26 clear cell carcinomas, and 12 normal ovarian tissues. All 4 carcinomas showed significant expression of LMX1A and OPN. In addition, higher immunostaining scores and percentage of cells stained for LMX1A in mucinous cystadenocarcinomas correlated with T stage, American Joint Committee on Cancer clinical stage, poorer tumor differentiation, and poorer survival rate. In serous cystadenocarcinoma, higher percentage of staining for OPN and higher intensity or immunostaining scores for LMX1A correlated with poorer tumor differentiation. Thus, the expression of LMX1A may be an independent prognostic risk factor in mucinous cystadenocarcinoma and a helpful marker in evaluating this tumor's aggressiveness.
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ABSTRACT: LIM homeobox genes are one of the most important subfamilies of homeobox genes which encode LIM-homeodomain (LIM-HD) proteins featuring two LIM domains in their amino termini and a centrally located HD that is used to interact with specific DNA elements in target genes. Numerous studies have reported their fundamental roles in the development of various organisms; however, little is known about their functions in cancer. Recently, research has shown that LIM homeobox genes also play an important role in cancer development. Among 12 human LIM homeobox genes, 10 LIM-HD proteins have been reported to be associated with cancer. In the present review, we mainly summarize the functions of these genes in various types of cancer and their potential as biomarkers and the related challenges. More in-depth research concerning LIM homeobox genes in cancer from a signaling pathway perspective may help to understand tumor profiles, establish biomarkers and guide choices for combinatorial drug therapies.Oncology Reports 03/2014; 31(5). DOI:10.3892/or.2014.3112 · 2.19 Impact Factor
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ABSTRACT: Patients with rectal cancer who achieve a complete pathological response after preoperative chemoradiation have an improved oncologic outcome. Identifying factors associated with a lack of response could help the understanding of the underlying biology of treatment resistance. This study aimed to develop a gene expression signature for chemoradiation (CRT) resistant rectal cancer using high-throughput nucleotide microarrays. Pretreatment biopsies of rectal adenocarcinomas were prospectively collected and freshly frozen according to an IRB-approved protocol. Total tumour mRNA was extracted and gene expression levels were measured using microarrays. Patients underwent proctectomy after completing standard long-course CRT and the resected specimens was graded for treatment response. Gene expression profiles for non-responders were compared with those of responders. Differentially expressed genes were analyzed for functional significance using the Ingenuity Pathway Analysis (IPA) software. Thirty three patients treated between 2006-2009 were included. An 812-gene and a 183-gene signature were derived separating non-responders from responders. The classifiers were able to identify non-responders with a sensitivity and specificity of 100% using the 812 gene signature and sensitivity and specificity of 100% and 33% using the 183 gene signature. IPA canonical pathway analysis revealed a significant ratio of differentially expressed genes in the "DNA double strand break repair by homologous recombination" pathway. Rectal cancer gene profiles are associated with poor response to CRT. Alterations in the DNA double strand break repair pathway could contribute to treatment resistance and provides an opportunity for further studies. This article is protected by copyright. All rights reserved.Colorectal Disease 08/2013; 16(1). DOI:10.1111/codi.12395 · 2.02 Impact Factor