Lecture

DNA Damage Response and Tumor Suppressor Genes

Graph Chat

Chat with Graph Search

Ask any question about EPFL courses, lectures, exercises, research, news, etc. or try the example questions below.

DISCLAIMER: The Graph Chatbot is not programmed to provide explicit or categorical answers to your questions. Rather, it transforms your questions into API requests that are distributed across the various IT services officially administered by EPFL. Its purpose is solely to collect and recommend relevant references to content that you can explore to help you answer your questions.

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 role of P53 in cancer, distinguishing between driver and passenger mutations, testing mutant genes, and identifying proteins involved in DNA damage response. It also explores the consequences of DNA damage during the cell cycle, the function of tumor suppressor genes like ARF and ATR, and the experimental approaches to study mutated P53. The instructor discusses methods such as complementation experiments, electromobility shift assays, and RNA-seq to understand the effects of mutations on P53 and other tumor suppressor genes.

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)

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.

Mutation

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA (such as pyrimidine dimers caused by exposure to ultraviolet radiation), which then may undergo error-prone repair (especially microhomology-mediated end joining), cause an error during other forms of repair, or cause an error during replication (translesion synthesis).

P53

p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates, where they prevent cancer formation. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene.

Somatic evolution in cancer

Somatic evolution is the accumulation of mutations and epimutations in somatic cells (the cells of a body, as opposed to germ plasm and stem cells) during a lifetime, and the effects of those mutations and epimutations on the fitness of those cells. This evolutionary process has first been shown by the studies of Bert Vogelstein in colon cancer. Somatic evolution is important in the process of aging as well as the development of some diseases, including cancer. Cells in pre-malignant and malignant neoplasms (tumors) evolve by natural selection.

Cell cycle

The cell cycle, or cell-division cycle, is the series of events that take place in a cell that causes it to divide into two daughter cells. These events include the duplication of its DNA (DNA replication) and some of its organelles, and subsequently the partitioning of its cytoplasm, chromosomes and other components into two daughter cells in a process called cell division. In cells with nuclei (eukaryotes, i.e., animal, plant, fungal, and protist cells), the cell cycle is divided into two main stages: interphase and the mitotic (M) phase (including mitosis and cytokinesis).

Related lectures (50)

Cancer Biology: p53 and DNA Repair

Explores p53's pivotal role in cellular stability, DNA repair, and tumor suppression, emphasizing TP53 mutations and DNA double-strand break repair mechanisms.

Cancer Biology: Hallmarks and Mechanisms

Covers the hallmarks of cancer, oncogenes, tumor suppressor genes, metastasis, and genetic alterations driving tumorigenesis.

Mutations and Cancer: The Role of P53 and HPV

Covers mutations, the role of P53 in cancer, and HPV's impact on tumorigenesis.

DNA Replication: Practical Applications and Errors

Explores practical applications of DNA replication, including PCR techniques and forensic analysis.

Evading Growth Suppression: TGFB Signaling

Explores how cells evade growth suppression, focusing on TGFB signaling and the role of tumor suppressors like PTEN and p53.

Related concepts (32)

Tumor suppressor gene

Mutation

P53

Somatic evolution in cancer

Cell cycle