Sarıtaş, Merve

Profile URL
https://hdl.handle.net/20.500.12573/2835
Name Variants
Saritas, Merve
Job Title
Arş. Gör.
Email Address
merve.saritas@agu.edu.tr
Main Affiliation
04.02. Moleküler Biyoloji ve Genetik
Status
Current Staff
Website
ORCID ID
0000-0003-4753-9372
Scopus Author ID
57741644800
Turkish CoHE Profile ID
DA5FC00C6CD52ED7
Google Scholar ID
WoS Researcher ID
No research topics data found.

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
Research Products
ZERO HUNGER2
ZERO HUNGER
0
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
1
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QUALITY EDUCATION4
QUALITY EDUCATION
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GENDER EQUALITY5
GENDER EQUALITY
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
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DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
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INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
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REDUCED INEQUALITIES10
REDUCED INEQUALITIES
0
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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CLIMATE ACTION13
CLIMATE ACTION
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LIFE BELOW WATER14
LIFE BELOW WATER
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LIFE ON LAND15
LIFE ON LAND
0
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PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
0
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PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
0
Research Products
Documents

6

Citations

6

h-index

1

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No records found in other affiliations.
Scholarly Output

2

Articles

2

Views / Downloads

1/8

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

0

Scopus Citation Count

0

Patents

0

Projects

0

WoS Citations per Publication

0.00

Scopus Citations per Publication

0.00

Open Access Source

1

Supervised Theses

0

JournalCount
European Journal of Medical Genetics1
Immunologic Research1
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2024 - 20252

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Author of Publication: search.filters.isAuthorOfPublication.922591f3-4645-4d09-ab37-6b6f17aa9ae8

Scholarly Output Search Results

Now showing 1 - 2 of 2
  • Article
    A Novel Germline Pregnane X Receptor (PXR) Variant Predisposing to Hodgkin Lymphoma in Two Siblings
    (Elsevier, 2024-12) Khodzhaev, Khusan; Sudutan, Tugce; Erbilgin, Yucel; Saritas, Merve; Yegen, Gulcin; Bozkurt, Ceyhun; Kebudi, Rejin
    Hodgkin's lymphoma (HL) is the most common cancer in adolescents and young adults. A family history of HL increases the risk of developing HL in other family members. Identification of genetic predisposition variants in HL is important for understanding disease aetiology, prognosis, and response to treatment. Aberrant activation of the NF-kappa B pathway is a hallmark feature of HL, contributing to the survival and proliferation of the malignant cells' characteristic of HL. The family with multiple consanguineous marriages with siblings of diagnosed HL was examined by whole-exome sequencing. We found a germline homozygous variation in the PXR ligand binding domain (NM_003889.3:c.811G>A, p.(Asp271Asn)), which was classified as pathogenic by prediction tools and segregated in HL cases. Increased PXR expression was found in homozygous variant carriers compared to heterozygous carriers by quantitative real time PCR (qRT-PCR) and immunofluorescence staining of patients' formalin-fixed paraffin-embedded tissues showed upregulation of PXR, particularly in Hodgkin Reed/Sternberg (HRS) cells. Patients with homozygous PXR variant showed significantly high expression compared to PXR wild-type HL, heterozygous and controls (p = 0.0001, p = 0.0004 and p = 0.0001, respectively). PXR homozygous HRS cells had significantly higher PXR expression compared to PXR wild-type HRS cells (p < 0.0001, 3.27-fold change). Albeit PXR's prominent expression in cytoplasm of HRS cells, homozygous PXR HRS cells showed increased PXR expression in nucleus (p < 0.001). PXR is a member of the nuclear receptor superfamily and previous studies have demonstrated a pleiotropic effect of PXR on malignant transformation. Expression analysis showed that cell proliferation, apoptosis and inflammation related genes were deregulated, in homozygous PXR HL cases. This study provided clinical evidence to previously reported Sxr(-/-) mice model that develop multifocal lymphomas, had an aberrantly increased NF-kappa B expression and consistent inflammation. Further functional studies are needed to elucidate the exact mechanisms of action of PXR in HL pathogenesis.
  • Article
    Identification of Nonsense Variants in the ATM Gene Mimicking SCID Phenotype: A Brief Report
    (Springer, 2025-05-16) Firtina, Sinem; Saritas, Merve; Ng, Yuk Yin; Nepesov, Serdar; Kiykim, Ayca; Bozkurt, Selcen; Sayitoglu, Muge
    Severe combined immunodeficiency (SCID) represents a life-threatening inborn error of immunity, necessitating rapid diagnosis and intervention to prevent fatal outcomes. While SCID is characterized by profound T-cell lymphopenia, it may overlap with other conditions like ataxia-telangiectasia (AT), which also presents with T-cell deficiencies. This study examines two cases of suspected SCID in infants, later identified as AT due to pathogenic variants in the ATM gene. Despite initial negative results from SCID-targeted gene panels, further genetic testing revealed nonsense mutations (p.Y2036X and p.E1996X) in the FAT domain of the ATM gene, confirmed by Sanger sequencing. The patients exhibited significant T-cell lymphopenia and reduced ATM protein activity, indicative of AT. These findings highlight the importance of comprehensive genetic screening beyond common SCID-associated genes, especially in patients with atypical presentations. Early and accurate diagnosis can prevent mismanagement and guide appropriate therapies, improving patient outcomes.