Lecture

DNA Repair Mechanisms

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In course

BIO-471: Cancer biology I

The course covers in detail molecular mechanisms of cancer development with emphasis on cell cycle control, genome stability, oncogenes, tumor suppressor genes, signaling pathways involved in cancer, genomic cancer analysis and rational cancer therapies. ...

Description

This lecture covers the mechanisms of DNA repair, focusing on topics such as DNA double-strand breaks, homologous recombination, and the role of key proteins like p53, BRCA1, and PARP1. It discusses the impact of mutations in DNA repair genes on cancer susceptibility and explores the concept of synthetic lethality.

Instructors (3)

Joachim Lingner

PhD at the Biocenter, University of Basel 1989-1992 (Supervisor: Walter Keller). Postdoc at the Howard Hughes Medical Institute, University of Colorado at Boulder 1993-1997 (Supervisor: Thomas Cech). Junior group leader at ISREC 1997-2001. Senior group leader at ISREC since 2002. Associate Professor at EPFL 2005-2008. Full Professor at EPFL since 2009. Honors: START-fellowship from the Swiss National Science Foundation in 1997; Friedrich Miescher Prize from the Swiss Society of Biochemistry in 2002; EMBO member in 2005; ERC advanced investigator grant in 2008.

Viesturs Simanis

Viesturs Simanis was awarded a degree in Biochemistry from Imperial College London. He carried out his doctoral studies with David Lane at Imperial College, London University, and postdoctoral studies with Paul Nurse (London and Oxford). He has been a group leader at ISREC since 1988. In 2006 he was appointed Associate Professor at the EPFL School of Life Sciences

Elisa Oricchio

Expertise Cancer geneticsMouse modelsTherapyStem cellsLymphoma Teaching & PhD PhD Students Vamsi Krishna Polavarapu, Asli Ece Kasapoglu, Konstantina Georgakopoulou, Eleni Balli Past EPFL PhD Students Maria Christine Donaldson, Elena Battistello, Daniel Pereira Duarte, Frédérica Schyrr, Ruxandra-Andreea Lambuta, Aaron Simone Petruzzella, Jixing Zhong, Justine Epiney Courses Cancer biology I BIO-471 The course covers in detail molecular mechanisms of cancer development with emphasis on cell

Official source

Ontological neighbourhood

Biology

Cell biology: Cancer

Related concepts (32)

DNA repair

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in tens of thousands of individual molecular lesions per cell per day. Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell's ability to transcribe the gene that the affected DNA encodes.

Tumor suppressor gene

A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is mutated, it results in a loss or reduction in its function. In combination with other genetic mutations, this could allow the cell to grow abnormally. The loss of function for these genes may be even more significant in the development of human cancers, compared to the activation of oncogenes.

Base excision repair

Base excision repair (BER) is a cellular mechanism, studied in the fields of biochemistry and genetics, that repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs bulky helix-distorting lesions. BER is important for removing damaged bases that could otherwise cause mutations by mispairing or lead to breaks in DNA during replication.

Genetic recombination

Genetic recombination (also known as genetic reshuffling) is the exchange of genetic material between different organisms which leads to production of offspring with combinations of traits that differ from those found in either parent. In eukaryotes, genetic recombination during meiosis can lead to a novel set of genetic information that can be further passed on from parents to offspring.

Oncogene

An oncogene is a gene that has the potential to cause cancer. In tumor cells, these genes are often mutated, or expressed at high levels. Most normal cells will undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered and malfunctioning. Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead. Most oncogenes began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis.

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