Alberto Bardelli (born 29 November 1967) is an Italian geneticist and cancer researcher, expert in the field of precision medicine. He is a full professor of histology at the Department of Oncology, University of Turin and Scientific Director of IFOM, the AIRC Institute of Molecular Oncology.
Alberto Bardelli was born in Turin on 29 November 1967. He studied Biological Sciences at the University of Turin and received his master's degree in 1991. After graduation, he moved to the Ludwig Institute for Cancer Research in London and obtained a PhD in Biochemistry and Molecular Biology from the University College London (UCL).
From 1999 to 2004, Bardelli has been a postdoctoral researcher at the Johns Hopkins University School of Medicine and the Howard Hughes Medical Institute, Baltimore (MD/USA), in the group led by Bert Vogelstein. Here Bardelli began studying the genomics of cancer. During his postdoctoral training at Johns Hopkins, Bardelli published multiple papers in high-profile journals such as Nature and Science.
In 2004, he returned to Italy as director of a research unit dedicated to the study of tumour genomes at the Candiolo Cancer Institute and Dept. of Oncology, University of Turin.
Since 2016, he has been a full professor of histology at the University of Turin. [1] [2]
From 2018 to 2020, he served as president of the European Association for Cancer Research (EACR).
He is a member of the scientific committee of the Italian Association for Cancer Research (AIRC). [3]
In 2005, he co-founded the gene editing company Horizon Discovery.
Since April 2022, he has been the scientific director of IFOM, the AIRC Institute of Molecular Oncology, Milan.
Bardelli performed the first comprehensive mutational profile of kinases in colorectal cancers (CRC). [4] He translated these findings into clinical practice by discovering the molecular landscape of response and resistance to EGFR, [5] [6] HER2 [7] and NTRK1 [8] blockades in CRC. One of the main focuses of his research is the study of the emergence and evolution of drug-resistant clones that can be restrained to improve the efficacy of anticancer agents to develop therapies that adapt to a tumour's evolution. [9] [10] [11] His group used several approaches in their work, including genetic analysis of clinical samples, a large collection of CRC cellular models, [12] patient-derived xenografts (xenopatients), and liquid biopsies. [13] [14] [15] In the last years his studies uncovered the molecular bases of primary and acquired resistance to anti-EGFR therapies in colorectal tumours. These findings have been rapidly translated into clinically applicable predictive biomarkers, which represent the first example of personalized medicine for colorectal tumours and are used to select patients for therapy. [16]
Bardelli also investigated the use of immunotherapy as a tool for precision medicine in CRC. His studies are built on an unconventional approach that an increased dynamic and mutational load in CRC cells can rouse an otherwise slack immune response, a vital requisite for effective immunosurveillance. Bardelli's team tweaked the clonal evolution of the tumour, via a pharmacological intervention, to provoke the persistent renewal of neoantigens. [17]
Bardelli's studies have been reported in high peer-reviewed scientific journals as Cancer Cell, Nature, JAMA, and Lancet Oncology. [ citation needed ]
Currently,[ when? ] Bardelli's team uses colorectal cancer models to establish personalized treatment for patients, focusing on:
Bardelli's team is composed of more than 20 members, including biologists, PH students, technicians and bioinformatics.
Bardelli has authored more than 200 scientific articles, of which 100 were written as an independent investigator. His research papers have been cited over 40,000 times. [18] Bardelli has been listed as a Highly Cited Researcher in the field of Clinical Medicine in Clarivate Web of Science (2014, 2018–2020). [19]
Bardelli was appointed "Officer" of the Order of Merit of the Italian Republic in 2021.[ citation needed ]
Glioblastoma, previously known as glioblastoma multiforme (GBM), is the most aggressive and most common type of cancer that originates in the brain, and has very poor prognosis for survival. Initial signs and symptoms of glioblastoma are nonspecific. They may include headaches, personality changes, nausea, and symptoms similar to those of a stroke. Symptoms often worsen rapidly and may progress to unconsciousness.
Cetuximab, sold under the brand name Erbitux, is an epidermal growth factor receptor (EGFR) inhibitor medication used for the treatment of metastatic colorectal cancer and head and neck cancer. Cetuximab is a chimeric (mouse/human) monoclonal antibody given by intravenous infusion.
The epidermal growth factor receptor is a transmembrane protein that is a receptor for members of the epidermal growth factor family of extracellular protein ligands.
Bert Vogelstein is director of the Ludwig Center, Clayton Professor of Oncology and Pathology and a Howard Hughes Medical Institute investigator at The Johns Hopkins Medical School and Sidney Kimmel Comprehensive Cancer Center. A pioneer in the field of cancer genomics, his studies on colorectal cancers revealed that they result from the sequential accumulation of mutations in oncogenes and tumor suppressor genes. These studies now form the paradigm for modern cancer research and provided the basis for the notion of the somatic evolution of cancer.
KRAS is a gene that provides instructions for making a protein called K-Ras, a part of the RAS/MAPK pathway. The protein relays signals from outside the cell to the cell's nucleus. These signals instruct the cell to grow and divide (proliferate) or to mature and take on specialized functions (differentiate). It is called KRAS because it was first identified as a viral oncogene in the KirstenRAt Sarcoma virus. The oncogene identified was derived from a cellular genome, so KRAS, when found in a cellular genome, is called a proto-oncogene.
Cripto is an EGF-CFC or epidermal growth factor-CFC, which is encoded by the Cryptic family 1 gene. Cryptic family protein 1B is a protein that in humans is encoded by the CFC1B gene. Cryptic family protein 1B acts as a receptor for the TGF beta signaling pathway. It has been associated with the translation of an extracellular protein for this pathway. The extracellular protein which Cripto encodes plays a crucial role in the development of left and right division of symmetry.
Matuzumab is a humanized monoclonal antibody for the treatment of cancer. It binds to the epidermal growth factor receptor (EGFR) with high affinity. The mouse monoclonal antibody (mAb425) from which matuzumab was developed at the Wistar Institute in Philadelphia, Pennsylvania
Lysosomal-associated transmembrane protein 4B is a protein that in humans is encoded by the LAPTM4B gene.
Oncology is a branch of medicine that deals with the study, treatment, diagnosis and prevention of cancer. A medical professional who practices oncology is an oncologist. The name's etymological origin is the Greek word ὄγκος (ónkos), meaning "tumor", "volume" or "mass". Oncology is concerned with:
A CDK inhibitor is any chemical that inhibits the function of CDKs. They are used to treat cancers by preventing overproliferation of cancer cells. The US FDA approved the first drug of this type, palbociclib (Ibrance), a CDK4/6 inhibitor, in February 2015, for use in postmenopausal women with breast cancer that is estrogen receptor positive and HER2 negative. While there are multiple cyclin/CDK complexes regulating the cell cycle, CDK inhibitors targeting CDK4/6 have been the most successful, with 4 CDK4/6 inhibitors haven been FDA approved. No inhibitors targeting other CDKs have been FDA approved, but several compounds are in clinical trials.
Combined small cell lung carcinoma is a form of multiphasic lung cancer that is diagnosed by a pathologist when a malignant tumor, arising from transformed cells originating in lung tissue, contains a component of;small cell lung carcinoma (SCLC), admixed with one components of any histological variant of non-small cell lung carcinoma (NSCLC) in any relative proportion.
Isogenic human disease models are a family of cells that are selected or engineered to accurately model the genetics of a specific patient population, in vitro. They are provided with a genetically matched 'normal cell' to provide an isogenic system to research disease biology and novel therapeutic agents. They can be used to model any disease with a genetic foundation. Cancer is one such disease for which isogenic human disease models have been widely used.
Angiokinase inhibitors are a new therapeutic target for the management of cancer. They inhibit tumour angiogenesis, one of the key processes leading to invasion and metastasis of solid tumours, by targeting receptor tyrosine kinases. Examples include nintedanib, afatinib and motesanib.
Molecular diagnostics is a collection of techniques used to analyze biological markers in the genome and proteome, and how their cells express their genes as proteins, applying molecular biology to medical testing. In medicine the technique is used to diagnose and monitor disease, detect risk, and decide which therapies will work best for individual patients, and in agricultural biosecurity similarly to monitor crop- and livestock disease, estimate risk, and decide what quarantine measures must be taken.
Patient derived xenografts (PDX) are models of cancer where the tissue or cells from a patient's tumor are implanted into an immunodeficient or humanized mouse. It is a form of xenotransplantation. PDX models are used to create an environment that allows for the continued growth of cancer after its removal from a patient. In this way, tumor growth can be monitored in the laboratory, including in response to potential therapeutic options. Cohorts of PDX models can be used to determine the therapeutic efficiency of a therapy against particular types of cancer, or a PDX model from a specific patient can be tested against a range of therapies in a 'personalized oncology' approach.
A cancer-associated fibroblast (CAF) is a cell type within the tumor microenvironment that promotes tumorigenic features by initiating the remodelling of the extracellular matrix or by secreting cytokines. CAFs are a complex and abundant cell type within the tumour microenvironment; the number cannot decrease, as they are unable to undergo apoptosis.
Luis Alberto Diaz, Jr. is the Head of the Division of Solid Tumor Oncology in Memorial Sloan Kettering’s Department of Medicine.
Paul S. Mischel is an American physician-scientist whose laboratory has made pioneering discoveries in the pathogenesis of human cancer. He is currently a Professor and Vice Chair of Research for the Department of Pathology and Institute Scholar of ChEM-H, Stanford University. Mischel was elected into the American Society for Clinical Investigation (ASCI), serving as ASCI president in 2010/11. He was inducted into the Association of American Physicians, and was elected as a fellow of the American Association for the Advancement of Science.
Urinary cell-free DNA (ucfDNA) refers to DNA fragments in urine released by urogenital and non-urogenital cells. Shed cells on urogenital tract release high- or low-molecular-weight DNA fragments via apoptosis and necrosis, while circulating cell-free DNA (cfDNA) that passes through glomerular pores contributes to low-molecular-weight DNA. Most of the ucfDNA is low-molecular-weight DNA in the size of 150-250 base pairs. The detection of ucfDNA composition allows the quantification of cfDNA, circulating tumour DNA, and cell-free fetal DNA components. Many commercial kits and devices have been developed for ucfDNA isolation, quantification, and quality assessment.
Yardena Samuels or Samuels-Lev is an Israeli molecular biologist who is the Director of the Ekard Institute for Cancer Diagnosis Research at the Weizmann Institute of Science. Her research considers the genetic mutations of melanoma.
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