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Tumour Suppressor Mechanisms in the Control of Chromosome Stability: Insights from BRCA2
Venkitaraman, Ashok R. Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.2
Cancer is unique amongst human diseases in that its cellular manifestations arise and evolve through the acquisition of somatic alterations in the genome. In particular, instability in the number and structure of chromosomes is a near-universal feature of the genomic alterations associated with epithelial cancers, and is triggered by the inactivation of tumour suppressor mechanisms that preserve chromosome integrity in normal cells. The nature of these mechanisms, and how their inactivation promotes carcinogenesis, remains enigmatic. I will review recent work from our laboratory on the tumour suppressor BRCA2 that addresses these issues, focusing on new insights into cancer pathogenesis and therapy that are emerging from improved understanding of the molecular basis of chromosomal instability in BRCA2-deficient cancer cells.
Tumour Suppressor Mechanisms in the Control of Chromosome Stability: Insights from BRCA2
Ashok R. Venkitaraman 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.2
Cancer is unique amongst human diseases in that its cellular manifestations arise and evolve through the acquisition of somatic alterations in the genome. In particular, instability in the number and structure of chromosomes is a near-universal feature of the genomic alterations associated with epithelial cancers, and is triggered by the inactivation of tumour suppressor mechanisms that preserve chromosome integrity in normal cells. The nature of these mechanisms, and how their inactivation promotes carcinogenesis, remains enigmatic. I will review recent work from our laboratory on the tumour suppressor BRCA2 that addresses these issues, focusing on new insights into cancer pathogenesis and therapy that are emerging from improved understanding of the molecular basis of chromosomal instability in BRCA2-deficient cancer cells.
Role of 68Ga-DOTATOC PET/CT in the Evaluation of Primary Pulmonary Carcinoids
( Tarun Jindal ),( Arvind Kumar ),( Balasubramanian Venkitaraman ),( Roman Dutta ),( Rakesh Kumar ) 대한내과학회 2010 The Korean Journal of Internal Medicine Vol.25 No.4
Background/Aims: Although carcinoid tumors usually have good prognosis, early and specific diagnosis is important. Computed tomography and magnetic resonance imaging do not provide findings that are specific for carcinoids, and somatostatin receptor scintigraphy suffers from low spatial resolution. 18-Fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) has limited sensitivity for carcinoids due to low uptake of the marker. A PET/CT system that uses the somatostatin receptor-based PET tracer 1,4,7,10-tetraazacyclododecane-NI,NII,NIII,NIIII-tetraacetic acid (D)-Phe1-thy3-octreotide (68Ga-DOTATOC) has also been used in the evaluation of carcinoids, although information regarding its use for the detection of primary pulmonary carcinoids is limited. Thus, we investigated the value of 68Ga-DOTATOC PET/CT for the diagnosis of primary pulmonary carcinoid tumors. Methods: This was a retrospective analysis of patients with primary pulmonary tumors who underwent 68Ga- DOTATOC PET/CT. All the patients had a histopathologic diagnosis of carcinoid. The rate of detection of primary pulmonary carcinoid tumors using 68Ga-DOTATOC PET/CT was assessed. Results: Twenty patients were diagnosed as having carcinoid, and 19 tumors showed significant uptake on 68Ga- DOTATOC (detection rate, 95%). The maximal standardized uptake value (SUVmax) ranged from 1.1 to 66, with a median value of 21.6. In one patient, 68Ga-DOTATOC PET/CT revealed additional lesions. Conclusions: Our results demonstrate that 68Ga-DOTATOC PET/CT is useful in the evaluation of primary pulmonary carcinoids and should be included in the diagnostic work-up of these patients. (Korean J Intern Med 2010;25:386-391)