Molecular mechanisms in metastasis of solid tumors

Metastasis occurs when cancer cells spread from the primary tumor site to other parts of the body, leading to the formation of secondary tumors. Metastasized cancer cells are more difficult to treat, resulting in decreased chances of survival. Understanding the mechanisms of metastasis is crucial for developing effective cancer treatments to prevent or treat metastatic disease. Identifying molecular targets and pathways involved in metastasis will also help develop new diagnostic and prognostic tools and targeted therapies, improving patient outcomes.

The most widely accepted mechanism explaining metastasis in cancer is EMT, but other mechanisms, including BMW, have recently been proposed. Recent research suggests that metastasis is a byproduct of stress-coping mechanisms facilitated by cancer-fitness genes. These genes enable the survival of metastatic cancer cells under stress during dissemination and colonization in distant organs. They are distinct from the classical driver oncogenes. Other factors, such as innate immunity, the tumor microenvironment, and hypoxia, may also play a pivotal role in the origin of metastasis.

Intended learning outcomes:
This project aims to familiarize the student with traditional and up-to-date molecular mechanisms involved in metastasis, and to allow the student to predict relevant differences between these mechanisms.
The intended learning outcomes of this research activity are:
1. To define the molecular mechanisms and genes involved in cancer metastasis.
2. To discuss the differences between these mechanisms including: a) onset time, b) role of microenviroment, c) role of hypoxia, d) genes involved.
3. To produce a database with genes involved in each mechanism involved in cancer metastasis.
4. To hypothesize the relationships between the genes for each of the mechanisms involved in metastasis.
5. To predict differences in gene expression in each of the mechanisms proposed.
6. To test the predicted differences in cell lines derived from primary tumor and metastasis.
7. To discuss how these mechanisms change in the onset and progression of metastasis.

Handledare: Oscar Bedoya Reina

E-post: oscar.bedoya-reina@oru.se

Telefon: 076-934 93 58

Etiktillstånd behövs inte

Termin 6 och 10

Typ av arbete: Modellering (AI - bioinformatik - sytembiologi), Systematisk litteraturstudie

Geografiskt område: Inte geografiskt avgränsat