Phd Clinical Biochemistry

Sheikh Mohd Shaffi, PhD

R/O Kawoosa Khalisa

P/O Kawoosa Magam,

Dist. Budgam, KMR, J&K-193401

Mob: +91-962*******

E-mail: **************@*****.***

***********@*****.**.**

OBJECTIVE

To obtain career position within an organization where I can meet challenges with the

able guidance, can prove my skills and can associate with growth of the institution to

further advance my knowledge, skills and excel in life.

CAREER HISTORY

Demonstrator, In-charge Chemistry diagnostic laboratory, Department of

Biochemistry, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard,

New Delhi, from Oct 2013 to Apr 2014.

Senior Resident, In-charge Emergency lab, Department of Clinical Biochemistry,

Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Kashmir (India), from

Aug 2011 till Oct 2013.

Tutor/Demonstrator in Biochemistry, Sher-I-Kashmir Institute of Medical Sciences-

Medical College, Srinagar Kashmir (India), from Nov 2010 to Jul 2011.

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PhD, in the Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical

Sciences, Srinagar Kashmir (India), from Nov 2006 to Jul 2010.

Thesis Title: Molecular analysis of TP53 gene and promoter hypermethylation of

MGMT gene in lung cancer patients of Kashmir Valley

EDUCATION

PhD at Sher-I-Kashmir Institute of Medical Sciences, Srinagar Kashmir (India), Nov

2006 to Jul 2010.

Master of Science (M.Sc.) in Biochemistry, Hamdard University, New Delhi (India),

2004-2006.

Bachelor of Science (B.Sc.) with Biotechnology, Chemistry and Zoology, from

Bangalore University, Bangalore (India), 2001-2004.

AWARDS & FELLOWSHIPS

Qualified National Eligibility Test (NET) for Lectureship/JRF-2006 conducted by

University Grants Commission (UGC) and Council for Scientific and Industrial

Research (CSIR), New Delhi.

Qualified Prestigious Common Entrance Test conducted by Sheri-I-Kashmir Institute

of Medical Sciences (SKIMS) for PhD programme in year 2006.

PUBLICATIONS

Sheikh M Shaffi, M Amin Shah

Promoter Methylation of MGMT in lung cancer patients of Kashmir Valley

International journal of medicine and public health, Apr-Jun,2013

http://www.ijmedph.org/text.asp?2013/3/2/89/115161

Sheikh M. Shaffi, M. Amin Shah, Imtiyaz A. Bhat, Parvaiz Koul, Syed Nisar A,

Mushtaq A. Siddiqi.

CYP1A1 polymorphism and risk of lung cancer in ethnic Kashmiri population

Asian Pacific J Cancer Prev, 2009,10,4, 651-656

http://www.ncbi.nlm.nih.gov/pubmed/19827888

M A Shah, Sheikh M Shaffi, Ghulam Nabi Lone, Syed Mudassar Jan

Splice site and germline variations of the MGMT gene in Esophageal cancer from kashmir

valley: India

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International journal of health sciences, Vol 7, No 3 (Nov 2013)

http://www.ncbi.nlm.nih.gov/pubmed/24533020

Mohd A Shah, Sheikh M Shaffi, Ghulam Nabi Lone, Syed Mudassar Jan

Lack of Influence of MGMT Codon Leu84Phe and Codon Ileu143Val Polymorphisms on

Esophageal Cancer Risk in the Kashmir Valley

Asian Pacific J Cancer Prev, 2012;13

http://www.ncbi.nlm.nih.gov/pubmed/22994708

Naveed A Chikan, Nadeem Shabir, Sheikh Shaffi, Manzoor R Mir, Trupti N Patel

N-Nitrosodimethylamine in the Kashmiri Diet and Possible Roles in the High

Incidence of Gastrointestinal Cancers

Asian Pacific J Cancer Prev 2012; 13, 1-4

http://www.ncbi.nlm.nih.gov/pubmed/22631641

Manzoor R. Mir, Nadeem Shabir, Khursheed A. Wani, Sheikh Shaffi, Ishraq Hussain,

Manzoor A. Banday, Naveed A. Chikan, S. Bilal and Sheikh Aejaz

Association between p16, hMLH1 and E-cadherin promoter hypermethylation and

intake of local hot salted tea and sundried foods in gastric tumors in Kashmiri

population. Asian Pacific J Cancer Prev, 2012;13,

http://www.ncbi.nlm.nih.gov/pubmed/22502664

Hussain I, ul Rehman S, Afroze D, Zahoor L, Abdullah S, Hafiz A, Shah ZA, Iqbal S,

Shaffi M, Das BC, Siddiqi MA.

Mutational spectrum of conserved regions of TP53 and PTEN genes in Kangri cancer

(of the skin) in the Kashmiri population.

Mutat Res. 2009 May 31;676(1-2):5-10.

http://www.ncbi.nlm.nih.gov/pubmed/19486858

BOOKS PUBLISHED

Sheikh Mohd Shaffi

Analysis of TP53 & promoter hypermethylation of MGMT in lung cancer

Lambert Academic Publishing (2011-08-24)

ISBN-13; 978-3-8454-3936-5

EAN; 978**********

Language; English

https://www.morebooks.de/store/gb/book/analysis-of-tp53-and-promoter-

hypermethylation-of-mgmt-in-lung-cancer/isbn/978-3-8454-3936-5

TECHNICAL EXPERTISE

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DNA/RNA Isolation and Purification from bacteria and mammalian systems

Isolation of DNA from formalin-fixed, paraffin embedded tissue, blood, serum and

plasma

Different versions of PCR including RT-PCR,MS-PCR

Single-Strand Conformational Polymorphism (SSCP) and Heteroduplex analysis

Western Blotting

RFLP

ELISA

Protein isolation and purification techniques

Eletrophoretic and chromatographic techniques

Basic Biochemical tests and working knowledge of fully automatic biochemistry

analysers

Blood gases analysis, electrolytes, CBC, Biochemistry baseline tests etc.

RESEARCH BACKGROUND

My PhD work was on ‘Molecular analysis of TP53 gene and promoter

hypermethylation of MGMT gene in lung cancer patients of Kashmir valley”.

Lung cancer is the second most common type of cancer in Kashmiri people. Since there

was no molecular data available on these regional people, made me interested to study the

most commonly altered gene (TP53) in lung cancer patients of this population.

In case of TP53, I studied the mutational spectrum of DNA Binding Domain of this gene

using PCR-SSCP followed by sequencing. The expression level of TP53 at mRNA level

was checked by using Semi-quantitative PCR. MGMT promoter hypermethylation has

been related to the type of mutational spectrum of TP53 gene, this became my obvious

choice to study along with TP53

MGMT encodes O-6-methylguanine-DNA methyltransferase, an enzyme involved in

DNA repair. This enzyme removes alkylating lesions at the O6 of guanine residues. This

can undermine cancer therapy using alkylating agents,and thus inhibitors of MGMT

activity are of interest in cancer research.The promoter hypermethylation of MGMT was

studied by using Bisulfite modification and Methylation specific PCR and results were

confirmed by restriction digestion.

The findings indicated that in Kashmiri population other than tobacco smoke carcinogens,

there are some other mutagens involved in the carcinogenesis of lung cancer (via TP53

route). Among the different variables studied, TP53 mutations were associated with

occupational category comprising of farmers with a history of pesticide exposure. Since

pesticides have already been considered as lung cancer carcinogen, I postulate a role for

this exposure for the unique TP53 mutational spectrum in this population.

Individual susceptibility to a particular cancer in an identical environmental exposure has

been a subject of curiosity in the scientific community. It is said that host factors,

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including polymorphism of genes involved in the carcinogenesis may account for the

difference. So my goal was to study the controversial role of Arg72Pro polymorphism

using PCR-RFLP methodology in lung cancer susceptibility of Kashmiri population. The

results confirmed that Pro variant is associated with the risk of lung cancer in this

population, supporting the findings of a recent meta-analysis wherein it has been

demonstrated that that Asians with Pro allele show a higher risk of lung cancer than those

with Arg allele. Besides, I found that Pro allele variant is a risk factor for developing lung

cancer in farmers with positive pesticide exposure. It is possible that pesticide

carcinogens might be interacting with Pro allele and increasing the lung cancer risk in

Kashmiri people. I also studied polymorphism at codon 47 of TP53 gene but found only

Pro homozygous alleles in all studied subjects, indicating that the other variants at this

position could be rare.

In recent years, cancer has begun to be understood not only as a genetic disease, but also

as an epigenetic one. The genetic and epigenetic pathways are not isolated, but rather

there is a complex network of connections between the two. The epigenetic silencing of

MGMT gene is an example of how abnormal methylation may lead to increased rates of

mutation. Alkylation of DNA at O6 position of guanine is an important step in the

formation of mutations in cancers, primarily because of the tendency of O 6-

methylguanine to pair with thymine during replication, resulting in conversion of

G:C A:T in DNA, which thus made me eager to study the promoter methylation of

MGMT gene by using Bisulfite modification and Methylation specific PCR. Theresults

were confirmed by doing restriction digestion and it was seen that MGMT methylation

was strongly associated with risk of lung cancer in patients with pesticide exposure which

further strengthened the basis for my postulation of the etio-pathogenetic role of pesticide

exposure in lung carcinogenesis in this part of the world.

Besides,I also found that MGMT promoter methylation is associated with TP53 mutation

spectrum, especially in those with G:C A:T type of transition mutation in our study

population, an effect found to be more pronounced in smokers and in those with

squamous cell carcinoma type of lung cancer.

Further, I have also been a part of other studies in our lab, like colorectal cancer ( TP53

mutations), Kangri cancer, a type of skin cancer (TP53 and PTEN mutations), esophageal

cancer (MGMT) and epidemiology and promoter hypermethylation of some of the

representative genes in gastric cancer.

RESEARCH INTERESTS

To study the molecular mechanisms of cancer development

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To study the genetic and epigenetic alterations associated with cancer

To study the human diseases in order to understand their etiology, diagnosis

and treatment

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