PhD Scientific Days 2025
Budapest, 7-9 July 2025
Poster Session III. - K: Theoretical and Translational Medicine
Pathological Role of Fibrin(ogen) in the Tumor Microenvironment under modulated Electro-Hyperthermia (mEHT) Treatment in a Triple Negative Breast Cancer (TNBC) Mouse Model.
Előadó neve
Al-murshidy Hakim Bahlok Jebur, MSc
Neptun code
A6EE9U
Előadó munkahelye
Institute of Translational Medicine, Semmelweis University.
Előadó telefonszáma
+36704235632
Előadó e-mail címe
Hakim.al@phd.semmelweis.hu
Az előadás címe
Pathological Role of Fibrin(ogen) in the Tumor Microenvironment under modulated Electro-Hyperthermia (mEHT) Treatment in a Triple Negative Breast Cancer (TNBC) Mouse Model.
Szerző(k) neve és munkahelye
Hakim Bahlok Jebur Al-murshidy1, Dániel Bócsi1, Mohamed I. Elsalahaty1, Qusay O. Abdalla1, Yibo Go1, Zoltán Koós1, Eslam Abdalalem1, Pedro Henrique Leroy Viana1, Csaba András Schvarcz1
1: Semmelweis University, Institute of Translational Medicine, 1094 Budapest, Tűzoltó u. 37-47.
Bemutatás módja
Poszter
Szekció
Poster Session III. - K: Theoretical and Translational Medicine
Language of the presentation
English
Preferred session
Theoretical and Translational Medicine
Összefoglaló szövege
Introduction: Effective therapy of triple-negative breast cancer (TNBC) has not yet been achieved. mEHT is a novel therapeutic approach based on selective heating and energy transfer to the tumor tissue using an electromagnetic field. mEHT induces tumor cell stress and may elicit a protective response within the tumor microenvironment (TME). Fibrinogen may play a non-canonical role when locally produced by cancer cells, particularly during mEHT treatment, potentially influencing the TME in distinct ways. Fibrinogen interacts with the integrin receptor αMβ2 (Mac-1) on myeloid cells, leads to leukocyte adhesion, migration, and the production of pro-inflammatory cytokines within TME.
Aim: To investigate how mEHT modulates fibrin(ogen) expression and its impact on inflammation and immune cell recruitment in the TNBC TME.
Methods: We analyzed transcriptomic data acquired from a previous murine TNBC model following mEHT treatment. Mouse TNBC 4T1 cells were inoculated orthotopically into female BALB/c mice. Tumor growth was measured by digital caliper and ultrasound. Expression of fibrinogen subunit genes (Fga, Fgb, Fgg) and inflammation-associated genes were assessed. qPCR validation of fibrinogen-related and inflammatory gene expression is in progress.
Result: qPCR validation of fibrinogen-related and inflammatory genes is currently underway. It is anticipated that repeated mEHT treatment will lead to a marked upregulation of stress-associated genes such as FGG, FGB, and FGA. Correspondingly, increased expression of inflammatory markers like Il-6 and Itgam1 (CD11b) is also expected in mEHT-treated tumors. These findings would support the idea that while mEHT exerts therapeutic pressure on tumors, it may also trigger a stress response that increases fibrinogen and pro-inflammatory factors in the tumor microenvironment.
Conclusion: It is anticipated that mEHT treatment will not only suppress tumor growth and proliferation in TNBC but also induce a stress-associated transcriptional response, characterized by upregulation of fibrinogen genes (FGG, FGB, FGA) and inflammatory markers (Il-6, Itgam/CD11b). This response is expected to result in increased fibrinogen deposition and immune cell recruitment within the tumor microenvironment (TME), potentially contributing to extracellular matrix remodeling and tumor adaptation.
Funding: SE250-2025-109.
University
Semmelweis University
Supervisor
Dr. Hamar Péter
Publication of my abstract
I give consent to the publication of my abstract on the website of the congress.
phd.section.field
in doctoral studies before complex exam (PhD)
Kind
Szabad
Status
elfogadva
Accepted presentation method
poszter
Előadás fájl jóváhagyás
nem rendelkezett róla
Előadó
9167
Start
14:48
End
14:54