Florian Markowetz | |
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Alma mater | Heidelberg University, Free University of Berlin |
Scientific career | |
Institutions | Cancer Research UK Cambridge Institute, University of Cambridge, Tailor Bio |
Thesis | (2006) |
Website | www |
Florian Markowetz is the Professor of Computational Oncology at the University of Cambridge. [1] He is a Senior Group Leader at the Cancer Research UK Cambridge Institute and Director and co-founder of Tailor Bio, a genomics company aiming to improve precision medicine for cancers with high levels of chromosomal instability. [2] [3]
Markowetz has degrees in Mathematics and Philosophy from Heidelberg University and completed his PhD in Computational Biology from the Free University of Berlin, for which he was awarded an Otto-Hahn Medal by the Max Planck Society. [4]
Markowetz's research combines machine learning and artificial intelligence with experimental techniques ranging from single cell sequencing to tissue imaging to understand the mechanisms behind chromosomal instability; how to target cancer weaknesses with therapies; how to overcome resistance to treatment; and how to improve the early detection of cancer.
His team have developed a compendium of 17 copy number signatures characterising different types of chromosomal instability. These chromosomal instability signatures were able to predict how tumours might respond to drugs, as well as helping in the identification of future drug targets. [5] [6] [7] [8] [9] [10] This research has led to the formation of Tailor Bio, a genomics company which aims to build a new pan-cancer precision medicine platform. [11]
Markowetz's research has created artificial intelligence approaches to analyse data from the Cytosponge, a minimally invasive device to detect a precursor of oesophageal cancer. This work automates labour-intensive tasks and refines pathology biomarkers to identify the patients at the highest risk of developing cancer. [12] [13] [14]
In 2016, Professor Markowetz was awarded the Future Leaders in Cancer Research Prize by Cancer Research UK. He was commended for his collaborative approach to research and his role as a champion of open science. [15]
Professor Markowetz received the Royal Society Wolfson Research Merit Award in 2017. [16]
Metastasis is a pathogenic agent's spread from an initial or primary site to a different or secondary site within the host's body; the term is typically used when referring to metastasis by a cancerous tumor. The newly pathological sites, then, are metastases (mets). It is generally distinguished from cancer invasion, which is the direct extension and penetration by cancer cells into neighboring tissues.
Breast cancer type 1 susceptibility protein is a protein that in humans is encoded by the BRCA1 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 and is responsible for repairing DNA.
Twist-related protein 1 (TWIST1) also known as class A basic helix–loop–helix protein 38 (bHLHa38) is a basic helix-loop-helix transcription factor that in humans is encoded by the TWIST1 gene.
Microsatellite instability (MSI) is the condition of genetic hypermutability that results from impaired DNA mismatch repair (MMR). The presence of MSI represents phenotypic evidence that MMR is not functioning normally.
Suppressor of tumorigenicity protein 7 is a protein that in humans is encoded by the ST7 gene. ST7 orthologs have been identified in all mammals for which complete genome data are available.
WAP four-disulfide core domain protein 2 - also known as Human Epididymis Protein 4 (HE4) - is a protein that in humans is encoded by the WFDC2 gene.
CDKN2A, also known as cyclin-dependent kinase inhibitor 2A, is a gene which in humans is located at chromosome 9, band p21.3. It is ubiquitously expressed in many tissues and cell types. The gene codes for two proteins, including the INK4 family member p16 and p14arf. Both act as tumor suppressors by regulating the cell cycle. p16 inhibits cyclin dependent kinases 4 and 6 and thereby activates the retinoblastoma (Rb) family of proteins, which block traversal from G1 to S-phase. p14ARF activates the p53 tumor suppressor. Somatic mutations of CDKN2A are common in the majority of human cancers, with estimates that CDKN2A is the second most commonly inactivated gene in cancer after p53. Germline mutations of CDKN2A are associated with familial melanoma, glioblastoma and pancreatic cancer. The CDKN2A gene also contains one of 27 SNPs associated with increased risk of coronary artery disease.
Dynein light chain roadblock-type 1 is a protein that in humans is encoded by the DYNLRB1 gene.
PIN2/TERF1-interacting telomerase inhibitor 1, also known as PINX1, is a human gene. PINX1 is also known as PIN2 interacting protein 1. PINX1 is a telomerase inhibitor and a possible tumor suppressor.
Eukaryotic translation initiation factor 5A-2 is a protein that in humans is encoded by the EIF5A2 gene.
Mitotic catastrophe has been defined as either a cellular mechanism to prevent potentially cancerous cells from proliferating or as a mode of cellular death that occurs following improper cell cycle progression or entrance. Mitotic catastrophe can be induced by prolonged activation of the spindle assembly checkpoint, errors in mitosis, or DNA damage and functioned to prevent genomic instability. It is a mechanism that is being researched as a potential therapeutic target in cancers, and numerous approved therapeutics induce mitotic catastrophe.
Alan D. D'Andrea is an American cancer researcher and the Fuller American Cancer Society Professor of Radiation Oncology at Harvard Medical School. D'Andrea's research at the Dana Farber Cancer Institute focuses on chromosome instability and cancer susceptibility. He is currently the director of the Center for DNA Damage and Repair and the director of the Susan F. Smith Center for Women's Cancer.
A hereditary cancer syndrome is a genetic disorder in which inherited genetic mutations in one or more genes predispose the affected individuals to the development of cancer and may also cause early onset of these cancers. Hereditary cancer syndromes often show not only a high lifetime risk of developing cancer, but also the development of multiple independent primary tumors.
Chromosomal instability (CIN) is a type of genomic instability in which chromosomes are unstable, such that either whole chromosomes or parts of chromosomes are duplicated or deleted. More specifically, CIN refers to the increase in rate of addition or loss of entire chromosomes or sections of them. The unequal distribution of DNA to daughter cells upon mitosis results in a failure to maintain euploidy leading to aneuploidy. In other words, the daughter cells do not have the same number of chromosomes as the cell they originated from. Chromosomal instability is the most common form of genetic instability and cause of aneuploidy.
High-grade serous carcinoma (HGSC) is a type of tumour that arises from the serous epithelial layer in the abdominopelvic cavity and is mainly found in the ovary. HGSCs make up the majority of ovarian cancer cases and have the lowest survival rates. HGSC is distinct from low-grade serous carcinoma (LGSC) which arises from ovarian tissue, is less aggressive and is present in stage I ovarian cancer where tumours are localised to the ovary.
Xin Lu is a Professor of Cancer Biology and Director of the Ludwig Institute for Cancer Research at the University of Oxford. She is known for her discovery of and research on the ASPP family of proteins.
Professor James D Brenton is a clinician scientist and Senior Group Leader at the Cancer Research UK Cambridge Institute and Professor of Ovarian Cancer Medicine in the Department of Oncology, University of Cambridge. He is an Honorary Consultant in Medical Oncology at Addenbrooke's Hospital, Cambridge University Hospitals, Ovarian Cancer Domain Lead for the 100,000 Genomes Project by Genomics England, and co-founder and Clinical Advisor to Inivata Ltd, a clinical cancer genomics company.
George Coukos is a physician-scientist in tumor immunology, professor and director of the Ludwig Cancer Research Lausanne Branch and director of the Department of oncology UNIL-CHUV of the University of Lausanne and the Lausanne University Hospital in Lausanne, Switzerland. He is known for his work on the mechanisms by which tumors suppress anti-cancer immune responses, and the role of the tumor vasculature in that suppression. In addition to his work in ovarian cancer, the combinatorial immune therapies proposed by Professor Coukos have been successfully tested and approved for lung, liver and kidney cancers.
Nissim Benvenisty is Professor of Genetics, the Herbert Cohn Chair in Cancer Research and the Director of “The Azrieli Center for Stem Cells and Genetic Research” at the Alexander Silberman Institute of Life Sciences, Hebrew University.
Nitzan Rosenfeld is a professor of Cancer Diagnostics at the University of Cambridge. He is a Senior Group Leader at the Cancer Research UK Cambridge Institute and co-founder of Inivata, a clinical cancer genomics company.