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RobertNagourneyMD
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- Oncology - Hematology/Oncology
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Professional Statement
Robert A. Nagourney, MD, is the medical and laboratory director at Rational Therapeutics, Inc., in Long Beach, California. He is board certified in internal medicine, medical oncology, and hematology.
Dr. Nagourney received his undergraduate degree in chemistry from Boston University and his doctor of medicine at McGill University in Montreal, where he was a University Scholar. After a residency in internal medicine at the University of California, Irvine, he went on to complete fellowship training in medical oncology at Georgetown University, as well as in hematology at the Scripps Institute in La Jolla.
During his medical oncology fellowship at Georgetown University, Dr. Nagourney confronted aggressive malignancies for which the standard therapies remained highly unsatisfactory. Responding to an unmet need, he pioneered the development of “personalized cancer therapy” applying a laboratory platform to match patients to therapies based on their unique response profiles.
As the founder of Rational Therapeutics, Dr. Nagourney has led in the development of “functional profiling” in human tumors. Using human tumor microspheroids isolated directly from surgical specimens, this platform known as the Ex Vivo Analysis of Programmed Cell Death (EVA-PCD®) measures drug-induced programmed cell death. The EVA-PCD® has been shown to be a robust method for the prediction of clinical response to therapy.
With more than twenty years experience in this field, Dr. Nagourney has authored numerous manuscripts, book chapters and abstracts. As co-investigator on national cooperative trials, he introduced the use of platinum/gemcitabine doublets in the management of advanced ovarian and breast cancers, treatments that today are used around the world.
Dr. Nagourney resides in Long Beach, California with his wife and two sons.
Dr. Nagourney received his undergraduate degree in chemistry from Boston University and his doctor of medicine at McGill University in Montreal, where he was a University Scholar. After a residency in internal medicine at the University of California, Irvine, he went on to complete fellowship training in medical oncology at Georgetown University, as well as in hematology at the Scripps Institute in La Jolla.
During his medical oncology fellowship at Georgetown University, Dr. Nagourney confronted aggressive malignancies for which the standard therapies remained highly unsatisfactory. Responding to an unmet need, he pioneered the development of “personalized cancer therapy” applying a laboratory platform to match patients to therapies based on their unique response profiles.
As the founder of Rational Therapeutics, Dr. Nagourney has led in the development of “functional profiling” in human tumors. Using human tumor microspheroids isolated directly from surgical specimens, this platform known as the Ex Vivo Analysis of Programmed Cell Death (EVA-PCD®) measures drug-induced programmed cell death. The EVA-PCD® has been shown to be a robust method for the prediction of clinical response to therapy.
With more than twenty years experience in this field, Dr. Nagourney has authored numerous manuscripts, book chapters and abstracts. As co-investigator on national cooperative trials, he introduced the use of platinum/gemcitabine doublets in the management of advanced ovarian and breast cancers, treatments that today are used around the world.
Dr. Nagourney resides in Long Beach, California with his wife and two sons.
Professional Info
Credential:
MD
Primary specialty:
Oncology - Hematology/Oncology
Medical school:
McGill University
Residency:
University of California, Irvine
Fellowship:
Georgetown University, Scripps Institute
Practice name:
Rational Therapeutics
Practice address:
750 E. 29th Street
Long Beach, CA
90806
Practice phone number:
562.989.6455
Webpage:
http://www.rational-t.com/
RobertNagourneyMD Activities
I have already described my thinking in this regard in a recent blog that surrounded the publication of an English study that clearly and unequivocally demonstrated the protective value of non-steroidal anti-inflammatory drugs in patient at high risk for colon cancer (http://robertanagourney.wordpress.com/category/colorectal-cancer-2/). To a large degree, cancer can be viewed as a wound that will not heal. Wound healing is a paradigm of inflammation. The more we can do in our lifestyles, diets, and therapies to reduce inflammation, the better.
I have already described my thinking in this regard in a recent blog that surrounded the publication of an English study that clearly and unequivocally demonstrated the protective value of non-steroidal anti-inflammatory drugs in patient at high risk for colon cancer (http://robertanagourney.wordpress.com/category/colorectal-cancer-2/). To a large degree, cancer can be viewed as a wound that will not heal. Wound healing is a paradigm of inflammation. The more we can do in our lifestyles, diets, and therapies to reduce inflammation, the better.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Health, Cancer Risk, Inflammation, Aspirin, Reduce Cancer Risk
1
Answer |
3 months ago
This is an excellent question. Caris is a member of a group of molecular profiling companies. These groups extract protein, DNA or RNA and measure the genetic information present in fixed tissue. Their intent is to match patients to therapy based on this static data. That is, the presence of a gene should, according to their reasoning, confer sensitivity to a drug. The proof of this concept, however, is sorely lacking. If we examine one publication in the literature (VonHoff D et al, J Clin Oncol Nov 2010), we find an objective response rate (measurable benefit in 66 patients treated using molecularly selected drugs) of 10%. Indeed, the positive results reported in this study reflected not a response rate but instead a 30% improvement in the time to disease progression, associated with molecular drug selection, compared with the patients prior, most recent (unsuccessful) therapies. To put this in context, a patient could arguably fail a physician-selected treatment after 1 month, and then receive a Caris selected therapy. If they responded for 1 month plus 10 days (a 30% improvement), they were counted as a success. The clinical relevance of that degree of improvement seems questionable.
While we fully understand the excitement surrounding genetic analyses, the more sophisticated researchers in the field are beginning to appreciate that the complexity of human biology demands more global (functional) analytic platforms that encompass all of the mechanisms of response and resistance. In this light, the presence of a gene cannot predict whether that gene will be expressed, active, counter-acted by a complementary gene, or functional.
We believe that human biology must be taken at face value in its most complex state. This is known as the phenotype and must be examined for the biological features that these interconnected cellular systems create. This field now known as biosystematics, or systems biology, recognizes the redundancies and uncertainties that separate the genotype (molecular profiling) from the phenotype (functional analyses) are not trivial. Our laboratory conducts phenotype analyses. Caris conducts genotype analyses. This is an excellent question. Caris is a member of a group of molecular profiling companies. These groups extract protein, DNA or RNA and measure the genetic information present in fixed tissue. Their intent is to match patients to therapy based on this static data. That is, the presence of a gene should, according to their reasoning, confer sensitivity to a drug. The proof of this concept, however, is sorely lacking. If we examine one publication in the literature (VonHoff D et al, J Clin Oncol Nov 2010), we find an objective response rate (measurable benefit in 66 patients treated using molecularly selected drugs) of 10%. Indeed, the positive results reported in this study reflected not a response rate but instead a 30% improvement in the time to disease progression, associated with molecular drug selection, compared with the patients prior, most recent (unsuccessful) therapies. To put this in context, a patient could arguably fail a physician-selected treatment after 1 month, and then receive a Caris selected therapy. If they responded for 1 month plus 10 days (a 30% improvement), they were counted as a success. The clinical relevance of that degree of improvement seems questionable.
While we fully understand the excitement surrounding genetic analyses, the more sophisticated researchers in the field are beginning to appreciate that the complexity of human biology demands more global (functional) analytic platforms that encompass all of the mechanisms of response and resistance. In this light, the presence of a gene cannot predict whether that gene will be expressed, active, counter-acted by a complementary gene, or functional.
We believe that human biology must be taken at face value in its most complex state. This is known as the phenotype and must be examined for the biological features that these interconnected cellular systems create. This field now known as biosystematics, or systems biology, recognizes the redundancies and uncertainties that separate the genotype (molecular profiling) from the phenotype (functional analyses) are not trivial. Our laboratory conducts phenotype analyses. Caris conducts genotype analyses.
While we fully understand the excitement surrounding genetic analyses, the more sophisticated researchers in the field are beginning to appreciate that the complexity of human biology demands more global (functional) analytic platforms that encompass all of the mechanisms of response and resistance. In this light, the presence of a gene cannot predict whether that gene will be expressed, active, counter-acted by a complementary gene, or functional.
We believe that human biology must be taken at face value in its most complex state. This is known as the phenotype and must be examined for the biological features that these interconnected cellular systems create. This field now known as biosystematics, or systems biology, recognizes the redundancies and uncertainties that separate the genotype (molecular profiling) from the phenotype (functional analyses) are not trivial. Our laboratory conducts phenotype analyses. Caris conducts genotype analyses. This is an excellent question. Caris is a member of a group of molecular profiling companies. These groups extract protein, DNA or RNA and measure the genetic information present in fixed tissue. Their intent is to match patients to therapy based on this static data. That is, the presence of a gene should, according to their reasoning, confer sensitivity to a drug. The proof of this concept, however, is sorely lacking. If we examine one publication in the literature (VonHoff D et al, J Clin Oncol Nov 2010), we find an objective response rate (measurable benefit in 66 patients treated using molecularly selected drugs) of 10%. Indeed, the positive results reported in this study reflected not a response rate but instead a 30% improvement in the time to disease progression, associated with molecular drug selection, compared with the patients prior, most recent (unsuccessful) therapies. To put this in context, a patient could arguably fail a physician-selected treatment after 1 month, and then receive a Caris selected therapy. If they responded for 1 month plus 10 days (a 30% improvement), they were counted as a success. The clinical relevance of that degree of improvement seems questionable.
While we fully understand the excitement surrounding genetic analyses, the more sophisticated researchers in the field are beginning to appreciate that the complexity of human biology demands more global (functional) analytic platforms that encompass all of the mechanisms of response and resistance. In this light, the presence of a gene cannot predict whether that gene will be expressed, active, counter-acted by a complementary gene, or functional.
We believe that human biology must be taken at face value in its most complex state. This is known as the phenotype and must be examined for the biological features that these interconnected cellular systems create. This field now known as biosystematics, or systems biology, recognizes the redundancies and uncertainties that separate the genotype (molecular profiling) from the phenotype (functional analyses) are not trivial. Our laboratory conducts phenotype analyses. Caris conducts genotype analyses.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Functional Profiling, Biomarkers, Tumor, Tumor Profiling, Biology, Molecular Profiling, Tumor Analysis
1
Answer |
3 months ago
Every medical oncologist wants to cure their patients. The problem has been when to stop. The general dictum that has guided medical oncology for 50 years can be summed up as “if some is good, more is better”. This regrettably may not be true. As a rule, patients will manifest benefit from therapy within 2-3 cycles. Thereafter, treatment is continued until complete remission, failure to respond, or intolerable toxicity. We witnessed the most glaring example of over treatment during the era of bone marrow transplantation for solid tumors which proved toxic and ineffective for most cancers, the exception being leukemias, myelomas and some lymphomas. Our preference is to use the right drugs from the start to achieve the best response with the least toxicity. Depending upon the tumor type, we complete treatment with 2 additional cycles beyond complete remission or in the highest risk cases, we may suggest a form of maintenance treatment. All of these therapies are administered with a very close attention to quality of life.
Every medical oncologist wants to cure their patients. The problem has been when to stop. The general dictum that has guided medical oncology for 50 years can be summed up as “if some is good, more is better”. This regrettably may not be true. As a rule, patients will manifest benefit from therapy within 2-3 cycles. Thereafter, treatment is continued until complete remission, failure to respond, or intolerable toxicity. We witnessed the most glaring example of over treatment during the era of bone marrow transplantation for solid tumors which proved toxic and ineffective for most cancers, the exception being leukemias, myelomas and some lymphomas. Our preference is to use the right drugs from the start to achieve the best response with the least toxicity. Depending upon the tumor type, we complete treatment with 2 additional cycles beyond complete remission or in the highest risk cases, we may suggest a form of maintenance treatment. All of these therapies are administered with a very close attention to quality of life.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Palliative Care, Oncology, Overtreatment, End Of Life
1
Answer |
3 months ago
Every patient must have a definitive determination of the tissue of origin. This is accomplished at the time of a careful review of the biopsy and provides a diagnosis. The second step is to determine where the disease has spread to at the time of diagnosis. This is done through x-rays, PET scans and MRIs, and is known as “staging”. At this point, most physicians begin treatment.
We add a third dimension to our workup. Knowing where it came from (diagnosis) and where it has gone to (stage), our laboratory then seeks to determine what to do about it (chemosensitivity). That is where our group is different from many. Every patient must have a definitive determination of the tissue of origin. This is accomplished at the time of a careful review of the biopsy and provides a diagnosis. The second step is to determine where the disease has spread to at the time of diagnosis. This is done through x-rays, PET scans and MRIs, and is known as “staging”. At this point, most physicians begin treatment.
We add a third dimension to our workup. Knowing where it came from (diagnosis) and where it has gone to (stage), our laboratory then seeks to determine what to do about it (chemosensitivity). That is where our group is different from many.
We add a third dimension to our workup. Knowing where it came from (diagnosis) and where it has gone to (stage), our laboratory then seeks to determine what to do about it (chemosensitivity). That is where our group is different from many. Every patient must have a definitive determination of the tissue of origin. This is accomplished at the time of a careful review of the biopsy and provides a diagnosis. The second step is to determine where the disease has spread to at the time of diagnosis. This is done through x-rays, PET scans and MRIs, and is known as “staging”. At this point, most physicians begin treatment.
We add a third dimension to our workup. Knowing where it came from (diagnosis) and where it has gone to (stage), our laboratory then seeks to determine what to do about it (chemosensitivity). That is where our group is different from many.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Oncology, Treatment, Treatment Options, Cancer
1
Answer |
3 months ago
Cancers produce novel proteins that can suggest, though not diagnose, a source of the tumor. The original blood tests included CEA, known to occur in many adenocarcinomas including lung, gastrointestinal and breast. CA 27-29 and CA15-3 have been most closely associated with breast cancers. CA 125 is the marker for ovarian as is HE4, a more recently developed test. PSA and prostatic acid phosphatase are used in prostate cancer. CA 19-9 is associated with pancreatic cancer. Germ cell tumors can produce B-HCG and AFP. AFP is also associated with hepatocellular cancer. Despite all of this, some tumors express no markers while other tumors express markers not generally associated with that disease type. This is part of the reason why markers are not promoted for general use at academic centers.
Cancers produce novel proteins that can suggest, though not diagnose, a source of the tumor. The original blood tests included CEA, known to occur in many adenocarcinomas including lung, gastrointestinal and breast. CA 27-29 and CA15-3 have been most closely associated with breast cancers. CA 125 is the marker for ovarian as is HE4, a more recently developed test. PSA and prostatic acid phosphatase are used in prostate cancer. CA 19-9 is associated with pancreatic cancer. Germ cell tumors can produce B-HCG and AFP. AFP is also associated with hepatocellular cancer. Despite all of this, some tumors express no markers while other tumors express markers not generally associated with that disease type. This is part of the reason why markers are not promoted for general use at academic centers.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Tumor Tests, Tumor, Blood Tests, Tumor Markers, Tests, Cancer Tests, Cancer
1
Answer |
3 months ago
There is a growing recognition that pathological findings may assist in prognosis. It is unclear from your question what disease this represented. Perineural extension is often noted in prostate cancer. This may confer a higher risk of recurrence in this disease. Again, this is disease specific. A growing number of algorithms are being developed that combine histology, nuclear grade, lymphatic invasion, vascular invasion, and molecular markers to provide better information regarding risk of recurrence.
There is a growing recognition that pathological findings may assist in prognosis. It is unclear from your question what disease this represented. Perineural extension is often noted in prostate cancer. This may confer a higher risk of recurrence in this disease. Again, this is disease specific. A growing number of algorithms are being developed that combine histology, nuclear grade, lymphatic invasion, vascular invasion, and molecular markers to provide better information regarding risk of recurrence.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Reduce Breast Cancer Risk, Perineural Invasion, Breast Cancer, Breast Cancer Risk
1
Answer |
3 months ago
This is a particularly controversial area of clinical medicine. While every patient desires close followup, the insurers and those engaged in the field of “evidence-based-medicine” point to the lack of survival benefit associated with the close monitoring of tumor markers and other harbingers of early relapse. It is indeed a dilemma, as both physicians and patients are comforted by negative workups and regular followups. It may, in the future, become necessary for patients to assume the costs of their followup visits after an adequate period of time has elapsed. As a rule, for most solid tumors, three years of followup with NED and certainly 5 years of followup with NED, is considered adequate. Despite this, some tumors, among them, ER+ breast cancers can manifest late relapses.
This is a particularly controversial area of clinical medicine. While every patient desires close followup, the insurers and those engaged in the field of “evidence-based-medicine” point to the lack of survival benefit associated with the close monitoring of tumor markers and other harbingers of early relapse. It is indeed a dilemma, as both physicians and patients are comforted by negative workups and regular followups. It may, in the future, become necessary for patients to assume the costs of their followup visits after an adequate period of time has elapsed. As a rule, for most solid tumors, three years of followup with NED and certainly 5 years of followup with NED, is considered adequate. Despite this, some tumors, among them, ER+ breast cancers can manifest late relapses.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Survivorship, Oncology, Post Treatment, Oncology Follow Up
1
Answer |
3 months ago
Interestingly, triple negative breast cancer (ER/PR/HER2 negative) is more than one disease. While some subsets reveal exquisite sensitivity to drugs like Cisplatin, other tumors may have features that render them better targets for agents that inhibit signaling pathways like AKT/mTOR. There may be other triple negatives for whom androgen therapy could hold benefit. Our experience with the Cisplatin/Gemcitabine doublet in this group, a regimen that we originally developed (Nagourney et al, J Clin Oncol 2000) is one example of good outcome with a appropriately selected chemotherapy.
Interestingly, triple negative breast cancer (ER/PR/HER2 negative) is more than one disease. While some subsets reveal exquisite sensitivity to drugs like Cisplatin, other tumors may have features that render them better targets for agents that inhibit signaling pathways like AKT/mTOR. There may be other triple negatives for whom androgen therapy could hold benefit. Our experience with the Cisplatin/Gemcitabine doublet in this group, a regimen that we originally developed (Nagourney et al, J Clin Oncol 2000) is one example of good outcome with a appropriately selected chemotherapy.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Triple Negative, Triple Negative Breast Cancer, Breast Cancer Treatments, Triple Negative Treatments
1
Answer |
3 months ago
One might imagine three platforms for the study of human tumor biology. Genomics studies information at the level of DNA, while proteomics examines protein expression. Functional analyses approximate the living organism by examining the behavior of cancer cells in their own environment. This allows heretofore unrecognized complexities to be examined in real time. A growing number of investigators around the world are beginning to recognize the important and clinical application of these techniques.
One might imagine three platforms for the study of human tumor biology. Genomics studies information at the level of DNA, while proteomics examines protein expression. Functional analyses approximate the living organism by examining the behavior of cancer cells in their own environment. This allows heretofore unrecognized complexities to be examined in real time. A growing number of investigators around the world are beginning to recognize the important and clinical application of these techniques.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Functional Profiling, Tumor Profiling, Biology, Tumor Biology, Tumore Functional Profiling
1
Answer |
3 months ago
Please visit our website at www.rational-t.com for additional information and references. In addition, the Ralph Moss’ book, “Customized Chemotherapy” Equinox Press 2011, is an excellent source regarding the history and application of these techniques.
Please visit our website at www.rational-t.com for additional information and references. In addition, the Ralph Moss’ book, “Customized Chemotherapy” Equinox Press 2011, is an excellent source regarding the history and application of these techniques.
New answer by RobertNagourneyMD (Physician - Oncology - Hematology/Oncology (Verified)) in topic(s) Functional Profiling, Tumor Functional Profiling, Research, Tumors
1
Answer |
3 months ago
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