Karin E. de Visser | |
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Alma mater | Netherlands Cancer Institute |
Scientific career | |
Institutions | Netherlands Cancer Institute University of California, San Francisco |
Thesis | The impact of self-antigen expression on the CD8+ T cell repertoire : implications for anti-tumor immunity (2002) |
Karina Elizabeth de Visser (Karin de Visser, 1975), [1] also named "Karin E. de Visser", is a researcher at the Netherlands Cancer Institute. Her research considers metastatic formation and how the immune system influences how people respond to cancer treatment.
In 1998 De Visser obtained her master's degree in Biomedical Science at Leiden University (cum laude). [2] De Visser was a postgraduate student at the Netherlands Cancer Institute, [3] supervised by prof. dr. Ada Kruisbeek. In 2002 she got her PhD degree at the Vrije Universiteit Amsterdam with her thesis The impact of self-antigen expression on the CD8+ T cell repertoire: Implications for anti-tumor immunity. [4]
In 2003 she was appointed a postdoctoral fellow with Lisa Coussens at the University of California, San Francisco. Here she started working on the interaction between the adaptive and innate immune system. She spent two years in California, before returning to the Netherlands Cancer Institute where she started working on inflammation and carcinogenesis.
De Visser launched her independent career at the Netherlands Cancer Institute, where she started working on tumour biology and immunology. De Visser looks to understand how the immune system impacts the formation of metastasis and response to cancer treatment. [5] In particular, De Visser has focussed on breast cancer, and how tumours can hijack the immune system to allow for metastatic spread. [5] She also identified that the precise genetic make-up of breast cancer determines pro-metastatic inflammation.
She works closely with Marleen Kok on translation of her findings to clinical environments, including looking to understand the landscape of breast cancer patients treated with checkpoint inhibitors. [5]
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.
Macrophages are a type of white blood cell of the innate immune system that engulf and digest pathogens, such as cancer cells, microbes, cellular debris, and foreign substances, which do not have proteins that are specific to healthy body cells on their surface. This process is called phagocytosis, which acts to defend the host against infection and injury.
The selectins are a family of cell adhesion molecules. All selectins are single-chain transmembrane glycoproteins that share similar properties to C-type lectins due to a related amino terminus and calcium-dependent binding. Selectins bind to sugar moieties and so are considered to be a type of lectin, cell adhesion proteins that bind sugar polymers.
E-selectin, also known as CD62 antigen-like family member E (CD62E), endothelial-leukocyte adhesion molecule 1 (ELAM-1), or leukocyte-endothelial cell adhesion molecule 2 (LECAM2), is a selectin cell adhesion molecule expressed only on endothelial cells activated by cytokines. Like other selectins, it plays an important part in inflammation. In humans, E-selectin is encoded by the SELE gene.
Chemokine ligand 9 (CXCL9) is a small cytokine belonging to the CXC chemokine family that is also known as monokine induced by gamma interferon (MIG). The CXCL9 is one of the chemokine which plays role to induce chemotaxis, promote differentiation and multiplication of leukocytes, and cause tissue extravasation.
Voltage-gated proton channels are ion channels that have the unique property of opening with depolarization, but in a strongly pH-sensitive manner. The result is that these channels open only when the electrochemical gradient is outward, such that their opening will only allow protons to leave cells. Their function thus appears to be acid extrusion from cells.
Toll-like receptor 9 is a protein that in humans is encoded by the TLR9 gene. TLR9 has also been designated as CD289. It is a member of the toll-like receptor (TLR) family. TLR9 is an important receptor expressed in immune system cells including dendritic cells, macrophages, natural killer cells, and other antigen presenting cells. TLR9 is expressed on endosomes internalized from the plasma membrane, binds DNA, and triggers signaling cascades that lead to a pro-inflammatory cytokine response. Cancer, infection, and tissue damage can all modulate TLR9 expression and activation. TLR9 is also an important factor in autoimmune diseases, and there is active research into synthetic TLR9 agonists and antagonists that help regulate autoimmune inflammation.
Tumor-infiltrating lymphocytes (TIL) are white blood cells that have left the bloodstream and migrated towards a tumor. They include T cells and B cells and are part of the larger category of ‘tumor-infiltrating immune cells’ which consist of both mononuclear and polymorphonuclear immune cells, in variable proportions. Their abundance varies with tumor type and stage and in some cases relates to disease prognosis.
Neutrophil collagenase, also known as matrix metalloproteinase-8 (MMP-8) or PMNL collagenase (MNL-CL), is a collagen cleaving enzyme which is present in the connective tissue of most mammals. In humans, the MMP-8 protein is encoded by the MMP8 gene. The gene is part of a cluster of MMP genes which localize to chromosome 11q22.3. Most MMP's are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. However, the enzyme encoded by this gene is stored in secondary granules within neutrophils and is activated by autolytic cleavage.
Joan Massagué, is a Spanish biologist and the current director of the Sloan Kettering Institute at Memorial Sloan Kettering Cancer Center. He is also an internationally recognized leader in the study of both cancer metastasis and growth factors that regulate cell behavior, as well as a professor at the Weill Cornell Graduate School of Medical Sciences.
Johannes (Hans) Carolus Clevers is a Dutch molecular geneticist, cell biologist and stem cell researcher. He became the Head of Pharma, Research and Early Development, and a member of the Corporate Executive Committee, of the Swiss healthcare company Roche in 2022. Previously, he headed a research group at the Hubrecht Institute for Developmental Biology and Stem Cell Research and at the Princess Máxima Center; he remained as an advisor and guest scientist or visiting researcher to both groups. He is also a Professor in Molecular Genetics at the University of Utrecht.
The tumor microenvironment (TME) is the environment around a tumor, including the surrounding blood vessels, immune cells, fibroblasts, signaling molecules and the extracellular matrix (ECM). The tumor and the surrounding microenvironment are closely related and interact constantly. Tumors can 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.
Cryoimmunotherapy, also referred to as cryoimmunology, is an oncological treatment for various cancers that combines cryoablation of tumor with immunotherapy treatment. In-vivo cryoablation of a tumor, alone, can induce an immunostimulatory, systemic anti-tumor response, resulting in a cancer vaccine—the abscopal effect. Thus, cryoablation of tumors is a way of achieving autologous, in-vivo tumor lysate vaccine and treat metastatic disease. However, cryoablation alone may produce an insufficient immune response, depending on various factors, such as high freeze rate. Combining cryotherapy with immunotherapy enhances the immunostimulating response and has synergistic effects for cancer treatment.
The Immunologic Constant of Rejection (ICR), is a notion introduced by biologists to group a shared set of genes expressed in tissue destructive-pathogenic conditions like cancer and infection, along a diverse set of physiological circumstances of tissue damage or organ failure, including autoimmune disease or allograft rejection. The identification of shared mechanisms and phenotypes by distinct immune pathologies, marked as a hallmarks or biomarkers, aids in the identification of novel treatment options, without necessarily assessing patients phenomenologies individually.
Stephanie S. Watowich is an American immunologist. Watowich is the deputy chair of the Department of Immunology at MD Anderson Cancer Center in Houston, TX. She is a professor within the department as well and serves as the co-director of the Center for Inflammation and Cancer at the MD Anderson Cancer Center. Watowich’s research has focused on transcriptional control of innate immunity, with specific interest in the actions of the cytokine-activated STAT transcriptional regulators.
Nancy Lin is an American oncologist who works at the Dana-Farber Cancer Institute and is an Associate Professor of Medicine at Harvard Medical School. Her research considers new diagnostic strategies and treatment pathways for HER2 positive breast cancer.
Julia Lesley Wilson is a British scientist who serves as associate director at the Wellcome Sanger Institute. Her research career investigates transplant rejection, cancer and inflammation. She previously worked at the World Cancer Research Fund and Breakthrough Breast Cancer.
Lisa M. Coussens is an American cancer scientist who is Chair of the Department of Cell, Developmental and Cancer Biology and Professor and Associate Director for Basic Research in the Knight Cancer Institute at the Oregon Health & Science University. She serves as President of the American Association for Cancer Research.
Reuven Agami is a Dutch cancer researcher. He is a professor of Oncogenomics at Erasmus University Rotterdam and head of the section of Oncogenomics at the Netherlands Cancer Institute-Antoni van Leeuwenhoekziekenhuis.
Janet Mary Lord is a British biologist who is a Professor of Cell Biology at the University of Birmingham. Her research considers immunity in old age, with a focus on the decline of neutrophil function. She was made a Commander of the British Empire in the 2023 New Year Honours List.