PhD Scientific Days 2025

Poster Session II. - B: Molecular Medicine

Genetic deficiency of Syk in platelets promotes solid tumor metastasis

Előadó neve

Ms. Sándor Luca

Neptun code

eij2nn

Előadó munkahelye

Department of Physiology

Előadó telefonszáma

+36301817993

Előadó e-mail címe

sandor.luca@phd.semmelweis.hu

Az előadás címe

Genetic deficiency of Syk in platelets promotes solid tumor metastasis

Szerző(k) neve és munkahelye

Luca Sándor¹

1: Department of Physiology

Bemutatás módja

Poszter

Szekció

Poster Session II. - B: Molecular Medicine

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Background: Spleen tyrosine kinase (Syk) is predominantly expressed in hematopoietic cells and plays a key role in B cell receptor, Fc receptor, and integrin signaling. Syk inhibitors have shown promise in clinical trials for hematological malignancies, such as chronic lymphoid leukemia, and are currently being explored for solid tumors. Beyond their classical role in hemostasis, platelets are increasingly implicated in cancer progression, including metastasis. However, the molecular mechanisms by which platelets influence metastasis, particularly via Syk, remain poorly understood.
Aims: This study investigates the role of platelet Syk in the formation of metastases by solid tumors using both pharmacological inhibitors and genetic models.
Methods: B16F10 malignant melanoma cells were injected intradermally or intravenously into C57Bl/6 mice. Syk inhibitors—fostamatinib (R788), entospletinib (GS-9973), and lanraplenib (GS-9876)—were administered orally or intraperitoneally. To selectively delete Syk in platelets, Pf4-Cre transgenic mice were crossed with Syk-floxed mice, generating platelet-specific Syk-deficient (SykΔPLT) mice. Primary tumor growth was monitored using caliper measurements. Lung metastases were quantified histologically following tissue collection.
Results: Pharmacological inhibition of Syk in wild-type mice resulted in significantly increased lung metastasis formation, with no effect on primary tumor growth. Similarly, SykΔPLT mice exhibited a substantial increase in melanin-rich metastatic lung deposits compared to wild-type controls. These results suggest that Syk in platelets plays a suppressive role in metastatic dissemination of melanoma cells.
Conclusions: Our findings reveal a critical function of platelet Syk in preventing metastasis of solid tumors. Understanding this pathway may enhance the safety and efficacy evaluation of Syk inhibitors, particularly when repurposed for non-hematological malignancies or used in patients with autoimmune conditions. Future studies will focus on the molecular mechanisms underlying Syk-dependent platelet functions during metastasis.
Funds: Semmelweis University

University

Semmelweis University

Supervisor

Dr. Győri Dávid Sándor

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8038

Start

18:48

End

18:54