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Jessica Kandel is the Mary Campau Ryerson Professor of Surgery and the Vice-Chair for Academic Affairs in the Department of Surgery at the University of Chicago.
Kandel graduated summa cum laude from Yale University in 1981, and completed her MD degree at Columbia University in 1985. She then went on to a General Surgery residency at the Massachusetts General Hospital in Boston (1986–1993). During her residency, Kandel completed a two-year surgical research fellowship with Dr. Judah Folkman at the Boston Children's Hospital, investigating mechanisms of tumor angiogenesis (new blood vessel development that "feeds" tumors).
Kandel joined Columbia University in 1995, becoming the Director of the Charles Edison Laboratory for Pediatric Surgical Research in 2000 and, in 2001, co-organized the first Columbia University Arden House Symposium on Angiogenesis. Kandel was a founding member of the Vascular Anomalies Group at Columbia, a multidisciplinary team treating children with vascular malformations, hemangioma, lymphatic tumors, and other disorders of vessel development. She was named the R. Peter Altman Chair in Pediatric Surgery at Columbia University in 2009, as a Professor of Surgery & Pediatrics in the Institute of Cancer Genetics at Columbia University.
In 1998, Kandel, Darrell Yamashiro, and colleagues at the Pediatric Tumor Biology Laboratory were the first to describe the way experimental pediatric tumor growth could be suppressed by blocking a molecule called vascular endothelial growth factor (VEGF) from performing its natural job. Their laboratory research provided key preclinical data about an antibody to VEGF, which was later humanized to become bevacizumab (Avastin, Genentech). Approved by the FDA in 2004 for adults with colorectal cancer, bevacizumab is now gaining use in the treatment of multiple adult and pediatric tumors.
Her current focus in the laboratory is to understand how tumors adapt to blockade of VEGF. Understanding how tumors become resistant to therapies that target recruited host cells may play an important role in the development of therapies for children with resistant cancers such as neuroblastoma, Wilms tumor, and hepatoblastoma.
Kandel has developed a novel mouse model of lymphatic malformations, with her coinvestigator, Carrie Shawber.
A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source. Krukenberg tumors are often found in both ovaries, consistent with its metastatic nature.
Bevacizumab, sold under the brand name Avastin among others, is a monoclonal antibody medication used to treat a number of types of cancers and a specific eye disease. For cancer, it is given by slow injection into a vein (intravenous) and used for colon cancer, lung cancer, ovarian cancer, glioblastoma, and renal-cell carcinoma. In many of these diseases it is used as a first-line therapy. For age-related macular degeneration it is given by injection into the eye (intravitreal).
Vascular endothelial growth factor, originally known as vascular permeability factor (VPF), is a signal protein produced by many cells that stimulates the formation of blood vessels. To be specific, VEGF is a sub-family of growth factors, the platelet-derived growth factor family of cystine-knot growth factors. They are important signaling proteins involved in both vasculogenesis and angiogenesis.
An angiogenesis inhibitor is a substance that inhibits the growth of new blood vessels (angiogenesis). Some angiogenesis inhibitors are endogenous and a normal part of the body's control and others are obtained exogenously through pharmaceutical drugs or diet.
Moses Judah Folkman was an American biologist and pediatric surgeon best known for his research on tumor angiogenesis, the process by which a tumor attracts blood vessels to nourish itself and sustain its existence. He founded the field of angiogenesis research, which has led to the discovery of a number of therapies based on inhibiting or stimulating neovascularization.
Vascular endothelial growth factor C (VEGF-C) is a protein that is a member of the platelet-derived growth factor / vascular endothelial growth factor (PDGF/VEGF) family. It is encoded in humans by the VEGFC gene, which is located on chromosome 4q34.
Steven Kenneth Libutti, M.D., F.A.C.S. is an American surgeon and scientist. In January 2017, he became the third permanent Director of the Rutgers Cancer Institute of New Jersey, Vice Chancellor for Cancer Programs for Rutgers Biomedical and Health Sciences and the Senior Vice President for Oncology Services for RWJBarnabas Health, the largest health system in New Jersey. He is a tenured Distinguished Professor of Surgery at the Rutgers Robert Wood Johnson Medical School. Libutti's work on the study of tumor angiogenesis and the tumor microenvironment has led to novel approaches for the treatment of cancer. He is also one of the pioneers of regional and targeted cancer therapy.
Vascular endothelial growth factor A (VEGF-A) is a protein that in humans is encoded by the VEGFA gene.
Napoleone Ferrara is an Italian-American molecular biologist who joined University of California, San Diego Moores Cancer Center in 2013 after a career in Northern California at the biotechnology giant Genentech, where he pioneered the development of new treatments for angiogenic diseases such as cancer, age-related macular degeneration (AMD), and diabetic retinopathy. At Genentech, he discovered VEGF—and made the first anti-VEGF antibody—which suppresses growth of a variety of tumors. These findings helped lead to development of the first clinically available angiogenesis inhibitor, bevacizumab (Avastin), which prevents the growth of new blood vessels into a solid tumor and which has become part of standard treatment for a variety of cancers. Ferrara's work led also to the development of ranibizumab (Lucentis), a drug that is highly effective at preventing vision loss in intraocular neovascular disorders.
Hope & Heroes is a 501(c)(3) non-profit organization based at Columbia University Medical Center (CUMC) in New York City. Hope & Heroes supports the Division of Pediatric Hematology, Oncology & Stem Cell Transplantation at Columbia University Medical Center. Hope & Heroes funds work on childhood cancer and blood disorders at Columbia University Medical Center—including research, support for families, and care.
Targeted therapy of lung cancer refers to using agents specifically designed to selectively target molecular pathways responsible for, or that substantially drive, the malignant phenotype of lung cancer cells, and as a consequence of this (relative) selectivity, cause fewer toxic effects on normal cells.
David Cheresh is a Michigan-born scientist who studies angiogenesis and cancer metastasis. His early research focused on the function of integrins, cellular receptors for the extracellular matrix, in cell migration and survival. His current work is on signaling aspects of cell invasion by vascular cells and tumor cells, with a focus on preventing tumor metastasis.
David Henry Gorski is an American surgical oncologist and professor of surgery at Wayne State University School of Medicine. He specializes in breast cancer surgery at the Karmanos Cancer Institute. Gorski is an outspoken skeptic and critic of alternative medicine and the anti-vaccination movement. A prolific blogger, he writes as Orac at Respectful Insolence, and as himself at Science-Based Medicine where he is the managing editor.
The tumor microenvironment is a complex ecosystem surrounding a tumor, composed of cancer cells, stromal tissue and the extracellular matrix. Mutual interaction between cancer cells and the different components of the tumor microenvironment support its growth and invasion in healthy tissues which correlates with tumor resistance to current treatments and poor prognosis. The tumor microenvironment is in constant change because of the tumor's ability to influence the microenvironment by releasing extracellular signals, promoting tumor angiogenesis and inducing peripheral immune tolerance, while the immune cells in the microenvironment can affect the growth and evolution of cancerous cells.
Anti–vascular endothelial growth factor therapy, also known as anti-VEGF therapy or medication, is the use of medications that block vascular endothelial growth factor. This is done in the treatment of certain cancers and in age-related macular degeneration. They can involve monoclonal antibodies such as bevacizumab, antibody derivatives such as ranibizumab (Lucentis), or orally-available small molecules that inhibit the tyrosine kinases stimulated by VEGF: sunitinib, sorafenib, axitinib, and pazopanib.
Tumor-associated endothelial cells or tumor endothelial cells (TECs) refers to cells lining the tumor-associated blood vessels that control the passage of nutrients into surrounding tumor tissue. Across different cancer types, tumor-associated blood vessels have been discovered to differ significantly from normal blood vessels in morphology, gene expression, and functionality in ways that promote cancer progression. There has been notable interest in developing cancer therapeutics that capitalize on these abnormalities of the tumor-associated endothelium to destroy tumors.
Bridget Anne Robinson is a New Zealand oncology academic. As of 2018, she is a full professor at the University of Otago, holding the Mackenzie Chair since 2010.
VEGFR-2 inhibitor, also known as kinase insert domain receptor(KDR) inhibitor, are tyrosine kinase receptor inhibitors that reduce angiogenesis or lymphangiogenesis, leading to anticancer activity. Generally they are small, synthesised molecules that bind competitively to the ATP-site of the tyrosine kinase domain. VEGFR-2 selective inhibitor can interrupt multiple signaling pathways involved in tumor, including proliferation, metastasis and angiogenesis.
The host response to cancer therapy is defined as a physiological response of the non-malignant cells of the body to a specific cancer therapy. The response is therapy-specific, occurring independently of cancer type or stage.
Bradley J. Monk is an American gynecologic oncologist, academician and researcher. He is a Professor on the Clinical Scholar Track in the Department of Obstetrics and Gynecology at the University of Arizona College of Medicine in Phoenix, Arizona, as well as at the Creighton University School of Medicine in Omaha, Nebraska. He also serves as Director of the Division of Gynecologic Oncology at the St. Joseph's Hospital and Medical Center in Phoenix.
