The molecular gas around the luminous blue variable star G24.73+0.69

Aims. We study the molecular environment of the luminous blue variable star G24.73+0.69 to investigate the origin of the two infrared shells around this massive star and determine its effects on the surrounding interstellar medium. Methods. We analyze the distribution of the molecular gas using the 13CO J = 1–0 emission extracted from the Galactic Ring Survey. We use near- and mid-infrared data from 2MASS and GLIMPSE to identify the young stellar objects in the field. Results. We discover the molecular counterpart to the outer infrared shell around G24.73+0.69. The CO shell was probably blown by the stellar wind of the star mainly during its main sequence phase. We also find molecular gas that corresponds to the inner infrared shell, although its origin remains uncertain. We identify seven young stellar objects within the molecular material, whose birth might have been triggered by the stellar wind of the luminous blue variable star. We suggest that both G24.73+0.69 and the progenitor of the nearby supernova remnant G24.7+0.6 were formed from the same natal cloud and represent the most evolved members of a so far undetected cluster of massive stars

Next-generation sequencing: advances and applications in cancer diagnosis

Simona Serratì, Simona De Summa, Brunella Pilato, Daniela Petriella, Rosanna Lacalamita, Stefania Tommasi, Rosamaria Pinto Molecular Genetics Laboratory, IRCCS Istituto Tumori Giovanni Paolo II, Bari, Italy Abstract: Technological advances have led to the introduction of next-generation sequencing (NGS) platforms in cancer investigation. NGS allows massive parallel sequencing that affords maximal tumor genomic assessment. NGS approaches are different, and concern DNA and RNA analysis. DNA sequencing includes whole-genome, whole-exome, and targeted sequencing, which focuses on a selection of genes of interest for a specific disease. RNA sequencing facilitates the detection of alternative gene-spliced transcripts, posttranscriptional modifications, gene fusion, mutations/single-nucleotide polymorphisms, small and long noncoding RNAs, and changes in gene expression. Most applications are in the cancer research field, but lately NGS technology has been revolutionizing cancer molecular diagnostics, due to the many advantages it offers compared to traditional methods. There is greater knowledge on solid cancer diagnostics, and recent interest has been shown also in the field of hematologic cancer. In this review, we report the latest data on NGS diagnostic/predictive clinical applications in solid and hematologic cancers. Moreover, since the amount of NGS data produced is very large and their interpretation is very complex, we briefly discuss two bioinformatic aspects, variant-calling accuracy and copy-number variation detection, which are gaining a lot of importance in cancer-diagnostic assessment. Keywords: hereditary breast cancer, melanoma, prostate cancer, thyroid cancer, lung cancer, colorectal cancer, hematologic cance

Oncosuppressor methylation: A possible key role in colon metastatic progression

K-RAS and BRAF gene mutations are mandatory to set anti-EGFR therapy in metastatic colorectal cancer (mCRC) patients. Due to the relationship of these mutations with tumor epigenotype, we hypothesized the potential role of oncosuppressor methylation of genes involved in K-RAS/BRAF pathway (CDKN2A, RASSF1A, and RARbeta suppressor genes) in inhibiting EGFR signaling cascade. Primary tumor and synchronous liver metastatic tissues of 75 mCRC patients were characterized for promoter methylation by QMSP and for K-RAS and BRAF mutations. RARbeta, RASSF1A, and CDKN2A genes were methylated in 82%, 35%, and 26% of primary tumors, respectively. RASSF1A resulted significantly more frequently methylated in liver metastasis than in primary site (P = 0.015), while RARbeta was significantly lower methylated in distant metastasis (P = 1.2 x 10(-6)). As regards methylation content, RASSF1A methylation status was significantly higher in liver metastasis with respect to primary tumor (P = 0.000) underlying the role of this gene in liver metastatic progression. In our series K-RAS and BRAF were mutated in 39% and 4% of cases, respectively. Methylation frequencies seemed to be unrelated to gene mutations; on the other hand, RASSF1A mean content methylation resulted significantly higher in liver than in primary tumor (288.78 vs. 56.23, respectively, P = 0.05) only in K-RAS wild-type cases sustaining a specific role of this gene in metastatic site thus supporting its function in strengthening the apoptotic role of K-RAS. These evidences held the role of oncosuppressor methylation in both colon tumorigenesis and progression and suggested that epigenetic events should be taken into account when biological therapies in mCRC patients have to be set. J. Cell. Physiol. 226: 1934-1939, 2011. (C) 2010 Wiley-Liss, Inc