Anti-CD137

Haven't heard anything about this one.  Best decriptions I could find were Here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776567/

and here:

http://meeting.ascopubs.org/cgi/content/abstract/26/15_suppl/3007

I couldn't find anything showing the effectiveness of the drug in early research.  The second link mainly talks about how the drug was tolerated (which seems quite well), and the immunological response achieved from the drug which also seemed pretty good.  Will be interesting to see what comes of this one.  To me it seems like it has potential to be used in combination with another treatment to enhance benefits.

Haven't heard anything about this one.  Best decriptions I could find were Here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776567/

and here:

http://meeting.ascopubs.org/cgi/content/abstract/26/15_suppl/3007

I couldn't find anything showing the effectiveness of the drug in early research.  The second link mainly talks about how the drug was tolerated (which seems quite well), and the immunological response achieved from the drug which also seemed pretty good.  Will be interesting to see what comes of this one.  To me it seems like it has potential to be used in combination with another treatment to enhance benefits.

Haven't heard anything about this one.  Best decriptions I could find were Here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776567/

and here:

http://meeting.ascopubs.org/cgi/content/abstract/26/15_suppl/3007

I couldn't find anything showing the effectiveness of the drug in early research.  The second link mainly talks about how the drug was tolerated (which seems quite well), and the immunological response achieved from the drug which also seemed pretty good.  Will be interesting to see what comes of this one.  To me it seems like it has potential to be used in combination with another treatment to enhance benefits.

CD137 is a member of the TNFR family and functions as a costimulatory molecule. In preclinical studies BMS- 663513, a fully human anti-CD137 agonist monoclonal antibody provided costimulation to CD8+ and CD4+ T-cells, leading to enhanced IFN production, cytolytic activity, and increased survival. This drug may work in combination with  yervoy and or anti-pd-1.

jimmy b

CD137 is a member of the TNFR family and functions as a costimulatory molecule. In preclinical studies BMS- 663513, a fully human anti-CD137 agonist monoclonal antibody provided costimulation to CD8+ and CD4+ T-cells, leading to enhanced IFN production, cytolytic activity, and increased survival. This drug may work in combination with  yervoy and or anti-pd-1.

jimmy b

CD137 is a member of the TNFR family and functions as a costimulatory molecule. In preclinical studies BMS- 663513, a fully human anti-CD137 agonist monoclonal antibody provided costimulation to CD8+ and CD4+ T-cells, leading to enhanced IFN production, cytolytic activity, and increased survival. This drug may work in combination with  yervoy and or anti-pd-1.

jimmy b

Thank you for bringing this potential new therapy to our attention. It seems to me that we are entering–no, we have entered– a "brave new world" of cancer immunotherapy made possible by the Human Genome Project, rapid technological advances and decades of basic research into how the immune system is regulated. I think that in the next 10 years we will see many exciting successes in this field, but an equal number of disappointments.

The key is that the immune system has evolved over the milennia to be able to recognize and kill every and any pathogen that enters the body while at the same time recognizing and not killing our own cells. Given the huge number of pathogens out there and the fact that the pathogens keep evolving, too, this is no easy task! And from an evolutionary point of view, the immune system's mission is to keep the species alive, not necessarily every individual.

For this reason, there are many, many different genes and variations of each gene that control the immune response. Because of this, for any given pathogen (or cancer) some people will have the "right" genetic makeup so that their immune system recognizes and cures the infection and many other people will not. Individuals will die but the species will continue. 

What this means for immunotherapies is two things: 1) there are and will continue to be more and more of these "co-stimulatory" or "inhibitory" molecules discovered and tested for their ability to kill cancer. Most of them will probably work. 2) None of them will work in every patient; each will work only in the subset of paitents who have the "right" or "matching" genetic makeup. Figuring out which genetic makeup will respond to which immunotheraputic agent is a huge area of research that is being called "personalized medicine". 

I am bringing this up because there is something we can do to speed up the process of discovering which genetic makeup will respond to which immunotherapy. You may have seen the headlines last week announcing that, for the first time, a number of large pharmaceutical companies agreed to form a consortium to pool their data from their clinical trials so that all could progress faster on their drug development. The main thing they will be pooling is the genetic information from their study participants together with the results– which genetic background responded to which immunostimulatory drug. Pooling all this (formerly proprietary) data from thousands and thousands of patients will really, really help all reseachers to target the RIGHT treatment to the RIGHT patient. But you know what? MELANOMA IS NOT ONE OF THE DISEASES THAT WAS INCLUDED IN THIS DATA-SHARING AGREEMENT!!!

Why is that? I don't know. I am dismayed by this. But I think that we, as patients, patient advocates and taxpayers can and should lobby our organizations– like the MRF and MIF and our governmental agencies like NIH and NCI– and insist that the data from melanoma patients be included in the pool. If these drug companies demand that we give them endless blood and tissue samples so they can analyze our genotypes for their own benefit, then in return they should make those samples and our personal data available to all other researchers. That should be a clause included in every clinical trial contract. 

We are getting screwed here. Clinical trial participants are being asked to participate in trials that, because of the genetic background issue, have little likelyhood of success for any one patient. We are rolling the dice for every trial. At the very least, the data that are generated should be shared so that future patients will have a greater probabiliy of success. 

Thank you for bringing this potential new therapy to our attention. It seems to me that we are entering–no, we have entered– a "brave new world" of cancer immunotherapy made possible by the Human Genome Project, rapid technological advances and decades of basic research into how the immune system is regulated. I think that in the next 10 years we will see many exciting successes in this field, but an equal number of disappointments.

The key is that the immune system has evolved over the milennia to be able to recognize and kill every and any pathogen that enters the body while at the same time recognizing and not killing our own cells. Given the huge number of pathogens out there and the fact that the pathogens keep evolving, too, this is no easy task! And from an evolutionary point of view, the immune system's mission is to keep the species alive, not necessarily every individual.

For this reason, there are many, many different genes and variations of each gene that control the immune response. Because of this, for any given pathogen (or cancer) some people will have the "right" genetic makeup so that their immune system recognizes and cures the infection and many other people will not. Individuals will die but the species will continue. 

What this means for immunotherapies is two things: 1) there are and will continue to be more and more of these "co-stimulatory" or "inhibitory" molecules discovered and tested for their ability to kill cancer. Most of them will probably work. 2) None of them will work in every patient; each will work only in the subset of paitents who have the "right" or "matching" genetic makeup. Figuring out which genetic makeup will respond to which immunotheraputic agent is a huge area of research that is being called "personalized medicine". 

I am bringing this up because there is something we can do to speed up the process of discovering which genetic makeup will respond to which immunotherapy. You may have seen the headlines last week announcing that, for the first time, a number of large pharmaceutical companies agreed to form a consortium to pool their data from their clinical trials so that all could progress faster on their drug development. The main thing they will be pooling is the genetic information from their study participants together with the results– which genetic background responded to which immunostimulatory drug. Pooling all this (formerly proprietary) data from thousands and thousands of patients will really, really help all reseachers to target the RIGHT treatment to the RIGHT patient. But you know what? MELANOMA IS NOT ONE OF THE DISEASES THAT WAS INCLUDED IN THIS DATA-SHARING AGREEMENT!!!

Why is that? I don't know. I am dismayed by this. But I think that we, as patients, patient advocates and taxpayers can and should lobby our organizations– like the MRF and MIF and our governmental agencies like NIH and NCI– and insist that the data from melanoma patients be included in the pool. If these drug companies demand that we give them endless blood and tissue samples so they can analyze our genotypes for their own benefit, then in return they should make those samples and our personal data available to all other researchers. That should be a clause included in every clinical trial contract. 

We are getting screwed here. Clinical trial participants are being asked to participate in trials that, because of the genetic background issue, have little likelyhood of success for any one patient. We are rolling the dice for every trial. At the very least, the data that are generated should be shared so that future patients will have a greater probabiliy of success. 

Thank you for bringing this potential new therapy to our attention. It seems to me that we are entering–no, we have entered– a "brave new world" of cancer immunotherapy made possible by the Human Genome Project, rapid technological advances and decades of basic research into how the immune system is regulated. I think that in the next 10 years we will see many exciting successes in this field, but an equal number of disappointments.

The key is that the immune system has evolved over the milennia to be able to recognize and kill every and any pathogen that enters the body while at the same time recognizing and not killing our own cells. Given the huge number of pathogens out there and the fact that the pathogens keep evolving, too, this is no easy task! And from an evolutionary point of view, the immune system's mission is to keep the species alive, not necessarily every individual.

For this reason, there are many, many different genes and variations of each gene that control the immune response. Because of this, for any given pathogen (or cancer) some people will have the "right" genetic makeup so that their immune system recognizes and cures the infection and many other people will not. Individuals will die but the species will continue. 

What this means for immunotherapies is two things: 1) there are and will continue to be more and more of these "co-stimulatory" or "inhibitory" molecules discovered and tested for their ability to kill cancer. Most of them will probably work. 2) None of them will work in every patient; each will work only in the subset of paitents who have the "right" or "matching" genetic makeup. Figuring out which genetic makeup will respond to which immunotheraputic agent is a huge area of research that is being called "personalized medicine". 

I am bringing this up because there is something we can do to speed up the process of discovering which genetic makeup will respond to which immunotherapy. You may have seen the headlines last week announcing that, for the first time, a number of large pharmaceutical companies agreed to form a consortium to pool their data from their clinical trials so that all could progress faster on their drug development. The main thing they will be pooling is the genetic information from their study participants together with the results– which genetic background responded to which immunostimulatory drug. Pooling all this (formerly proprietary) data from thousands and thousands of patients will really, really help all reseachers to target the RIGHT treatment to the RIGHT patient. But you know what? MELANOMA IS NOT ONE OF THE DISEASES THAT WAS INCLUDED IN THIS DATA-SHARING AGREEMENT!!!

Why is that? I don't know. I am dismayed by this. But I think that we, as patients, patient advocates and taxpayers can and should lobby our organizations– like the MRF and MIF and our governmental agencies like NIH and NCI– and insist that the data from melanoma patients be included in the pool. If these drug companies demand that we give them endless blood and tissue samples so they can analyze our genotypes for their own benefit, then in return they should make those samples and our personal data available to all other researchers. That should be a clause included in every clinical trial contract. 

We are getting screwed here. Clinical trial participants are being asked to participate in trials that, because of the genetic background issue, have little likelyhood of success for any one patient. We are rolling the dice for every trial. At the very least, the data that are generated should be shared so that future patients will have a greater probabiliy of success.