Lani
04-24-2013, 10:01 AM
Rituxin was the first approved monoclonal antibody (used vs lymphoma)
Only now are we discovering mechanisms to help it create ADCC (also mechanism of action --or one of them-- of herceptin) so well and how to help it do so better
I cannot formulate a link, but if someone goes to http://www.eurekalert.org/bysubject/medicine.php within 24 hours, perhaps they can
Public release date: 24-Apr-2013
Contact: Morwenna Grills
Morwenna.Grills@manchester.ac.uk
44-161-275-2111
University of Manchester
Video reveals cancer cells' Achilles' heel
VIDEO: The Natural Killer white blood cell in red is drawn to the cancerous B cell which has been treated with rituximab. It latches on to the side of the cell...
Click here for more information.
Scientists from the Manchester Collaborative Centre for Inflammation Research (MCCIR) have discovered why a particular cancer drug is so effective at killing cells. Their findings could be used to aid the design of future cancer treatments.
Professor Daniel Davis and his team used high quality video imaging to investigate why the drug rituximab is so effective at killing cancerous B cells. It is widely used in the treatment of B cell malignancies, such as lymphoma and leukaemia - as well as in autoimmune diseases like rheumatoid arthritis.
Using high-powered laser-based microscopes, researchers made videos of the process by which rituximab binds to a diseased cell and then attracts white blood cells known as natural killer (NK) cells to attack. They discovered that rituximab tended to stick to one side of the cancer cell, forming a cap and drawing a number of proteins over to that side. It effectively created a front and back to the cell - with a cluster of protein molecules massed on one side.
But what surprised the scientists most was how this changed the effectiveness of natural killer cells in destroying these diseased cells. When the NK cell latched onto the rituximab cap on the B cell, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this cluster of proteins on one side, it was killed only 40% of the time.
bringing together industry and academia, demonstrates a real catalyst of scientific change within the UK, and I am excited by the potential of the MCCIR to bring further innovation that could ultimately bring benefit to patients."
Much of the research for this study was carried out during Professor Davis' time at Imperial College London. He will be continuing to use high quality video imaging at a microscopic level to investigate immunology at the MCCIR.
###
Professor Davis and MedImmune would like to acknowledge the funding they received from the Medical Research Council which helped make this study possible. The aim of the grant was to bring industry and academia closer together.
Only now are we discovering mechanisms to help it create ADCC (also mechanism of action --or one of them-- of herceptin) so well and how to help it do so better
I cannot formulate a link, but if someone goes to http://www.eurekalert.org/bysubject/medicine.php within 24 hours, perhaps they can
Public release date: 24-Apr-2013
Contact: Morwenna Grills
Morwenna.Grills@manchester.ac.uk
44-161-275-2111
University of Manchester
Video reveals cancer cells' Achilles' heel
VIDEO: The Natural Killer white blood cell in red is drawn to the cancerous B cell which has been treated with rituximab. It latches on to the side of the cell...
Click here for more information.
Scientists from the Manchester Collaborative Centre for Inflammation Research (MCCIR) have discovered why a particular cancer drug is so effective at killing cells. Their findings could be used to aid the design of future cancer treatments.
Professor Daniel Davis and his team used high quality video imaging to investigate why the drug rituximab is so effective at killing cancerous B cells. It is widely used in the treatment of B cell malignancies, such as lymphoma and leukaemia - as well as in autoimmune diseases like rheumatoid arthritis.
Using high-powered laser-based microscopes, researchers made videos of the process by which rituximab binds to a diseased cell and then attracts white blood cells known as natural killer (NK) cells to attack. They discovered that rituximab tended to stick to one side of the cancer cell, forming a cap and drawing a number of proteins over to that side. It effectively created a front and back to the cell - with a cluster of protein molecules massed on one side.
But what surprised the scientists most was how this changed the effectiveness of natural killer cells in destroying these diseased cells. When the NK cell latched onto the rituximab cap on the B cell, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this cluster of proteins on one side, it was killed only 40% of the time.
bringing together industry and academia, demonstrates a real catalyst of scientific change within the UK, and I am excited by the potential of the MCCIR to bring further innovation that could ultimately bring benefit to patients."
Much of the research for this study was carried out during Professor Davis' time at Imperial College London. He will be continuing to use high quality video imaging at a microscopic level to investigate immunology at the MCCIR.
###
Professor Davis and MedImmune would like to acknowledge the funding they received from the Medical Research Council which helped make this study possible. The aim of the grant was to bring industry and academia closer together.