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Your search keyword '"Palanisamy, Nallasivam"' showing total 3 results
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3 results on '"Palanisamy, Nallasivam"'

1. Fibroblast growth factor family aberrations as a putative driver of head and neck squamous cell carcinoma in an epidemiologically low-risk patient as defined by targeted sequencing

Author

Tillman, Brittny N, Yanik, Megan, Birkeland, Andrew C, Liu, Chia-Jen, Hovelson, Daniel H, Cani, Andi K, Palanisamy, Nallasivam, Carskadon, Shannon, Carey, Thomas E, Bradford, Carol R, Tomlins, Scott A, McHugh, Jonathan B, Spector, Matthew E, and Brenner, J Chad

Subjects
DNA Copy Number Variations, Class I Phosphatidylinositol 3-Kinases, DNA Mutational Analysis, Clinical Sciences, amplification, head and neck squamous cell carcinoma, Rare Diseases, Clinical Research, fibroblast growth factor, Genetics, Humans, 2.1 Biological and endogenous factors, mutant, Dental/Oral and Craniofacial Disease, Aetiology, Cancer, Neoplastic, Carcinoma, Human Genome, High-Throughput Nucleotide Sequencing, Middle Aged, Fibroblast Growth Factors, Neoplasm Recurrence, Good Health and Well Being, Squamous Cell, Local, Gene Expression Regulation, Otorhinolaryngology, Head and Neck Neoplasms, Dentistry, fibroblast growth factor receptor, Female
Abstract

BackgroundTargeted sequencing of patients with epidemiologically low-risk (ELR) head and neck squamous cell carcinoma (HNSCC) could help identify novel drivers or lost suppressors leading to precision medicine protocols and improved survival rates.MethodsA patient with ELR-HNSCC was selected for targeted sequencing. We then assessed next generation sequencing cohorts from the Oncomine Powertool Database, which contains pan-cancer data from The Cancer Genome Atlas (TCGA).ResultsTargeted sequencing revealed fibroblast growth factor receptor-1 (FGFR1) amplifications as a putative driver of the patient's tumor. Patients with HNSCC from TCGA data demonstrated fibroblast growth factor (FGF) family mutations, rearrangements, or amplifications in over 35% of HNSCC cases, with a statistically significant higher frequency in African American populations. FGF alterations were unique from activating phosphatidylinositol 3-kinase (PIK3CA) mutations.ConclusionTogether, these data suggest that FGF signaling may be critical for a subset of patients with HNSCC independent of other known pathways and provides rationale for leveraging patients with ELR-HNSCC to define molecular subsets of high-risk HNSCC. © 2016 Wiley Periodicals, Inc. Head Neck 38: E1646-E1652, 2016.

Published
2016

2. A subset of solitary fibrous tumors express nuclear PAX8 and PAX2: a potential diagnostic pitfall

Author

McDaniel, Andrew S., Palanisamy, Nallasivam, Smith, Steven C., Robinson, Dan R., Wu, Yi-Mi, Chinnaiyan, Arul M., McHugh, Jonathan B., Greenson, Joel K., and Kunju, Lakshmi P.

Subjects
Solitary fibrous tumors, PAX2, 6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU], PAX8, Immunohistochemistry
Abstract

Solitary fibrous tumor (SFT), a mesenchymal neoplasm with widespread anatomic distribution, can be diagnostically challenging in limited samples. We recently encountered an aspirate of a pancreatic mass, incorrectly interpreted as metastatic renal cell carcinoma based on strong PAX8 expression by immunohistochemistry (IHC). After resection, morphologic features with additional IHC (CD34 positivity) correctly identified this lesion as a SFT. PAX8 and PAX2 are commonly used as renal tumor markers; however, no series has investigated PAX8 or PAX2 expression in SFT. IHC for PAX8 and PAX2 was performed on 41 SFTs (biopsy and resections) from varying sites. Eight were histologically malignant and eight were recurrences of previous resections. PAX8 staining was observed at least focally in 26.8% (11 of 41) SFT cases; additionally, PAX2 was positive in 12.2% (5 of 41 cases) of SFTs. For PAX8 and PAX2 positive cases 45.6% and 40%, respectively, showed diffuse expression. No correlation was found between PAX8/PAX2 positivity and age, tumor size, site, malignancy, or recurrence. In conclusion, a substantial minority of SFTs express PAX8 and PAX2 via IHC. This presents a diagnostic pitfall when evaluating possible metastases from the kidney, particularly when primary tumors show sarcomatoid or spindle cell morphologies.

Published
2016

3. Alternative translocation breakpoint cluster region 5' to BCL-6 in B-cell non-Hodgkin's lymphoma

Author

Marion P, Butler, Shinsuke, Iida, Daniela, Capello, Davide, Rossi, Pulivarthi H, Rao, Palanisamy, Nallasivam, Diane C, Louie, Seeta, Chaganti, Thomas, Au, Randy D, Gascoyne, Gianluca, Gaidano, Raju S K, Chaganti, and Riccardo, Dalla-Favera

Subjects
Chromosomes, Human, Pair 14, Lymphoma, B-Cell, Base Sequence, Molecular Sequence Data, Chromosome Breakage, Proto-Oncogene Mas, Translocation, Genetic, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-6, Humans, Chromosomes, Human, Pair 3, Cloning, Molecular, Transcription Factors
Abstract

Chromosomal translocations involving band 3q27 with various different partner chromosomes represent a recurrent cytogenetic abnormality in B-cell non-Hodgkin's lymphoma. In a fraction of these translocations, the chromosomal breakpoint is located within the 5' noncoding region of the BCL-6 proto-oncogene where the BCL-6 major breakpoint region (MBR) maps. As a result of the translocation, BCL-6 expression is deregulated by promoter substitution. However, between 30 and 50% of lymphomas with cytogenetically detectable translocations affecting band 3q27 retain a germ-line configuration at the BCL-6 locus. To identify possible additional breakpoint clusters within 3q27, we cloned a t(3;14)(q27;q32) lymphoma without MBR rearrangement and found a novel breakpoint site located between 245 and 285 kb 5' to BCL-6. Breakpoints within this newly described region, which we called the alternative breakpoint region (ABR), were found to be recurrent in lymphomas carrying t(3q27) chromosomal translocations but devoid of BCL-6 MBR rearrangements. Comparative analysis of multiple lymphomas carrying rearrangements within the ABR showed that the breakpoints cluster within a 20-kb distance. Translocations involving the ABR may juxtapose BCL-6 to distantly acting, heterologous transcriptional regulatory elements which cause deregulation of the proto-oncogene. The identification of BCL-6 ABR provides new tools for the diagnosis of lymphomas carrying aberrations at 3q27 and deregulated BCL-6 genes.

Published
2002

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