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Saturday, April 7, 2018

Patents by Inventor Nallasivam Palanisamy

Patents by Inventor Nallasivam Palanisamy
Nallasivam Palanisamy has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
  • Patent number: 9657350
    Abstract: Provided herein are kits, compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present invention relates to recurrent RNA fusions as diagnostic markers and clinical targets for leukemia.
    Type: Grant
    Filed: May 6, 2014
    Date of Patent: May 23, 2017
    Assignee: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Kojo Elenitoba-Johnson, Thirunavukkarasu Velusamy, Nallasivam Palanisamy, Anagh Sahasrabuddhe, Megan Lim, Arul Chinnaiyan
  • Publication number: 20170081731
    Abstract: The present disclosure relates to compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present disclosure relates to RAF gene fusions as diagnostic markers and clinical targets for cancer.
    Type: Application
    Filed: December 6, 2016
    Publication date: March 23, 2017
    Inventors: Arul Chinnaiyan, Nallasivam Palanisamy, Shanker Kalyana-Sundaram
  • Patent number: 9567644
    Abstract: The present disclosure relates to compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present disclosure relates to RAF gene fusions as diagnostic markers and clinical targets for cancer.
    Type: Grant
    Filed: January 5, 2015
    Date of Patent: February 14, 2017
    Assignee: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Arul Chinnaiyan, Nallasivam Palanisamy, Shanker Kalyana-Sundaram
  • Publication number: 20150191795
    Abstract: The present disclosure relates to compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present disclosure relates to RAF gene fusions as diagnostic markers and clinical targets for cancer.
    Type: Application
    Filed: January 5, 2015
    Publication date: July 9, 2015
    Inventors: Arul Chinnaiyan, Nallasivam Palanisamy, Shanker Kalyana-Sundaram
  • Patent number: 8945556
    Abstract: The present disclosure relates to compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present disclosure relates to RAF gene fusions as diagnostic markers and clinical targets for cancer.
    Type: Grant
    Filed: November 18, 2011
    Date of Patent: February 3, 2015
    Assignee: The Regents of The University of Michigan
    Inventors: Arul Chinnaiyan, Nallasivam Palanisamy, Shanker Kalyana-Sundaram
  • Publication number: 20140364481
    Abstract: Provided herein are kits, compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present invention relates to recurrent RNA fusions as diagnostic markers and clinical targets for leukemia.
    Type: Application
    Filed: May 6, 2014
    Publication date: December 11, 2014
    Applicant: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Kojo Elenitoba-Johnson, Thirunavukkarasu Velusamy, Nallasivam Palanisamy, Anagh Sahasrabuddhe, Megan Lim, Arul Chinnaiyan
  • Publication number: 20120142549
    Abstract: The present disclosure relates to compositions and methods for cancer diagnosis, research and therapy, including but not limited to, cancer markers. In particular, the present disclosure relates to RAF gene fusions as diagnostic markers and clinical targets for cancer.
    Type: Application
    Filed: November 18, 2011
    Publication date: June 7, 2012
    Applicant: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Arul Chinnaiyan, Nallasivam Palanisamy, Shanker Kalyana-Sundaram
  • Patent number: 7964345
    Abstract: Probes and methods of using the probes to detect chromosomal rearrangements and/or deletions are provided. The methods utilize probes that are free of repeat sequences to provide greater selectivity and sensitivity; methods for producing such probes are also disclosed. The probe sets utilized in the detection methods are designed to hybridize to chromosomes at regions outside known breakpoints, instead of spanning the breakpoint as with conventional FISH methods, and, in some instances, are further designed to bind to regions located outside the genes involved in the rearrangement. Methods utilizing probe sets with two and four colors are also described, as are automated methods for analyzing rearrangements.
    Type: Grant
    Filed: April 5, 2005
    Date of Patent: June 21, 2011
    Assignee: Cancer Genetics, Inc.
    Inventors: Nallasivam Palanisamy, Raju S. Chaganti
  • Publication number: 20100285475
    Abstract: There is provided at least one isolated fused gene comprising at least one first gene and/or fragment thereof fused to at least one second gene and/or fragment thereof, wherein at least the first and/or the second gene, independently, is selected from the group consisting of: RCC2, CENPF, ARFGEF2, SULF2, MTAP, ATXN7, BCAS3, RPS6KB1, TMEM49, EAP30, a gene having the nucleotide sequence SEQ ID NO:1, and a gene having the nucleic acid SEQ ID NO:2, or a fragment thereof. There is also provided a diagnostic method and/or a kit for detecting the susceptibility, prognosis, and/or to tumour in a subject.
    Type: Application
    Filed: October 22, 2007
    Publication date: November 11, 2010
    Applicant: AGENCY FOR SCIENCE, TECHNOLOGY AND RESEARCH
    Inventors: Nallasivam Palanisamy, Kalpana Ramnarayanan, Edison T. Liu
  • Patent number: 7585964
    Abstract: Probes and methods of using the probes to detect chromosomal rearrangements and/or deletions are provided. The methods utilize probes that are free of repeat sequences to provide greater selectivity and sensitivity; methods for producing such probes are also disclosed. The probe sets utilized in the detection methods are designed to hybridize to chromosomes at regions outside known breakpoints, instead of spanning the breakpoint as with conventional FISH methods, and, in some instances, are further designed to bind to regions located outside the genes involved in the rearrangement. Methods utilizing probe sets with two and four colors are also described, as are automated methods for analyzing rearrangements.
    Type: Grant
    Filed: May 14, 2002
    Date of Patent: September 8, 2009
    Assignee: Cancer Genetics, Inc.
    Inventors: Nallasivam Palanisamy, Raju S. Chaganti
  • Publication number: 20070166749
    Abstract: Probes and methods of using the probes to detect chromosomal rearrangements and/or deletions are provided. The methods utilize probes that are free of repeat sequences to provide greater selectivity and sensitivity; methods for producing such probes are also disclosed. The probe sets utilized in the detection methods are designed to hybridize to chromosomes at regions outside known breakpoints, instead of spanning the breakpoint as with conventional FISH methods, and, in some instances, are further designed to bind to regions located outside the genes involved in the rearrangement. Methods utilizing probe sets with two and four colors are also described, as are automated methods for analyzing rearrangements.
    Type: Application
    Filed: March 12, 2007
    Publication date: July 19, 2007
    Applicant: Cancer Genetics, Inc.
    Inventors: Nallasivam Palanisamy, Raju Chaganti
  • Publication number: 20050214842
    Abstract: Probes and methods of using the probes to detect chromosomal rearrangements and/or deletions are provided. The methods utilize probes that are free of repeat sequences to provide greater selectivity and sensitivity; methods for producing such probes are also disclosed. The probe sets utilized in the detection methods are designed to hybridize to chromosomes at regions outside known breakpoints, instead of spanning the breakpoint as with conventional FISH methods, and, in some instances, are further designed to bind to regions located outside the genes involved in the rearrangement. Methods utilizing probe sets with two and four colors are also described, as are automated methods for analyzing rearrangements.
    Type: Application
    Filed: April 5, 2005
    Publication date: September 29, 2005
    Applicant: Cancer Genetics, Inc.
    Inventors: Nallasivam Palanisamy, Raju Chaganti
  • Publication number: 20020192692
    Abstract: Probes and methods of using the probes to detect chromosomal rearrangements and/or deletions are provided. The methods utilize probes that are free of repeat sequences to provide greater selectivity and sensitivity; methods for producing such probes are also disclosed. The probe sets utilized in the detection methods are designed to hybridize to chromosomes at regions outside known breakpoints, instead of spanning the breakpoint as with conventional FISH methods, and, in some instances, are further designed to bind to regions located outside the genes involved in the rearrangement. Methods utilizing probe sets with two and four colors are also described, as are automated methods for analyzing rearrangements.
    Type: Application
    Filed: May 14, 2002
    Publication date: December 19, 2002
    Applicant: Cancer Genetics, Inc.
    Inventors: Nallasivam Palanisamy, Raju S. Chaganti

Publication in American Journal of Surgical Pathology

 2017 Dec;41(12):1642-1656. doi: 10.1097/PAS.0000000000000940.

Solitary Fibrous Tumors of the Head and Neck: A Multi-Institutional Clinicopathologic Study.

Author information

1
*Departments of Pathology and Surgery, VCU School of Medicine, Richmond, VA †Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA §Biostatistics Facility, University of Pittsburgh Cancer Institute **Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA ∥Department of Pathology, SUNY Upstate Medical University, Syracuse, NY Departments of ‡Pathology ¶Dermatology ††Oral and Maxillofacial Surgery, University of Michigan Health System, Ann Arbor #Department of Urology, Henry Ford Health System, Detroit, MI.

Abstract

Solitary fibrous tumors (SFTs) of the head and neck are uncommon. Lesions previously diagnosed in the head and neck as hemangiopericytomas (HPCs), giant cell angiofibromas (GCAs), and orbital fibrous histiocytomas (OFHs) are now recognized as within the expanded spectrum of SFTs. To better understand the clinicopathologic profile of head and neck SFTs, we performed a multi-institutional study of 88 examples. There was no sex predilection (F:M ratio 1.2), and the median patient age was 52 years (range: 15 to above 89 y). The sinonasal tract and orbit were the most common sites involved (30% and 25%), followed by the oral cavity and salivary glands (15% and 14%). Original diagnoses included HPC (25%), SFT (67%), and OFH (6%), with 1 SFT and 1 OFH noted as showing GCA-like morphology. On review, the predominant histologic pattern was classic SFT-like in 53% and cellular (former HPC-like) in 47%; lipomatous differentiation (8%) and GCA-like pattern (7%) were less prevalent. Subsets demonstrated nuclear atypia (23%), epithelioid morphology (15%), or coagulative necrosis (6%). Infiltrative growth (49%) and osseous invasion (82%) were prevalent among evaluable cases. Of the 48 SFTs with follow-up (median: 43 mo), 19 showed recurrence (40%). Of these, 4 patients were alive with disease and 4 dead of disease. Size and mitotic rate were negative prognosticators using a joint prognostic proportional hazards regression model. Three patients experienced metastasis, to lungs, parotid, bone, and skull base, including one case showing overtly sarcomatous "dedifferentiation." As a group, SFTs present in a wide anatomic and morphologic spectrum in the head and neck. Only rare examples metastasize or cause death from disease. However, the fairly high local recurrence rate underscores their aggressive potential and highlights the importance of prospective recognition.
PMID:
 
28877055
 
PMCID:
 
PMC5680135
 [Available on 2018-12-01]
 
DOI:
 
10.1097/PAS.0000000000000940

Friday, April 6, 2018

Publication in Oncology Reports

 2018 Mar 30. doi: 10.3892/or.2018.6342. [Epub ahead of print]

Enrichment and mutation detection of circulating tumor cells from blood samples.

Abstract

The potential of circulating tumor cells (CTCs) in the diagnosis and prognosis of cancer patients has become increasingly attractive. However, molecular analysis of CTCs is hindered by low sensitivity and a high level of background leukocytes in CTC enrichment technologies. We have developed a novel protocol using a microfluidic device, which enriches and retrieves CTCs from blood samples. The principle of CTC capturing is that tumor cells are larger and less deformable than normal blood cells. To evaluate the potential of utilizing Celsee PREP100 in CTC molecular analysis, we prepared prostate cancer cell lines PC3 and LNCaP, retrieved the captured cells and analyzed them using PCR amplicon sequencing. We were able to recover an average of 79% of 110‑1,100 PC3 and 60‑1,500 LNCaP cells, and detect the p.K139fs*3 deletion of the p53 gene in PC3 cells and p.T877A mutation of the androgen receptor gene in LNCaP cells. Next, we spiked these two types of cells into normal donor blood samples, captured the cells and analyzed them using PCR amplicon sequencing. The PC3 and LNCaP cells were captured and retrieved with the ratio of captured CTCs to the background leukocytes reaching 1:1.5 for PC3 and 1:2.9 for LNCaP cells. We further revealed that the p.K139fs*3 deletion and p.T877A mutation can be detected in the captured PC3 and LNCaP cells, respectively. We successfully validated this approach using clinical blood samples from patients with metastatic prostate cancer. Our results demonstrated a novel approach for CTC enrichment and illustrated the potential of CTC molecular characterization for diagnosis, prognosis and treatment selection of patients with metastatic malignancy.
PMID:
 
29620284
 
DOI:
 
10.3892/or.2018.6342

Thursday, April 5, 2018

Publication in Histopathology

Histopathology. 2018 Apr 4. doi: 10.1111/his.13526. [Epub ahead of print]

Pseudosarcomatous Myofibroblastic Proliferations of the Genitourinary Tract are Genetically Different from Nodular Fasciitis and Lack USP6, ROS1, and ETV6 Gene Rearrangements.

Jebastin JA, Smith SC, Perry KD, Gupta NS, Alanee S, Carskadon S, Chitale DA, Palanisamy N, Williamson SR.

AIMS:
Pseudosarcomatous myofibroblastic proliferations of the genitourinary tract have a debatable relationship to inflammatory myofibroblastic tumour (generally lacking ALK rearrangement); however, they share several overlapping features with nodular fasciitis of soft tissue. Since rearrangement of the USP6 gene has been recently recognized as a recurrent alteration in soft tissue nodular fasciitis, and several other alternative gene fusions have been recently recognized in inflammatory myofibroblastic tumour, we studied whether USP6, ROS1, or ETV6 gene rearrangements were present in these lesions (12 cases).

METHODS AND RESULTS:
Fluorescence in-situ hybridization (FISH) analysis was performed using bacterial artificial chromosome (BAC) derived break-apart probes against USP6, ROS1, and ETV6. Two cases with adequate genetic material from recent paraffin tissue blocks were also tested by using a solid tumour gene fusion detection assay via next-generation sequencing, targeting over 50 known genes involved in recurrent fusions. None of the genitourinary pseudosarcomatous myofibroblastic proliferations was detected to harbour USP6 (0/12), ROS1 (0/8), or ETV6 (0/7) rearrangement and no gene fusions were detected in 2 cases studied by sequencing.

CONCLUSIONS:
Despite overlap in histologic and immunohistochemical features between pseudosarcomatous myofibroblastic proliferation and nodular fasciitis, these tumours lack the recently recognized USP6 gene rearrangements that occur in nodular fasciitis, as well as alternative fusions found in ALK-negative inflammatory myofibroblastic tumours. At present, this diagnosis remains based primarily on clinical, histologic, and immunohistochemical features. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

KEYWORDS:
USP6; inflammatory myofibroblastic tumour; pseudosarcomatous myofibroblastic proliferation; soft tissue tumours; urinary bladder

PMID: 29617048 DOI: 10.1111/his.13526

Sunday, September 17, 2017

கோரக்பூரில் ஒரு கோர நிகழ்வு

பிராண வாயு இல்லாமல்
பிராணனை விட்ட
பிஞ்சுக் குழந்தைகள் !

இது விபத்தல்ல !
விபரீதம் !

Wednesday, August 2, 2017

"குயில் கூவுவதைக்கேட்கும் போதெல்லாம் காக்கைக்கு நன்றி சொல்ல மறக்காதே"



குயிலுக்கு கூடு கட்டத்தெரியாது 
காக்கை கூட்டுக்குள் குயில்  முட்டையிடும் 
குஞ்சுபொரித்து வளர்ந்த பிறகு கூவும் போதுதான் 
காக்கை விழித்துக்கொண்டு கொத்த  ஆரம்பிக்கும் 
இயற்கையின் அற்புதத்தால் குயிலுக்கு பறக்கும் சக்தி வந்து பறந்து விடும்.

இதன் நீதி

அடுத்தவரை அண்டிப்பிழைப்பவர்கள் காக்கை கூட்டுக்குள் குயில்போல் கூவித்திரியாமல் அடக்கமாக இருப்பதுவரை அண்டிப்பிழைக்கலாம் 
தின்றுவிட்டு திமிர்  பேசும்போது காக்கை போல் கொத்தித்துரத்தப்படும் நிலை ஏற்படும்.


குயிலுக்காவது பறக்கும் சக்தி உண்டு,

கோழைகளுக்கு ???குறுக்கு வழியில் போவதைத்தவிர வேறு  வழி ???

Tuesday, August 1, 2017

Webinar on Novel technology to isolate circulating tumor cells in cancer

Novel Microfluidic Platforms Enrich Rare Cancer Cells to Study Heterogeneity and Identify Genetic Variants


August 2, 2017 | 11 am to 12 pm EDT

Cancer is comprised of heterogeneous cell populations, and research is increasingly becoming dependent on the ability to isolate rare cells, both enriched populations as well as individual, single cells. Employing advanced molecular cytogenetic technologies to analyze isolated rare cells, such as circulating tumor cells, provides a unique opportunity to interrogate the cancer transcriptome to identify novel genetic variations. These variations could lead to the development of novel cancer biomarkers.
Learning Objectives:
  • Introduction to advanced microfluidic technologies to isolate and characterize rare cells
  • Applications of NGS approaches to characterize isolated cells
  • Importance of characterization and summary of select results
Speakers:
Yixing Wang, Ph.D.
Nallasivam Palanisamy, Ph.D.
Kalyan Handique, Ph.D.

Tuesday, July 25, 2017

Publication in Human Pathology

Increased Expression of EZH2 in Merkel Cell Carcinoma Is Associated with Disease Progression and Poorer Prognosis

DOI: http://dx.doi.org/10.1016/j.humpath.2017.07.009


Highlights

  • EZH2 is a histone methyltransferase that affects tumorigenesis by epigenetic gene silencing.
  • We found strong/moderate EZH2 immunohistochemical expression in 54% of Merkel cell carcinomas.
  • EZH2 is expressed at higher levels in nodal metastases compared to primary tumors.
  • Weaker EZH2 expression in primary tumors correlated with improved prognosis.
  • These findings suggest EZH2 may play a role in MCC progression.

Summary

Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase that affects tumorigenesis by epigenetic gene silencing. Merkel cell carcinoma (MCC) is a rare cutaneous neuroendocrine carcinoma that has a high risk of disease progression with nodal and distant metastases. Here, we evaluated EZH2 expression by immunohistochemistry in a cohort of 85 MCC tumors (29 primary tumors, 41 lymph node metastases, 13 in-transit metastases, and 2 distant metastases) with clinical follow-up. We show strong/moderate EZH2 expression in 54% of tumors. Importantly, weak expression of EZH2 in the primary tumor, but not nodal metastases, correlated with improved prognosis compared to moderate/strong EZH2 expression (5-year MCC-specific survival of 68% versus 22%, respectively, P = .024). In addition, EZH2 was expressed at higher levels in nodal metastases compared to primary tumors (P = .005). Our data demonstrate that EZH2 has prognostic value and may play an oncogenic role in MCC.
http://www.humanpathol.com/article/S0046-8177(17)30259-9/fulltext


Monday, July 24, 2017

Publication in Clinical Cancer Research

Clin Cancer Res. 2017 Jun 12. pii: clincanres.0299.2017. doi: 10.1158/1078-0432.CCR-17-0299. [Epub ahead of print]
Age and gender associations of virus positivity in Merkel cell carcinoma characterized using a novel RNA in situ hybridization assay.

Wang L, Harms PW, Palanisamy N, Carskadon S, Cao X, Siddiqui J, Patel RM, Zelenka-Wang S, Durham AB, Fullen DR, Harms K, Su F, Shukla S, Mehra R, Chinnaiyan AM.

Abstract
Purpose: Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine tumor of the skin. Merkel cell polyomavirus (MCPyV) plays an oncogenic role in the majority of MCCs. Detection of MCPyV in MCCs has diagnostic utility and prognostic potential. We investigated whether RNAscope, an RNA in situ hybridization (ISH) assay for detection of RNA transcripts in tissues, is useful for MCPyV detection. Experimental Design: We applied an RNAscope probe targeting MCPyV T antigen transcripts on tissue microarrays (TMAs) and whole tissue sections encompassing 87 MCCs from 75 patients, 14 carcinomas of other types, and benign tissues. For comparison, quantitative PCR (qPCR) was performed on 57 cases of MCC from 52 patients.  
Results: RNA-ISH demonstrated the presence of MCPyV in 37/75 (49.3%) cases. Notably, tumors from younger patients (< 73 years) had a significantly higher virus positivity than those from elderly patients (≥ 73 years) (64.9% vs. 34.2%, P =0.011). Female patients had a higher positive rate of MCPyV than male patients (66.7% vs. 39.6%, P =0.032). Data from both RNA-ISH and qPCR were available for 57 samples. Considering MCPyV qPCR as the gold standard for determining MCPyV status, RNAscope had 100% sensitivity and 100% specificity. There was a strong correlation between qPCR copy number and RNA-ISH product score (Spearman's correlation coefficient R2 = 0.932, P < 0.0001).
Conclusions: RNA-ISH is comparably sensitive to qPCR for detection of MCPyV and allows for correlation with tissue morphology. This study also reveals a significant association between age, gender, and MCPyV positivity.
Copyright ©2017, American Association for Cancer Research.

PMID: 28606924 DOI: 10.1158/1078-0432.CCR-17-0299

Saturday, July 22, 2017

Publication in Cancer Research

Cancer Res. 2017 Jul 17. pii: canres.2072.2016. doi: 10.1158/0008-5472.CAN-16-2072. [Epub ahead of print]
Poor Prognosis Indicated by Venous Circulating Tumor Cell Clusters in Early Stage Lung Cancers.

Murlidhar V, Reddy RM, Fouladdel S, Zhao L, Ishikawa MK, Grabauskiene S, Zhang Z, Lin J, Chang AC, Carrott PW, Lynch WR, Orringer MB, Kumar-Sinha C, Palanisamy N, Beer DG, Wicha MS, Ramnath N, Azizi E, Nagrath S.

Abstract
Early detection of metastasis can be aided by circulating tumor cells (CTCs), which also show potential to predict early relapse. Due to the limited CTC numbers in peripheral blood in early stages, we investigated CTCs in pulmonary vein blood accessed during surgical resection of tumors. Pulmonary vein (PV) and peripheral vein (Pe) blood specimens from patients with lung cancer were drawn during the perioperative period and assessed for CTC burden using a microfluidic device. From 108 blood samples analyzed from 36 patients, PV had significantly higher number of CTCs compared to pre-operative Pe p<(0.0001) and intra-operative Pe p<(0.001) blood. CTC clusters with large number of CTCs were observed in 50% of patients, with PV often revealing larger clusters. Long term surveillance indicated that presence of clusters in pre-operative Pe blood predicted a trend toward poor prognosis. Gene expression analysis by RT-qPCR revealed enrichment of p53 signaling and extracellular matrix involvement in PV and Pe samples.  Ki67 expression was detected in 62.5% of PV samples and 59.2% of Pe samples, with the majority (72.7%) of patients positive for Ki67 expression in PV having single CTCs as opposed to clusters. Gene ontology analysis revealed enrichment of cell migration and immune-related pathways in CTC clusters, suggesting survival advantage of clusters in circulation. Clusters display characteristics of therapeutic resistance, indicating the aggressive nature of these cells. Thus, CTCs isolated from early stages of lung cancer are predictive of poor prognosis and can be interrogated to determine biomarkers predictive of recurrence.
Copyright ©2017, American Association for Cancer Research.
PMID: 28716896 DOI: 10.1158/0008-5472.CAN-16-2072

Publication in Modern Pathology

Mod Pathol. 2017 Jul 21. doi: 10.1038/modpathol.2017.72. [Epub ahead of print]

Renal cell tumors with clear cell histology and intact VHL and chromosome 3p: a histological review of tumors from the Cancer Genome Atlas database.

Favazza L, Chitale DA, Barod R, Rogers CG, Kalyana-Sundaram S, Palanisamy N, Gupta NS, Williamson SR.

Abstract

Clear cell renal cell carcinoma is by far the most common form of kidney cancer; however, a number of histologically similar tumors are now recognized and considered distinct entities. The Cancer Genome Atlas published data set was queried (http://cbioportal.org) for clear cell renal cell carcinoma tumors lacking VHL gene mutation and chromosome 3p loss, for which whole-slide images were reviewed. Of the 418 tumors in the published Cancer Genome Atlas clear cell renal cell carcinoma database, 387 had VHL mutation, copy number loss for chromosome 3p, or both (93%). Of the remaining, 27/31 had whole-slide images for review. One had 3p loss based on karyotype but not sequencing, and three demonstrated VHL promoter hypermethylation. Nine could be reclassified as distinct or emerging entities: translocation renal cell carcinoma (n=3), TCEB1 mutant renal cell carcinoma (n=3), papillary renal cell carcinoma (n=2), and clear cell papillary renal cell carcinoma (n=1). Of the remaining, 6 had other clear cell renal cell carcinoma-associated gene alterations (PBRM1, SMARCA4, BAP1, SETD2), leaving 11 specimens, including 2 high-grade or sarcomatoid renal cell carcinomas and 2 with prominent fibromuscular stroma (not TCEB1 mutant). One of the remaining tumors exhibited gain of chromosome 7 but lacked histological features of papillary renal cell carcinoma. Two tumors previously reported to harbor TFE3 gene fusions also exhibited VHL mutation, chromosome 3p loss, and morphology indistinguishable from clear cell renal cell carcinoma, the significance of which is uncertain. In summary, almost all clear cell renal cell carcinomas harbor VHL mutation, 3p copy number loss, or both. Of tumors with clear cell histology that lack these alterations, a subset can now be reclassified as other entities. Further study will determine whether additional entities exist, based on distinct genetic pathways that may have implications for treatment.Modern Pathology advance online publication, 21 July 2017; doi:10.1038/modpathol.2017.72.PMID: 28731045 DOI: 10.1038/modpathol.2017.72

Saturday, June 24, 2017

பல தோல்விகளையும் 
பல துரோகிகளையும் 
சந்தித்தாலொழிய 
வாழ்க்கையில் 
வெற்றி பெற முடியாது !

Sunday, May 7, 2017


பாசம் வைத்து மோசம் போகவேண்டாம் !
மோசக்காரர்களிடம் பாசம் வைக்கவேண்டாம்!

Saturday, April 29, 2017

என் வாழ்க்கையில் மூன்று பேர்களை மறக்க முடியாது 

1. துன்பம்  கொடுத்தவர்கள் 
2. துன்பத்திலிருக்கும்போது  என்னை விட்டு விலகியவர்கள் 
3. துன்பம் செய்யாமல் நன்மை செய்தவர்கள் 
நம்பிக்கை, நாணயம் , நேர்மை , நல்லொழுக்கம் 
இவை விலை மதிப்பில்லாத பொருட்கள் 
இவையணைத்தும் கீழ்த்தரமான மனிதர்களிடம் இருப்பதில்லை 

Saturday, April 8, 2017


முட்டாள் 



எல்லா உண்மையும் தெரிந்தும் பொய்யை நம்புகிறவன் 

Sunday, April 2, 2017

Father-in-law

"Person who accepts the responsibility of an irresponsible person"

Tuesday, March 14, 2017

Wayne State University-Pathology Lecture Series

March 15, 2017 | 12:00 p.m. - 1:00 p.m.
Category: Lecture
Location: Scott Hall #9364
Cost: Free
Nallasivam Palanisamy, MSc., MPhil., PhD.
Associate Scientist
Henry Ford Health System
Vattikutti Urology Institute
Medical Group Urology - Prostate Cancer Research
Detroit, Michigan

 “Understanding the diverse heterogeneity of molecular alterations in prostate cancer”

Sunday, March 12, 2017

உறவாடிக் கெடுக்கும் உறவுகளால் யாதொரு பயனும் இல்லை 

Wednesday, March 8, 2017

கோவிலுக்குப் போனேன்
மனம் உருகிப் பிரார்த்திக்கும் போது
அர்ச்சகர்
சாமிக்குத் தட்சிணை போடு என்றார்
கல்லான சாமியைக் கண்டு மனம் உருகி
தாராளமாய்ப் போட்டேன்
மனமெல்லாம் நிறைந்து
கோவிலுக்கு வெளியே வந்தபோது
பிச்சைக்காரர்
சாமி பிச்சை போடுங்கள் என்றார்
உயிருள்ள மனிதனின் நிலையைக்கண்டு
மனம் இறுகிக் கல்லானது
சற்று சிந்தித்தபோது உறைத்தது
சாமிக்கு தட்சிணை போடுபவனும் நான்
பிச்சைக்காரனுக்கு பிச்சை போடுபவனும் நான்
கோவிலுக்கு உள்ளே ஆசாமியாக இருந்த நான்
கோவிலுக்கு வெளியே சாமியாகிவிட்டேன்
கல்லான சாமி எதுவும் கொடுக்கப்போவதில்லை
கோவிலுக்கு உள்ளேயும் வெளியேயும் கொடுப்பது நான்
ஆக,
என்னுள்ளேயே சாமி இருக்கிறது என்ற உண்மை புரிந்தது
கோவிலுக்குப் போவதை நிறுத்தி விட்டேன்
.N.P.

Sunday, March 5, 2017

"எதிர்மறையான எண்ணம் மற்றும் செயலில் ஈடுபடுபவர்களிடம் உறவாடுவதால் நிச்சயம் நம் வாழ்க்கை நிம்மதியாக செல்லாது "
சொந்தக்காலில் நிற்க முடியாதவனுக்கு 
பந்தக்கால் போடும் யோக்கியதை கிடையாது !

Thursday, March 2, 2017

ரத்த உறவுகளா ? அல்லது ரத்தத்தை உறிஞ்சும் உறவுகளா ?
எல்லாம் தலையெழுத்து !
"பெற்றவர்களிடமே திருடும் கையாலாகாத கபோதிகள் செய்யும் கொடுமையை என்னவென்று சொல்வது "
"கையாலாகாத்தனம் மற்றும் பொறாமையில் மற்றவர்கள் நம்மைப் பற்றி தவறாகப் பேசுகிறார்கள் அல்லது கேடு செய்கிறார்கள் என்றால் நாம்  சரியான பாதையில் செல்கிறோம் என்று அர்த்தம் "






Monday, February 20, 2017

Saturday, January 14, 2017

நித்திரை இல்லாமல் உழைத்தால் 
இத்தரையில் நிச்சயம் 
முத்திரை பதிக்கலாம் 

Thanks to the central government and Supreme Court for making sallikattu more popular, it used to be played/celebrated invery few places in Tamilndu, now it is popular all over the world.

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