Ekspresija gena IL1B i CXCR4 kod EGFR-pozitivnog karcinoma pluća nemalih stanica

master's thesis

• Title (english): The expression of IL1B and CXCR4 genes in EGFR-positive non-small cell lung cancer
• Author: Jelena Vojvodić
• Mentor: Petra Korać (mentor)
• Mentor: Paula Gršković (komentor)
• Committee member: Petra Korać (predsjednik povjerenstva)
• Committee member: Inga Urlić (član povjerenstva)
• Committee member: Željka Vidaković-Cifrek (član povjerenstva)
• Committee member: Nenad Malenica (član povjerenstva)
• Granter: University of Zagreb; Faculty of Science; (Department of Biology); Zagreb
• Defense date and country: 2024-02-02, Croatia
• Scientific / art field, discipline and subdiscipline: NATURAL SCIENCES; Biology

Abstract

Karcinom pluća vodeći je uzrok smrtnosti povezane s tumorima u svijetu. Ovisno o molekularnim
karakteristikama, karcinom pluća dijeli se na podtipove, a njihova precizna karakterizacija nužna
je za primjenu ciljane, što efikasnije terapije. Za jedan od podtipova karcinoma pluća nemalih
stanica, adenokarcinom, osobito je važna mutacija gena EGFR. Vodeća mutacija u genu za receptor
epidermnog faktora rasta definira podtip karcinoma pluća, a povezana je i s promjenama u
tumorskom mikrookolišu. Interakcija stanica tumorskog mikrookoliša putem brojnih signalnih
molekula ključna je za imunosni odgovor organizma na tumor, a uključena je i u odgovor na
terapiju. U ovom radu istražena je ekspresija interleukina-1β i kemokina CXCR4 koji su dio
imunosnog odgovora kod pacijenata s karcinomom pluća. Kako bi se utvrdila potencijalna
povezanost između ekspresije gena IL1B, koji kodira proupalni citokin interleukin-1β, i gena
CXCR4, koji kodira kemokinski receptor 4, s mutacijom u genu EGFR, izolirana je RNA iz uzoraka
karcinoma pluća nemalih stanica koji ima mutaciju gena EGFR, provedena je reverzna
transkripcija te je lančanom reakcijom polimerazom u stvarnom vremenu utvrđena razina
ekspresije tih dvaju gena. Dobiveni podaci uspoređeni su s podacima za karcinom pluća nemalih
stanica koji nema mutaciju gena EGFR i pokazano je da je ekspresija gena IL1B i CXCR4 statistički
značajno niža kod tumora s mutacijom.

Abstract (english)

Lung cancer is the leading cause of cancer-related mortality worldwide. There are several subtypes
of lung cancer, depending on molecular characteristics, which must be precisely characterized to
apply targeted, most efficient possible therapy. Adenocarcinoma, one of the subtypes of non-small
cell lung cancer, is often characterized by the mutation of the EGFR gene. This driver mutation in
the epidermal growth factor not only defines a specific subtype of cancer but is also associated with
specific changes in the tumor microenvironment. Cells of the tumor microenvironment
communicate through an intricate net of signaling molecules which is crucial for the body’s
immune response to the tumor and the tumor’s response to therapy. In this thesis, the expression
of interleukin 1β and chemokine CXCR4, both part of the immune response, is investigated. To
determine a potential association between their expression and the EGFR gene mutation, RNA was
isolated from non-small cell lung cancer samples, reversely transcribed into cDNA with which
polymerase chain reaction in real time was performed. Expression levels of these genes were also
compared to the data for non-small cell lung cancer lacking the EGFR mutation. It was shown that
the expression of the IL1B and CXCR4 genes is significantly lower in the tumors with the EGFR
gene mutation.

• Keywords: epidermni faktor rasta; tumorski mikrookoliš; imunosni odgovor
• Keywords (english): epidermal growth factor; tumor microenvironment; immune response
• Language: croatian
• URN:NBN: urn:nbn:hr:217:577767
• Study programme: Title: Molecular Biology-University graduate programme; Study programme type: university; Study level: graduate; Academic / professional title: sveučilišni/a magistar/magistra molekularne biologije (sveučilišni/a magistar/magistra molekularne biologije)
• Type of resource: Text
• File origin: Born digital
• Access conditions: Embargoed access; Embargo expiration date: 2026-02-02
• Created on: 2024-02-27 11:49:18