Lecture

Cancer Biology: p53 and DNA Repair

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 delves into the role of p53 as the 'Master Guardian' in cellular and genetic stability, focusing on its functions in DNA damage response, cell cycle regulation, and apoptosis. The prevalence and impact of TP53 mutations in various tumors are discussed, along with the mechanisms of missense mutations in the DNA-binding domain. The lecture also covers the classification of oncogenes and tumor suppressor genes based on mutation patterns, as well as the repair mechanisms for DNA double-strand breaks. Key concepts include the synthetic lethality concept and the sensitivity of BRCA-deficient cells to PARP inhibitors.

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.

BRCA1

Breast cancer type 1 susceptibility protein is a protein that in humans is encoded by the BRCA1 (ˌbrækəˈwʌn) gene. Orthologs are common in other vertebrate species, whereas invertebrate genomes may encode a more distantly related gene. BRCA1 is a human tumor suppressor gene (also known as a caretaker gene) and is responsible for repairing DNA. BRCA1 and BRCA2 are unrelated proteins, but both are normally expressed in the cells of breast and other tissue, where they help repair damaged DNA, or destroy cells if DNA cannot be repaired.

Germline mutation

A germline mutation, or germinal mutation, is any detectable variation within germ cells (cells that, when fully developed, become sperm and ova). Mutations in these cells are the only mutations that can be passed on to offspring, when either a mutated sperm or oocyte come together to form a zygote. After this fertilization event occurs, germ cells divide rapidly to produce all of the cells in the body, causing this mutation to be present in every somatic and germline cell in the offspring; this is also known as a constitutional mutation.

Missense mutation

In genetics, a missense mutation is a point mutation in which a single nucleotide change results in a codon that codes for a different amino acid. It is a type of nonsynonymous substitution. Missense mutation refers to a change in one amino acid in a protein, arising from a point mutation in a single nucleotide. Missense mutation is a type of nonsynonymous substitution in a DNA sequence.

Related lectures (64)

DNA Repair Mechanisms

Explores DNA repair mechanisms, DNA damage response, and synthetic lethality in cancer.

Mutations and Cancer: The Role of P53 and HPV

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

Cancer Biology: Hallmarks and Mechanisms

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

Cancer Biology: Base Excision Repair

Covers cancer biology topics on base excision repair, cellular responses to DNA damage, p53 regulation, and apoptosis mechanisms.

DNA Damage Response and Tumor Suppressor Genes