Publication in Oncogene

Oncogene. 2011 May 2. [Epub ahead of print]
The tumor suppressor gene rap1GAP is silenced by miR-101-mediated EZH2 overexpression in invasive squamous cell carcinoma.

Banerjee R, Mani RS, Russo N, Scanlon CS, Tsodikov A, Jing X, Cao Q, Palanisamy N, Metwally T, Inglehart RC, Tomlins S, Bradford C, Carey T, Wolf G, Kalyana-Sundaram S, Chinnaiyan AM, Varambally S, D'Silva NJ.

Abstract

Rap1GAP is a critical tumor suppressor gene that is downregulated in multiple aggressive cancers, such as head and neck squamous cell carcinoma, melanoma and pancreatic cancer. However, the mechanistic basis of rap1GAP downregulation in cancers is poorly understood. By employing an integrative approach, we demonstrate polycomb-mediated repression of rap1GAP that involves Enhancer of Zeste Homolog 2 (EZH2), a histone methyltransferase in head and neck cancers. We further demonstrate that the loss of miR-101 expression correlates with EZH2 upregulation, and the concomitant downregulation of rap1GAP in head and neck cancers. EZH2 represses rap1GAP by facilitating the trimethylation of histone 3 at lysine 27, a mark of gene repression, and also hypermethylation of rap1GAP promoter. These results provide a conceptual framework involving a microRNA-oncogene-tumor suppressor axis to understand head and neck cancer progression.Oncogene advance online publication, 2 May 2011; doi:10.1038/onc.2011.141.

PMID:21532618

Publication in Science Translational Medicine

Sci Transl Med. 2011 Apr 6;3(77):77ra30.

CD44-SLC1A2 Gene Fusions in Gastric Cancer.

Tao J, Deng NT, Ramnarayanan K, Huang B, Oh HK, Leong SH, Lim SS, Tan IB, Ooi CH, Wu J, Lee M, Zhang S, Rha SY, Chung HC, Smoot DT, Ashktorab H, Kon OL, Cacheux V, Yap C, Palanisamy N, Tan P.

Abstract

Fusion genes are chimeric genes formed in cancers through genomic aberrations such as translocations, amplifications, and rearrangements. To identify fusion genes in gastric cancer, we analyzed regions of chromosomal imbalance in a cohort of 106 primary gastric cancers and 27 cell lines derived from gastric cancers. Multiple samples exhibited genomic breakpoints in the 5' region of SLC1A2/EAAT2, a gene encoding a glutamate transporter. Analysis of a breakpoint-positive SNU16 cell line revealed expression of a CD44-SLC1A2 fusion transcript caused by a paracentric chromosomal inversion, which was predicted to produce a truncated but functional SLC1A2 protein. In primary tumors, CD44-SLC1A2 gene fusions were detected in 1 to 2% of gastric cancers, but not in adjacent matched normal gastric tissues. When we specifically silenced CD44-SLC1A2, cellular proliferation, invasion, and anchorage-independent growth were significantly reduced. Conversely, CD44-SLC1A2 overexpression in gastric cells stimulated these pro-oncogenic traits. CD44-SLC1A2 silencing caused significant reductions in intracellular glutamate concentrations and sensitized SNU16 cells to cisplatin, a commonly used chemotherapeutic agent in gastric cancer. We conclude that fusion of the SLC1A2 gene coding region to CD44 regulatory elements likely causes SLC1A2 transcriptional dysregulation, because tumors expressing high SLC1A2 levels also tended to be CD44-SLC1A2-positive. CD44-SLC1A2 may represent a class of gene fusions in cancers that establish a pro-oncogenic metabolic milieu favoring tumor growth and survival.

PMID: 21471434

Publication in Clinical Cancer Research

Clin Cancer Res. 2011 Mar 17. [Epub ahead of print]

Genomic Loss of miR-486 Regulates Tumor Progression and the OLFM4 Anti-apoptotic Factor in Gastric Cancer.

Oh HK, Tan AL, Das K, Ooi CH, Deng NT, Tan IB, Beillard E, Lee J, Ramnarayanan K, Rha SY, Palanisamy N, Voorhoeve PM, Tan P.

Cellular and Molecular Research, National Cancer Centre, Singapore.

Abstract

PURPOSE: MicroRNAs (miRNAs) play pivotal oncogenic and tumor suppressor roles in several human cancers. We sought to discover novel tumor suppressor miRNAs in gastric cancer (GC).

EXPERIMENTAL DESIGN: Using Agilent miRNA microarrays, we compared miRNA expression profiles of 40 primary gastric tumors and 40 gastric normal tissues, identifying miRNAs significantly downregulated in gastric tumors.

RESULTS: Among the top 80 miRNAs differentially expressed between gastric tumors and normals (FDR<0.01), we identified hsa-miR-486 (miR-486) as a significantly downregulated miRNA in primary GCs and GC cell lines. Restoration of miR-486 expression in GC cell lines (YCC3, SCH and AGS) caused suppression of several pro-oncogenic traits, while conversely inhibiting miR-486 expression in YCC6 GC cells enhanced cellular proliferation. Array-CGH analysis of 106 primary GCs revealed genomic loss of the miR-486 locus in ~25-30% of GCs, including two tumors with focal genomic losses specifically deleting miR-486, consistent with miR-486 playing a tumor suppressive role. Bioinformatic analysis identified the secreted anti-apoptotic glycoprotein OLFM4 as a potential miR-486 target. Restoring miR-486 expression in GC cells decreased endogenous OLFM4 transcript and protein levels, and also inhibited expression of luciferase reporters containing a OLFM4 3' untranslated region (UTR) with predicted miR-486 binding sites. Supporting the biological relevance of OLFM4 as a miR-486 target, proliferation in GC cells was also significantly reduced by OLFM4 silencing.

CONCLUSIONS: miR-486 may function as a novel tumor suppressor miRNA in GC. Its anti-oncogenic activity may involve the direct targeting and inhibition of OLFM4.

PMID: 21415212

Meeting with James D. Watson, the co discoverer of Structure of DNA and the winner of The Nobel Prize in Physiology or Medicine 1962

This is a great moment in my life. Dr. Watson is the great inspiring personality whom I wanted to meet him in person and it happened very recently at a meeting in Washington, DC USA.

Click on the title to learn more about James D Watson and his Nobel Prize winning work which has changed the way we do medicine and many aspects of our life today.

சொர்க்கம் உன் காலடியில்

எல்லோரும் அஞ்சுவது இறப்பிற்கு
இறக்கும் நாள் தெரிந்தால் வாழும் நாட்கள்  நரகமாகும்

சொர்க்கம் இருப்பது  உண்மை என்றால்
நரகம் இருப்பதும் கூட உண்மையாகும்
சொர்க்கத்தில் எல்லாம் கிடைக்கும் என்றாலும்
அங்கு செல்வதற்கு யாரும் இறக்கத் தயாரில்லை

நாம்  இருக்கும் இடம் நரகம் என்றாலும்
யாரும் இறக்கத் தேவையில்லை
சொர்க்கமோ, நரகமோ
இல்லாத ஒன்றை, யாரும் காணாத ஒன்றை
காணத் துடிக்கும் மனமே

ஒரு கணம் நில்!

நான் வாழும் பூமியே சொர்க்கபூமி
இங்கு இல்லாதது எங்கு இருக்க முடியும்

என்ன இல்லை இங்கு?

எல்லோருடைய ஆசைக்குத்  தேவையானது இங்கு இல்லாது  இருக்கலாம்
ஆனால் எல்லோருடைய தேவைக்கு வேண்டியது இங்கு எல்லாம் இருக்கிறது
அதற்க்கு மேல்
இல்லாததைப்  படைக்க உனக்கு அறிவு இருக்கிறது

உன் தேவை என்ன?
உன் ஆசை என்ன?

இது சொர்க்கமா?
இல்லை நரகமா?

தேர்ந்தெடுப்பதும் அல்லது மாற்றுவதும் உன்கையில்

மனிதனே உழைக்கத் தயாராகு
உழைக்கத் தயாரானால்
சொர்க்கம் உன் காலடியில்
நரகம் உன் கனவில் கூட தெரியாது

வெற்றி

௧. வெற்றி என்றால் என்ன?
௨. வெற்றியின் அளவுகோல் எது ?
௩. வெற்றியின் ரகசியம் என்ன?
௪. வெற்றி பெற வழிகள் என்ன?
௫. வெற்றியை நிர்ணயிப்பது யார்?
பணம், பதவி, புகழ், அந்தஸ்து, கல்வி - இதுதான் வெற்றியா?


என் பார்வையில் வெற்றிபெறுவதற்கு
௧.     நீ நீயாக இரு
௨.     உனக்கு உண்மையாய் இரு
௩.     நேர் வழியில் தைரியமாய் செல்
௪.     விரும்பியதை விருப்பமுடன் செய்
௫.     அடுத்தவன் உழைப்பை அனுபவிக்காதே

இவை ஐந்தும் உன்னிடம் இருந்தால்
பணம், பதவி, புகழ், அந்தஸ்து, கல்வி எல்லாம் உன்னைத்   தேடி வரும்
அப்புறம் என்ன? நிச்சயம் நீ வெற்றி பெற்றவன்தான்

இவை எல்லாம் எல்லோராலும் செய்ய முடியும்
இதைமட்டும் செய்தால் எல்லோரும் வெற்றி பெற்றவரே!

வரதட்சணை

சோம்பேறியை மேலும் சோம்பேறியாக்குவது
வசதியுள்ளவனை வரியவனாக்குவது
காரணமில்லாமல் காஸ் அடுப்பு வெடிப்பது
மகனுக்கு வாங்கும் தட்சனையில் மகளுக்கு வாழ்வு கொடுப்பது
வீட்டு மாப்பிள்ளை என்று வெட்கமில்லாமல் வாழவைப்பது
கையாலாகதவன் கட்டிய மனைவியிடம் வீரத்தை காட்டுவது
வரட்டுக் கவுரவத்தால் இன்னும் ஒழிக்க முடியாதது

மேலும் பல கொடுமைகள் இந்த மண்ணில் ........

வரதட்சணையால் பாழ்பட்ட சமுதாயம் திருந்துவது எப்போது?

பயனில்லை

ஆபத்துக்கு உதவாத பிள்ளை
அரும்பசிக்கு உதவாத அன்னம்
தாகத்தை தீராத் தீர்த்தம்
தரித்திரம் அறியா பெண்டிர்
கோபத்தை அடக்கா வேந்தன்
குரு மொழி கொள்ளாச் சீடன்

---எப்போதோ படித்தது

இது எப்படி வழக்கில் வந்தது?!

காபி கீப்பி
மருந்து கிருந்து
சாப்பாடு கீப்பாடு
தண்ணி கிண்ணி
கார் கீர்
சண்டை கிண்டை
பாம்பு கீம்பு
பூனை கீன
பல்லி கில்லி
குழந்தை கிழந்தை
தூது கீது

...............மேலும் பல

கடவுள் இருந்தால் இப்படி நடக்காது

மனிதனுக்கு சாகும் நாள் தெரியாது
ஆனால் மனிதன்
பல உயிர்கள் பரலோகம் போவதற்கு நாள் குறிக்கிறான்

மிருகங்களுக்கு மனிதன் -
     கடவுளுக்கு திருவிழா என்ற பெயரில் 

     காட்டில் வேட்டை என்ற பெயரில்
     நேர்த்திகடன் என்ற பெயரில்
கடவுள் இருந்தால் இப்படி நடக்காது

மனிதனுக்கு மனிதன் -
     நரபலி என்ற பெயரில்
     போட்டி பொறாமை என்ற பெயரில்
     பேராசை என்றால் பெயரில்
கடவுள் இருந்தால் இப்படி நடக்காது

     கருவறையில் காமம்
     உண்டியல் உடைத்து திருட்டு
     ஆன்மிகம் என்றபெயரில் அயோக்கியத்தனம்
கடவுள் இருந்தால் இப்படி நடக்காது

     அரசாங்க சொத்து அபகரிப்பு
     அதிகார துஸ்பிரயோகம்
     கடமையை செய்ய லஞ்சம்
கடவுள் இருந்தால் இப்படி நடக்காது

அண்ட சராசரங்களை படைத்தவன் எவனோ
அவனே இதற்கெல்லாம் முடிவு காணட்டும்
அவன் பெயர் கடவுளா?

என் ஆசைகள்

அகங்காரம்: அறிவாளிகளிடம் மட்டுமே இருக்க வேண்டும்
ஆசை:அடுத்தவர்களுக்கு கொடுப்பவர்களிடம்  இருக்க வேண்டும்
இல்லாமை:இருப்பவனிடம் இருக்க வேண்டும்
ஈகை: பேராசை பிடித்தவர்களிடம் இருக்க வேண்டும்
உற்சாகம்:சோம்பேறிகளிடம் இருக்க வேண்டும்
கோபம்: பொறுமைசாலிகளுக்கு மட்டுமே வர  வேண்டும்
வெற்றி: திறமைசாலிகளுக்கு  மட்டுமே கிடைக்க வேண்டும்
பதவி: தகுதி உள்ளவருக்கே கிடைக்க வேண்டும்
தண்டனை:தவறு செய்பவர்களுக்கு மட்டுமே கிடைக்க வேண்டும்
புகழ்:நல்லவர்களுக்கே கிடைக்க வேண்டும்
மதம்: யானைக்கு மட்டுமே பிடிக்க வேண்டும்
பொய்: உண்மை பேசுபவனிடம் மட்டுமே இருக்க வேண்டும்
உழைப்பு:சோம்பேறிகளிடம் இருக்க வேண்டும்
பசி:வசதி உள்ளவனுக்கே இருக்க வேண்டும்
வறுமை:பணக்காரனுக்கு மட்டுமே இருக்க வேண்டும்
பணிவு:அதிகாரம் உள்ளவர்களிடம் இருக்க வேண்டும்
துணிவு:கோழைகளிடம் இருக்க வேண்டும்
கடவுள்:உருவத்துடன் இருக்க வேண்டும்

அம்மா

அம்மா என்றாலே பிரம்மா
ஏனென்றால்
அனைத்தையும் படைப்பவள் அம்மாதான்

ஆசை

மரம் செடி கொடிகளுக்கு இல்லாத ஆசை
மிருகங்களுக்கு இல்லாத ஆசை
மனிதனுக்குள் எப்படி வந்தது இந்த பேராசை

சண்டை

நிரந்தரமில்லாத இந்த உலகத்தில்
நிரந்தரமில்லாத மனிதர்கள்
நிரந்தரமில்லாத பொருள்களின்மேல்
நிரந்தரமாக போடுவது

Publication in Cancer Research

Activation of NF-kB by TMPRSS2/ERG fusion isoforms through Toll-like receptor-4

Jianghua Wang, Yi Cai, Long-jiang Shao, Javed Siddiqui, Nallasivam Palanisamy, Rile Li,Chengxi Ren, Gustavo Ayala, and Michael M Ittmann

Abstract

The TMPRSS2/ERG (T/E) fusion gene is present and thought to be an oncogenic driver of approximately half of all prostate cancers. Fusion of the androgen regulated TMPRSS2 promoter to the ERG oncogene results in constitutive high level expression of ERG which promotes prostate cancer invasion and proliferation. Here we report the characterization of multiple alternatively spliced T/E fusion gene isoforms which have differential affects on invasion and proliferation. We found that T/E fusion gene isoforms differentially increase NF-κB mediated transcription, which may explain in part the differences in biological activities of the T/E fusion isoforms. This increased activity is due to phosphorylation of NF-κB p65 on Ser536. Tissue microarray immunochemistry revealed that p65 phospho-Ser536 is present in the majority of prostate cancers where it is associated with ERG protein expression. The T/E fusion gene isoforms differentially increase expression of a number of NF-κB associated genes including PAR1, CCL2, FOS, TLR3 and TLR4 (Toll-like receptor 4). TLR4 activation is known to promote p65 Ser536 phosphorylation and knockdown of TLR4 with ShRNA decreases Ser536 phosphorylation in T/E fusion gene expressing cells. TLR4 can be activated by proteins in the tumor microenvironment and lipopolysacharide from Gram (-) bacteria. Our findings suggest that bacterial infection of the prostate and/or endogenous microenvironment proteins may promote progression of high-grade prostatic intraepithelial neoplasia and/or prostate cancers that express the T/E fusion gene, where the NF-κB pathway might be targeted as a rational therapeutic approach.

Published OnlineFirst December 17, 2010; doi: 10.1158/0008-5472.CAN-10-2210

UK Cancer Convention Focus on Prostate

UK Cancer Convention Focus on Prostate

Invited Speaker 

Presentations:  http://ukcancerconvention.org/prostate/index.html

Click the link above to Listen to the presentations

American Society of Clinical Pathology - Teleconference

8702 Transcriptome Sequencing To Detect Gene Fusions in Cancer
Date: 3/30/2011 Wed
Time: 1:00 PM CT

Faculty:

Nallasivam Palanisamy, PhD
Assistant Research Professor, University of Michigan, Ann Arbor, MI

Description:

Multiple complex chromosome translocations and aneuploidy are the hallmark of solid tumors. The occurrence, frequency, and significance of these aberrations are poorly understood. Identifying the complex aberrations that drive mutations is limited by available methods. Are the complex translocations in solid tumors random events? Important gene fusions have been identified in hematologic malignancies and soft tissue sarcomas. Recent discovery of recurrent gene fusions in prostate and lung cancers using new approaches has identified recurrent gene fusions as a new class mutation in solid cancer. Similar approaches did not detect recurrent aberrations in other solid cancers. Therefore, new approaches are needed to analyze solid cancer at the whole genome and transcriptome level to understand the genetic complexity. Research activities are using new approaches directed toward understanding the nature of all rearrangements in solid tumor genomes, particularly to identify the deregulated genes and/or fusion genes, to establish clinical correlations, and to identify recurrent cytogenetic markers. Application of next-generation sequencing technology (RNAseq) will unravel the genetic complexity of solid cancers. These and other topics for presentation include molecular stratification of cancers, and current understanding on the molecular mechanisms involved in the genesis of gene fusions in prostate cancer.

After attending this session, participants will be able to:

Explain gene fusions and their importance in cancer

Describe the methods used to discover gene fusion

Discuss the concept of molecular classification of cancer

Describe the process of identifying druggable targets in cancer

Core Competencies: PC, MK, PBL

Intended Audience: Practicing Pathologists, Residents, Doctoral Scientists, Pathologists' Assistants, Laboratory Managers, Bench Supervisors, Bench Technologists & Technicians, Cytotechnologists, Histotechnologists, Research Investigators in Cancer Genomics, Students.

 -Register for this event

Hematopathology- expert Consult - Nallasivam Palanisamy contributed to Chapter 7 in this Book

Editorial Reviews

Book Description

A landmark new reference for more definitive hematologic diagnoses

Introducing HEMATOPATHOLOGY, a definitive new diagnostic reference on diseases of the hematopoietic system by Dr. Elaine S. Jaffe and her fellow editors, all collaborators on the World Health Organization's classification of lymphoid and myeloid disorders. These experts provide you with today's most effective guidance in evaluating specimens from the lymph nodes, bone marrow, peripheral blood, and more, equipping you to deliver more accurate and actionable pathology reports. More than 1,100 high-quality color images mirror the findings you encounter in practice, and full-text online access lets you search the contents rapidly and download any illustration.

Overcome the toughest diagnostic challenges with authoritative guidance from the world's leading experts.

Make optimal use of the newest diagnostic techniques, including molecular, immunohistochemical, and genetic studies.

Compare specimens to more than 1,100 high-quality color images to confirm or challenge your diagnostic interpretations.

Amazon.com

Research Profile of Palanisamy, Nallasivam

http://www.researchprofiles.collexis.com/umichigan/expert.asp?n=Palanisamy%2C+Nallasivam&u_id=1186

A book Chapter by Nallasivam Palanisamy

Chromosomal Aberrations in solid tumors.

Chinnaiyan AM, Palanisamy N.
Prog Mol Biol Transl Sci. 2010;95:55-94.
PMID: 21075329 [PubMed - in process]

Abstract

Ever since the identification of the exact number of human chromosomes in 1956, several cancer-specific chromosomal abnormalities have been identified in different tumors. Among the various genetic changes, such as alterations in oncogenes, tumor suppressor genes, and microRNA genes, recurrent chromosome translocations have been identified as an important class of mutations in hematological malignancies, soft tissue sarcomas, and more recently in prostate cancer and lung cancer. Recurrent gene fusions are used for cancer classification and as diagnostic markers, and some have been successfully targeted for drug development. Recent advances in high-throughput sequencing technology and the ambitious undertaking of "The Cancer Genome Atlas" (TCGA) project will help drive the identification of the underlying genetic aberrations in most of the solid cancers. This chapter presents an overview on the current status of the knowledge on chromosome aberrations in solid cancers, cytogenetic and noncytogenetic methods for the characterization of changes at the DNA and RNA levels, technological advancements in high-throughput characterization of the cancer genome and transcriptome, and the current understanding of the molecular mechanism involved in the formation of gene fusions in solid cancer.

Cytogenetics Resources

Atlas of Genetics and Cytogenetics in Oncology and Haematology

Please click on the title

UK Cancer Convention - Focus on Prostate

Click on the title for more information about this conference

http://www.ur.umich.edu/0910/Nov02_09/11.php

Remembering Mahatma Gandhi on his 141st Birthday

Born	2 October 1869(1869-10-02) Porbandar, Bombay Presidency, British India
Died	30 January 1948 (aged 78) New Delhi, Union of India

50 years of 46 Chromosomes

The correct human chromosome number was reported in 1956.

Tjio, H. J. & Levan, A. The chromosome numbers of man.
Hereditas 42, 1–6 (1956).

A symposium celebrating the 50th Anniversary of the discovery of correct human chromosome number.

July 20-21 2006

National Institutes of Health, Bethesda, Maryland

Meeting with Scientific Leaders - Dr. Thomas Ried

Dr. Ried developed Spectral Karyotyping (SKY), a multi-color chromosome painting method for the identification of complex chromosomal aberrations in human cancer and mouse models.

Spectral karyotype of normal human male (left), mouse cell line (right)

Thirukural in Tamil and English

knowledge is power........

Thirukural - The Classic of Tamil Literature

Invention -Nallasivam Palanisamy

there is no substitute for hard work.......

United States Patent 7,585,964
Inventors: Palanisamy , et al. September 8, 2009
---------------------------------------------------------------------------
Methods of analyzing chromosomal translocations using fluorescence in situ hybridization (FISH)

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.
Click on the title to go to USPTO web site, then go to 'SEARCH" and type the keyword "Palanisamy N" to view the entire patent.

New Drug for Melanoma

never give up..........

This is a remarkable achievement in melanoma research.

Research Publication in Nature

think differently.......

Transcriptome Sequencing to Detect Gene Fusions in Cancer

Maher CA, Kumar-Sinha C, Cao X, Kalyana-Sundaram S, Han B, Jing X, Sam L, Barrette T, Palanisamy N, Chinnaiyan AM.

Nature. 2009 Mar 5;458(7234):97-101. Epub 2009 Jan 11.
Editor's Summary
http://www.nature.com/nature/journal/v458/n7234/edsumm/e090305-12.html

Recurrent gene fusions, typically associated with haematological malignancies and rare bone and soft-tissue tumours, have recently been described in common solid tumours. Here we use an integrative analysis of high-throughput long- and short-read transcriptome sequencing of cancer cells to discover novel gene fusions. As a proof of concept, we successfully used integrative transcriptome sequencing to ‘re-discover’ the BCR–ABL1 gene fusion in a chronic myelogenous leukaemia cell line and the TMPRSS2–ERG, gene fusion in a prostate cancer cell line and tissues. Additionally, we nominated, and experimentally validated, novel gene fusions resulting in chimaeric transcripts in cancer cell lines and tumours. Taken together, this study establishes a robust pipeline for the discovery of novel gene chimaeras using high-throughput sequencing, opening up an important class of cancer-related mutations for comprehensive characterization.

Cancer Terms - Dictionary

cancer (KAN-ser)
A term for diseases in which abnormal cells divide without control and can invade nearby tissues. Cancer cells can also spread to other parts of the body through the blood and lymph systems. There are several main types of cancer. Carcinoma is a cancer that begins in the skin or in tissues that line or cover internal organs. Sarcoma is a cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. Leukemia is a cancer that starts in blood-forming tissue such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the blood. Lymphoma and multiple myeloma are cancers that begin in the cells of the immune system. Central nervous system cancers are cancers that begin in the tissues of the brain and spinal cord. Also called malignancy.

Click on the title to go to NCI web page
http://www.cancer.gov/dictionary/?expand=

List of Cancers

divide and conquer...........

You will find the complete list of Cancers

Click on the title or copy and paste this link to open in a new window

http://www.cancer.gov/cancertopics/alphalist

Nallasivam Palanisamy

 be who you are........


MCTP Personnel Page

http://mctp.path.med.umich.edu/mctp/main/index.jsp

Quotable Quotes

Harry Truman

"It is amazing what you can accomplish if you do not care who gets the credit."
-- Harry Truman

Cancer Chromosome Abnormalities from the publications of Palanisamy and colleagues

-Click the title and use keyword " Palanisamy N" to search

List of Cancer Chromosome Abnormalities from my publications

Citation Report -Nallasivam Palanisamy Publications, ISI Web of Knowledge

Click on the title

Nallasivam Palanisamy - Peer reviewed publications

It is all in your genes...........

Click on the title

My contributions to the identification of Gene Fusions in Cancer

My primary research interest is to characterize genomic rearrangements in cancer and understand their molecular consequences in a translational research perspective.

Identification of gene fusions at breakpoint junctions on chromosomes is an active area of research since the discovery of BCR-ABL gene fusion from t(9;22) translocation in chronic myeloid leukemia.

• Gene fusions are important mutations identified in a variety of cancer.
• Common in hematological malignancies (leukemia and lymphoma), sarcoma and some solid cancer including prostate cancer and lung cancer.
• Difficult to identify in solid cancer by conventional cytogenetic methods
• Inter and intra chromosomal rearrangements cause gene fusions.
• Intra chromosomal, unbalanced rearrangements are common in solid cancers.
• Molecualr consequences of rearrangement result in activation of an oncogene or formation of gene fusion.
• During my research on cancer since 1996 - 2010, I was involved in the identification and characterization of the following genomic rearrangements and associated gene fusions in different types of cancer.

To learn more about the gene fusions in cancer please read the publications and related work provided in the link. - click the title of this page

http://cgap.nci.nih.gov/Chromosomes/MSearchForm

Chen et al 2001, Oncogene
	Follicular lymphoma
	IGH@/FCGR2B
	t(1;14)(q21;q32)
	B-Lineage
Dyomin et al 2000, Blood
	Mature B-cell neoplasm, NOS
	IGH@/MUC1
	t(1;14)(q22;q32)
	B-Lineage
Han et al 2008, Cancer Res
	Adenocarcinoma	Prostate
	SLC45A3/ERG
	t(1;21)(q32;q22)
	Adenocarcinoma	Prostate
	FLJ35294/ETV1
	t(7;17)(p21;p13)
	Adenocarcinoma	Prostate
	CANT1/ETV4
	t(17;17)(q25;q21)
	Adenocarcinoma	Prostate
	DDX5/ETV4
	t(17;17)(q21;q24)
Hatzivassiliou et al 2001, Immunity
	Multiple myeloma
	IGH@/FCRL4
	t(1;14)(q23;q32)
	B-Lineage
Maher et al 2009, Nature
	Adenocarcinoma	Prostate
	USP10/ZDHHC7
	del(16)(q24q24)
	Adenocarcinoma	Prostate
	HJURP/EIF4E2
	t(2;2)(q37;q37)
	Adenocarcinoma	Prostate
	INPP4A/HJURP
	t(2;2)(q11;q37)
	Adenocarcinoma	Prostate
	MIPOL1/DGKB
	t(7;14)(p21;q13-21)
	Adenocarcinoma	Prostate
	STRN4/GPSN2
	t(19;19)(p13;q13)
	Adenocarcinoma	Prostate
	RC3H2/RGS3
	t(9;9)(q32;q33)
	Adenocarcinoma	Prostate
	LMAN2/AP3S1
	t(5;5)(q23;q35)
	Adenocarcinoma	Prostate
	SLC45A3/ELK4
	t(1;1)(q32;q32)
	Adenocarcinoma	Prostate
	MRPS10/HPR
	t(6;16)(p21;q22)
	Adenocarcinoma	Prostate
	ZNF649/ZNF577
	t(19;19)(q13;q13)
	Adenocarcinoma	Prostate
	MBTPS2/YY2
	t(X;X)(p22;p22)
	Adenocarcinoma	Prostate
	C19ORF25/APC2
	t(19;19)(p13;p13)
	Adenocarcinoma	Prostate
	WDR55/DND1
	t(5;5)(q31;q31)
Maher et al 2009, Proc Natl Acad Sci U S A
	Adenocarcinoma	Breast
	AHCYL1/RAD51C
	t(1;17)(p13;q22)
	Adenocarcinoma	Breast
	ARHGAP19/DRG1
	t(10;22)(q24;q12)
	Adenocarcinoma	Prostate
	AX747630/ETV1
	t(7;17)(p21;p13)
	Adenocarcinoma	Breast
	BC017255/TMEM49
	t(17;17)(q22;q23)
	Adenocarcinoma	Prostate
	HERPUD1/ERG
	t(16;21)(q13;q22)
	Adenocarcinoma	Breast
	MYO9B/FCHO1
	del(19)(p13p13)
	Adenocarcinoma	Breast
	PAPOLA/AK7
	del(14)(q32q32)
	Adenocarcinoma	Prostate
	TIA1/DIRC2
	t(2;3)(p13;q21)
	Adenocarcinoma	Prostate
	ZDHHC7/ABCB9
	t(12;16)(q24;q24)
	Adenocarcinoma	Prostate
	DLEU2/PSPC1
	t(13;13)(q12;q14)
	Adenocarcinoma	Prostate
	PIK3C2A/TEAD1
	del(11)(p15p15)
	Adenocarcinoma	Prostate
	SPOCK1/TBC1D9B
	t(5;5)(q31;q35)
	Adenocarcinoma	Prostate
	RERE/PIK3CD
	del(1)(p36p36)
Palanisamy et al 2010, Nat Med
	Adenocarcinoma	Prostate
	SLC45A3/BRAF
	t(1;7)(q32;q34)
	Adenocarcinoma	Prostate
	ESRP1/RAF1
	t(3;8)(p25;q22)
	Adenocarcinoma	Stomach
	AGTRAP/BRAF
	t(1;7)(p36;q34)
Schmidt et al 2004, Oncogene
	Chronic lymphocytic leukemia
	IGH@/CHST11
	t(12;14)(q23;q32)
	B-Lineage
Wang et al 2009, Nat Biotechnol
	Carcinoma, NOS	Lung
	R3HDM2/NFE2
	del(12)(q13q13)

---------------------------------------------------------------------------------------------------------------------

Butler et al 2002, Cancer Res

                    
                        Follicular lymphoma                                             Lymphoma

                        IGH@/BCL6

                        t(3;14)(q27;q32)

                        B-Lineage

                     
                        Diffuse large B-cell lymphoma                              Lymphoma

                        BCL6+

                        t(2;3)(q21;q27)

                        B-Lineage

                       
                        Diffuse large B-cell lymphoma                              Lymphoma

                        BCL6+

                        t(3;8)(q27;q13)

                        B-Lineage

                        Diffuse large B-cell lymphoma                              Lymphoma

                        BCL6+

                        t(3;9)(q27;p13)

                        B-Lineage

                        Diffuse large B-cell lymphoma                              Lymphoma

                        BCL6+

                        t(2;3)(q12;q27)

                        B-Lineage

                        Diffuse large B-cell lymphoma                              Lymphoma

                        BCL6+

                        t(3;6;14)(q27;p35;q32)

                        B-Lineage

--------------------------------------------------------------------------------------------------------

Iida et al 1996, Blood

                       
                        Lymphoplasmacytic lymphoma                             Lymphoma

                        IGH@/PAX5

                        t(9;14)(p13;q32)

                        B-Lineage

Meeting with Scientific Leaders - Dr. Francis Collins

With Dr. Francis Collins during his visit to Genome Institute of Singapore

Dr. Collins led the international human genome project.

be a positive role model..........

Cancer Cytogenomics Microarray Consortium (CCMC)

In my opinion this is a timely and a needed effort. Together we can succeed in helping the innumerable cancer patients who have exhausted all options but to try whatever the new therapeutic options available.

I am confident that this effort will help to identify new markers for cancer diagnosis, treatment and followup.

Congratulations to all the participants.

Nallasivam Palanisamy