Hamar Balázs

Dr. Hamar Balázs

orcid

Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 April 2023 in International Journal of Gynecology & Obstetrics
Verified
Journal Article
Open access
HBHamar Balázs
Hamar Balázs
BTBrigitta Teutsch
Brigitta Teutsch
EHEszter Hoffmann
Eszter Hoffmann
PHPéter Hegyi
Péter Hegyi
AVAlex Váradi
Alex Váradi
ZMZsolt Melczer
Zsolt Melczer
Background: Trichomonas vaginalis infection is the most prevalent non‐viral sexually transmitted infection (STI) in women and has been suggested as a risk factor for developing cervical cancer.Objective: We aimed to investigate the associations between T. vaginalis infection and cervical carcinogenesis.Search Strategy: A comprehensive systematic search was conducted in five databases on 21 October 2021.Selection Criteria: Studies assessing the relationship between T. vaginalis infection, HPV co‐infections, cervical dysplasia, and cervical cancer were found eligible.Data Collection and Analysis: Summary estimates for pooled odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated with a random‐effects model. Statistical heterogeneity was measured with I2 and Cochran's Q tests.Main Results: The 29 articles included 473 740 women, of whom 8518 were T. vaginalis‐positive. Our results showed that T. vaginalis‐infected women had 1.79 times higher odds of being diagnosed with HPV co‐infection (95% CI 1.27–2.53; I2 95%). We also found that T. vaginalis infection was associated with high‐grade squamous intraepithelial lesion diagnosis (OR 2.34, 95% CI 1.10–4.95; I2 75%) and cervical cancer (OR 5.23, 95% CI 3.03–9.04; I2 3%).Conclusions: Our results showed an association between T. vaginalis and cervical carcinogenesis in sexually active women.

22 April 2024 in Cancers
Verified
Journal Article
Open access
PDF file
HBHamar Balázs
Hamar Balázs
BTBrigitta Teutsch
Brigitta Teutsch
EHEszter Hoffmann
Eszter Hoffmann
Peter HegyiPeter Hegyi
Peter Hegyi
AHAndrea Harnos
Andrea Harnos
ZMZsolt Melczer
Zsolt Melczer
Introduction: Topical Imiquimod is an immune response modifier approved for the off-label use of vulvar intraepithelial neoplasia. We conducted this systematic review and meta-analysis to investigate the efficacy and safety of Imiquimod in treating cervical intraepithelial neoplasia (CIN) and human papillomavirus (HPV)-positive patients. Methods: The study was prospectively registered (CRD420222870) and involved a comprehensive systematic search of five medical databases on 10 October 2022. We included articles that assessed the use of Imiquimod in cervical dysplasia and HPV-positive patients. Pooled proportions, risk ratios (RRs), and corresponding 95% confidence intervals (CIs) were calculated using a random effects model to generate summary estimates. Statistical heterogeneity was assessed using I2 tested by the Cochran Q tests. Results: Eight articles reported on 398 patients who received Imiquimod out of 672 patients. Among CIN-2–3 patients, we observed a pooled regression rate of 61% (CI: 0.46–0.75; I2: 77%). When compared, Imiquimod was inferior to conization (RR: 0.62; CI: 0.42–0.92; I2: 64%). The HPV clearance rate in women who completed Imiquimod treatment was 60% (CI: 0.31–0.81; I2: 57%). The majority of side effects reported were mild to moderate in severity. Conclusions: Our findings indicate that topical Imiquimod is safe and effective in reducing cervical intraepithelial neoplasia and promoting HPV clearance. However, it was found to be inferior compared to conization. Imiquimod could be considered a potential medication for high-grade CIN patients and should be incorporated into guidelines for treating cervical dysplasia.

7 July 2026 in Frontiers in Toxicology
Verified
Journal Article
Open access
PDF file
BCBernadett Csókay
Bernadett Csókay
EREszter Ruff
Eszter Ruff
ZSZsuzsanna Szőke
Zsuzsanna Szőke
LSLevente Sára
Levente Sára
BKBalázs Komoróczy
Balázs Komoróczy
HBHamar Balázs
Hamar Balázs
Background: Mycotoxins are widespread food contaminants that pose a significant global health concern. While their hepatotoxic, nephrotoxic, and carcinogenic effects are well established and characterized, their effects on adipose tissue biology and systemic lipid regulation remain incompletely understood. Given adipose tissue’s central role in lipid homeostasis, endocrine regulation, and as a storage reservoir for adipophilic compounds, understanding these effects is critical. Methods: This systematic review was conducted in accordance with the PRISMA 2020 guidelines, and prospectively registered to PROSPERO (CRD42022287044). A comprehensive literature search was conducted in CENTRAL, Embase, and MEDLINE (PubMed) through 16 January 2026. Experimental in vivo and in vitro studies examining the effects of mycotoxins on adipose tissue, lipid metabolism, or mycotoxin distribution in fat tissue were included. Risk of bias in animal studies was assessed using the SYRCLE Risk of Bias Tool. A descriptive qualitative synthesis was performed. Results: Twenty-one experimental studies met the inclusion criteria. Across animal models, mycotoxin exposure consistently disrupted lipid homeostasis, leading to elevated serum triglyceride, cholesterol, LDL, and VLDL levels, alongside reduced HDL concentrations. These effects were mediated through toxin-specific mechanisms, including inhibition of ppar α signaling by aflatoxins and ochratoxin, suppression of pparγ by deoxynivalenol, and activation of pparγ by zearalenone. Mycotoxins also impaired adipokine secretion, with reduced leptin and adiponectin levels, and were associated with insulin resistance and altered glucose metabolism. Importantly, although mycotoxins are primarily metabolized in the liver, multiple studies demonstrated substantial accumulation and prolonged retention in adipose tissue, suggesting a secondary toxicokinetic reservoir. Conclusion: Mycotoxins exert significant, toxin-specific effects on lipid metabolism and adipose tissue function and may contribute to cardiometabolic dysfunction. Adipose tissue appears to play a key role in mycotoxin bioaccumulation, with potential implications for chronic exposure and delayed systemic toxicity.