Public defense “Modeling the interactions between cancer cells, endothelial cells, and monocytes under flow: The driving role of oxidized LDL in cancer-associated atherosclerosis” by Mr. SCALIA Alessandro

When?
On 01 July 2026 at 12:00
Where?
Campus Plaine de Nimy - Centre Vésale - Aud. La Fontaine

Organized by

Service de Cardiologie (Stéphane Carlier)

Date and Time

Wednesday, July 1, 2026

12:00 – 17:00

(UTC+01:00) Brussels, Copenhagen, Madrid, Paris

 

About this event

Public defense of doctoral thesis for the academic degree of Doctor of Medical Sciences

Supervisor: Prof. Stéphane Carlier, Head of the Cardiology Department, UMONS

Co-supervisor: Prof. Pierre Duez, Department of Therapeutic Chemistry and Pharmacognosy, UMONS

Jury President : Prof. Fabrice Journe, Department of Oncology, UMONS

Jury Secretary : Prof. Nadège Kindt, Department of Oncology, H.U.B.

Jury Members:

  • Gabrielle Sylvain, Interfaces and Complex Fluids Laboratory
  • Fabian Demeure, Lipid Clinic and Cardiometabolic Prevention – UCL Namur University Hospital (BE)
  • Carmine Gentile, School of Biomedical Engineering – University of Technology Sydney (AUS)
  • Robert Krams, Molecular Bioengineering – Queen Mary University of London (UK)

 

Thesis Approach and Objectives

The overall objective is to explore the bidirectional pathophysiological overlap between cardiovascular diseases and cancer, demonstrating that solid tumors act as systemic drivers of atherogenesis and also the influence of oxidized lipids (oxLDL) on tumor cell behavior, covering the entire pathological continuum: from cellular impact at the level of the vascular endothelium to the evaluation of preventive phytotherapeutic interventions.

The specific objectives are as follows:

  • To determine the effect of oxLDL on the aggressiveness of head and neck squamous cell carcinomas and the expression of their specific receptors.
  • To evaluate the ability of tumor secretome from breast cancers to induce a pro-inflammatory “athero-mimetic” state on the vascular endothelium.
  • To identify the potential of compounds derived from ginger (Zingiber officinale) to block the atherosclerotic process, and to validate these adhesion mechanisms within a dynamic model reproducing blood flow.

 

Approaches and Results

The methodology used in this work consists of:

In vitro cellular and molecular models: The approach begins with the development of a standardized method for producing oxLDL, subsequently tested on head and neck cancer cell lines (HPV-positive and negative) and breast cancer cells. The analyses rely on Boyden chamber migration assays, immunofluorescence to quantify adhesion and capture receptors (LOX-1, CD36, ICAM-1, E-selectin, etc.), and Western blots to explore cell signaling pathways such as Wnt/β-catenin.
Pharmacognostic evaluation: Specific fractions of ginger extracts are tested on monocyte-derived macrophages (THP-1) exposed to oxLDL. Inhibition of lipid accumulation is measured via Oil Red O staining, coupled with analysis of cell adhesion receptor and inflammasome attenuation.
3D millifluidic tissue engineering: To validate the in vitro results under physiological conditions, a 3D millifluidic model was developed. This model incorporates endothelial cells (HUVECs) perfused under a constant flow to faithfully reproduce the shear stress present in blood vessels.

 

Results:

Experiments have revealed major pathological interactions between oncology and cardiology:
Pro-tumor impact and vascular remodeling: oxLDL promotes tumor aggressiveness by increasing the expression of scavenger receptors (LOX-1, CD36) on cancer cells, which actively absorb these lipids. Conversely, the secretome of breast cancer cells induces an athero-mimetic state on the endothelium, which drastically increases the expression of adhesion markers (ICAM-1, E-selectin, Connexin-43) and promotes monocyte recruitment. Tumor cells have also demonstrated an autonomous capacity to oxidize LDL.

Efficacy of the phytotherapeutic intervention: The study suggested that specific fractions of ginger significantly inhibit foam cell formation, reduce the expression of pro-atherogenic receptors, and block NLRP3 inflammasome activation. These results highlight the emergence of strong preventive potential in cardio-oncology.
Hemodynamic validation: Flow perfusion assays in the millifluidic model confirmed that monocytes, pre-conditioned by the cancerous environment, exhibit firm and increased adhesion to endothelial cells. This result demonstrates, both mechanistically and dynamically, that solid tumors act directly as systemic drivers in the initiation of atherosclerosis.

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