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Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
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play increasing roles. Highly aggressive tumours will need particular care, including the use of TMZ and newer agents. What is clear is that we need molecular markers able to predict future behaviour, and these are still unavailable. Perhaps the next
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strong prognostic molecular marker in ER-positive breast cancer. Positive Stat5 expression predicts response to endocrine therapy and increases post-relapse survival in metastatic breast cancer patients who received first-line treatment with endocrine
Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain
Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain
Biomedical Research Networking Center in Rare Diseases (CIBERER), Institute of Health Carlos III (ISCIII), Madrid, Spain
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Department of Endocrinology, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Princesa, Madrid, Spain
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Hospital General Universitario de Alicante-Institute for Health and Biomedical Research (ISABIAL), Alicante, Spain
Department of Clinical Medicine, Miguel Hernández University, Elche, Spain
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Hospital General Universitario de Alicante-Institute for Health and Biomedical Research (ISABIAL), Alicante, Spain
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Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania, USA
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Department of Endocrinology, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Princesa, Madrid, Spain
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-0565 . Influence of SRL treatment given before or after surgery in the expression of molecular markers Molecular markers expression was compared between patients who had received SRL treatment before surgery ( n = 67) and those that had not received it ( n = 33
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). Histopathological and molecular markers of malignant chromaffin-cell tumours There is considerable controversy as to whether the histopathological appearance of chromaffin cell tumours can predict malignancy in the absence of distant metastases
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that 17p13 LOH could be used as a molecular marker of malignancy in adrenocortical tumors. In a large prospective study of patients with ACT, 17p13 LOH was demonstrated to be an independent variable predictive of recurrence after complete surgical
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Selection of novel molecular markers is an important goal of cancer genomics studies. The aim of our analysis was to apply the multivariate bioinformatical tools to rank the genes – potential markers of papillary thyroid cancer (PTC) according to their diagnostic usefulness. We also assessed the accuracy of benign/malignant classification, based on gene expression profiling, for PTC. We analyzed a 180-array dataset (90 HG-U95A and 90 HG-U133A oligonucleotide arrays), which included a collection of 57 PTCs, 61 benign thyroid tumors, and 62 apparently normal tissues. Gene selection was carried out by the support vector machines method with bootstrapping, which allowed us 1) ranking the genes that were most important for classification quality and appeared most frequently in the classifiers (bootstrap-based feature ranking, BBFR); 2) ranking the samples, and thus detecting cases that were most difficult to classify (bootstrap-based outlier detection). The accuracy of PTC diagnosis was 98.5% for a 20-gene classifier, its 95% confidence interval (CI) was 95.9–100%, with the lower limit of CI exceeding 95% already for five genes. Only 5 of 180 samples (2.8%) were misclassified in more than 10% of bootstrap iterations. We specified 43 genes which are most suitable as molecular markers of PTC, among them some well-known PTC markers (MET, fibronectin 1, dipeptidylpeptidase 4, or adenosine A1 receptor) and potential new ones (UDP-galactose-4-epimerase, cadherin 16, gap junction protein 3, sushi, nidogen, and EGF-like domains 1, inhibitor of DNA binding 3, RUNX1, leiomodin 1, F-box protein 9, and tripartite motif-containing 58). The highest ranking gene, metallophosphoesterase domain-containing protein 2, achieved 96.7% of the maximum BBFR score.
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Endometrial cancer is the most common gynecological malignancy in developed countries and represents the eighth leading cause of cancer related death in women. The growing incidence of endometrial cancer leads scientists and oncologists to identify effective preventive measures and also molecular markers for diagnosis and prognosis. Chemotherapy and hormone therapy is the mainstay treatment option for advanced and recurrent endometrial cancer and response to therapy is one of the most important factor which favors prognosis and overall survival. In recent years, there have been major advances in the treatment of patients with endometrial cancer. Despite advances made in the treatment of this cancer, the overall survival of patients has not significantly improved because considerable number of patients harbor tumor refractory to these therapies and the majority of the initially responsive tumors become refractory to treatments. Therefore, determination of sensitivity/resistance is becoming increasingly important for individualization of endometrial cancer therapy. The aim of this review is to present the existing knowledge about the molecular markers that could play a crucial role in determining resistance to chemo- and hormone therapy. Extensive literature search for the cell signaling pathways and factors responsible for chemoresistance have been performed and reviewed. Several recent studies suggest that deregulations in the apoptotic pathways (such as p53, Fas/FasL, Bcl-2 family proteins, inhibitor of apoptosis proteins), survival pathways (PI3K/AKT, MAPK), hormone receptor signaling pathways (progesterone receptor), Cyclooxygenase-2 and Her-2 are considered as key factors involved in the onset and maintenance of therapeutic resistance, suggesting that resistance is a multi-factorial phenomenon.
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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Both external and internal exposure to ionizing radiation are strong risk factors for the development of thyroid tumors. Until now, the diagnosis of radiation-induced thyroid tumors has been deduced from a network of arguments taken together with the individual history of radiation exposure. Neither the histological features nor the genetic alterations observed in these tumors have been shown to be specific fingerprints of an exposure to radiation. The aim of our work is to define ionizing radiation-related molecular specificities in a series of secondary thyroid tumors developed in the radiation field of patients treated by radiotherapy. To identify molecular markers that could represent a radiation-induction signature, we compared 25K microarray transcriptome profiles of a learning set of 28 thyroid tumors, which comprised 14 follicular thyroid adenomas (FTA) and 14 papillary thyroid carcinomas (PTC), either sporadic or consecutive to external radiotherapy in childhood. We identified a signature composed of 322 genes which discriminates radiation-induced tumors (FTA and PTC) from their sporadic counterparts. The robustness of this signature was further confirmed by blind case-by-case classification of an independent set of 29 tumors (16 FTA and 13 PTC). After the histology code break by the clinicians, 26/29 tumors were well classified regarding tumor etiology, 1 was undetermined, and 2 were misclassified. Our results help shed light on radiation-induced thyroid carcinogenesis, since specific molecular pathways are deregulated in radiation-induced tumors.
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Endocrine pancreatic tumors (EPTs) comprise a highly heterogeneous group of tumors with different clinical behavior and genetic makeup. Insulinomas represent the predominant syndromic subtype of EPTs. The metastatic potential of insulinomas can frequently not be predicted using histopathological criteria, and also molecular markers indicating malignant progression are unreliable because of the small number of cases per subtype studied so far. For the identification of reliable indicators of metastatic disease, we investigated 62 sporadic insulinomas (44 benign and 18 tumors with metastases) by means of comparative genomic hybridization (CGH). In addition, the role of MEN1 (multiple endocrine neoplasia type 1) gene mutations was determined to assess specific chromosomal alterations associated with dysfunction of this endocrine tumor-related tumor suppressor gene. Only one case with a somatic MEN1 mutation was identified (1527del7bp), indicating that the MEN1 gene plays a minor pathogenic role in sporadic insulinomas. CGH analysis revealed that the total number of aberrations per tumor differs strongly between the benign and the malignant group (4.2 vs 14.1; P<0.0001). Furthermore, chromosome 9q gain was found to be the most frequent aberration in both benign and malignant insulinomas, whereas chromosome 6q losses and 12q, 14q and 17pq gains are strongly associated with metastatic disease. Our study shows that chromosomal instability, as defined by ≥5 gains together with ≥5 losses, or total number of gains and losses ≥8, rather than parameters such as tumor size and proliferation index, is the most powerful indicator for the development of metastatic disease in patients with sporadic insulinoma.
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Noninvasive encapsulated follicular variants of papillary thyroid carcinomas have been recently reclassified as noninvasive follicular thyroid neoplasms with papillary-like nuclear features (NIFTPs). NIFTPs exhibit a behavior that is very close to that of follicular adenomas but different from the infiltrative and invasive follicular variants of papillary thyroid carcinomas (FVPTCs). The importance of miRNAs to carcinogenesis has been reported in recent years. miRNAs seem to be promising diagnostic and prognostic molecular markers for thyroid cancer, and the combination of miRNA expression and mutational status might improve cytological diagnosis. The aim of the present study was to evaluate the miRNA expression profile in wild-type, RAS - or BRAF-mutated NIFTPs, infiltrative and invasive FVPTCs, and follicular adenomas using the nCounter miRNA Expression assay (NanoString Technologies). To identify the significant Kyoto Encyclopedia of Genes and Genomes (KEGG) molecular pathways associated with deregulated miRNAs, we used the union of pathways option in DNA Intelligent Analysis (DIANA) miRPath software. We have shown that the miRNA expression profiles of wild-type and mutated NIFTPs could be different. The expression profile of wild-type NIFTPs seems comparable to that of follicular adenomas, whereas mutated NIFTPs have an expression profile similar to that of infiltrative and invasive FVPTCs. The upregulation of 4 miRNAs (miR-221-5p, miR-221-3p, miR-222-3p, miR-146b-5p) and the downregulation of 8 miRNAs (miR-181a-3p, miR-28-5p, miR-363-3p, miR-342-3p, miR-1285-5p, miR-152-3p, miR-25-3p, miR-30e-3) in mutated NIFTPs compared to wild-type ones suggest a potential invasive-like phenotype by deregulating the specific pathways involved in cell adhesion and cell migration (Hippo signaling pathway, ECM-receptor interaction, adherens junction, regulation of actin cytoskeleton, fatty acid biosynthesis and metabolism).
