EvanLipsonMD
(Physician
- Oncology - Hematology/Oncology
(Verified)
)
| Communities:
Melanoma
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Thank You's:
1
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| Member Since: Feb. 2012 |
Questions:
0
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Answers:
8
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Professional Statement
Dr. Lipson received his Bachelor of Arts in economics from the University of Maryland in 1996. After working as a producer at CNN's "Larry King Live" for a few years, he completed a post-baccalaureate program at Georgetown University in Washington, DC. He received his medical degree in 2005 from the Mount Sinai School of Medicine in New York City, where he graduated with distinction in research. He completed his internship and residency in Internal Medicine at the Johns Hopkins Hospital, and completed his Medical Oncology fellowship at the Johns Hopkins Kimmel Cancer Center.
Dr. Lipson's primary research interest is in early phase clinical trials for melanoma and other cutaneous malignancies. As a member of the Johns Hopkins Melanoma Program and the Immunology Program at the Kimmel Cancer Center, he focuses on evaluating novel therapies for patients with high risk or advanced disease. Dr. Lipson is a co-investigator on multiple trials, involving partners from both industry and academia, which address two major areas of opportunity in melanoma therapeutics: immunotherapy and molecular pathway inhibition. With an eye toward developing synergistic combinatorial therapies, Dr. Lipson is leading clinical research to test a cellular melanoma vaccine – melanoma GVAX – designed to stimulate T-cell immunity in melanoma patients. Other immunomodulatory therapies under investigation, including monoclonal antibodies such as anti-PD-1 and anti-B7-H1, have shown early promise in clinical trials led by Johns Hopkins investigators and may eventually be combined with vaccine therapies. Dr. Lipson and his colleagues recently authored a book chapter reviewing the state-of-the-art on these therapies.
In related research, Dr. Lipson is collaborating with Hopkins' expert Dr. Jim Herman to evaluate the impact of gene silencing (epigenetics) on immunoregulatory and anti-angiogenesis pathways in melanoma. These studies aim to better identify early stage melanoma patients who are at risk for disease progression, and to select those patients with advanced disease who are most likely to respond to immune-based therapy.
In addition to his research activities, Dr. Lipson conducts a regular clinical practice as part of the multidisciplinary Melanoma Program at Johns Hopkins. To learn more or schedule an appointment, call 410-616-7660.
Dr. Lipson is also the founder of “Seize the Days,” a non-profit organization that chronicles the stories of cancer patients who, with power and determination, find interesting and meaningful ways to add life to their days. For more information, visit
http://seizethedays.org.
Professional Info
Primary specialty:
Oncology - Hematology/Oncology
Secondary specialty:
Internal Medicine
Medical school:
Mount Sinai School of Medicine
Residency:
The Johns Hopkins Hospital
Fellowship:
The Johns Hopkins Hospital
Board certifications:
American Board of Internal Medicine
Areas of expertise:
Basal Cell Carcinoma, Clinical Trials, Immunotherapy, Medical Oncology, Melanoma, Merkel Cell Carcinoma, Oncology, Skin Cancer
Practice name:
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Hospital
Practice address:
401 N. Broadway
Baltimore, MD
21231
Practice phone number:
410-614-0040
EvanLipsonMD Activities
The FDA’s approval in 2011 of Zelboraf (vemurafenib) is another important step in what is a rapidly changing landscape for melanoma and cancer therapy in general. Some cancers are formed when, inside a cell, a signal is passed from one molecule to another, like a game of telephone. Zelboraf stops that signal from being sent and, in doing so, stops the growth of the cancer. Data published in February of 2012 in the New England Journal of Medicine showed that Zelboraf extended average survival to about 16 months for stage IV melanoma patients whose tumors had BRAF mutations. The drug was generally well tolerated with minimal side effects. These results, while promising on their own, are a stepping stone to another exciting prospect in cancer research: combining drugs like vemurafenib with other therapies, where two treatments used together might be more effective than each one by itself.
The FDA’s approval in 2011 of Zelboraf (vemurafenib) is another important step in what is a rapidly changing landscape for melanoma and cancer therapy in general. Some cancers are formed when, inside a cell, a signal is passed from one molecule to another, like a game of telephone. Zelboraf stops that signal from being sent and, in doing so, stops the growth of the cancer. Data published in February of 2012 in the New England Journal of Medicine showed that Zelboraf extended average survival to about 16 months for stage IV melanoma patients whose tumors had BRAF mutations. The drug was generally well tolerated with minimal side effects. These results, while promising on their own, are a stepping stone to another exciting prospect in cancer research: combining drugs like vemurafenib with other therapies, where two treatments used together might be more effective than each one by itself.
Melanoma spreads to other parts of the body in two ways: through the lymphatics and through the bloodstream. If caught early, the large majority of melanomas are removed before spreading to other parts of the body. In later stages, however, melanoma often spreads through either or both of these routes.
Melanoma spreads to other parts of the body in two ways: through the lymphatics and through the bloodstream. If caught early, the large majority of melanomas are removed before spreading to other parts of the body. In later stages, however, melanoma often spreads through either or both of these routes.
The answer to this question depends on many things, including the stage of disease. The more advanced the disease that was removed by surgery, the more likely it is to come back. There are several clinical trials in progress that are investigating ways to reduce the chance that melanoma will return once someone is declared N.E.D. It’s difficult to compare melanoma to other cancers in terms of likelihood of disease recurrence.
The answer to this question depends on many things, including the stage of disease. The more advanced the disease that was removed by surgery, the more likely it is to come back. There are several clinical trials in progress that are investigating ways to reduce the chance that melanoma will return once someone is declared N.E.D. It’s difficult to compare melanoma to other cancers in terms of likelihood of disease recurrence.
In the United States there are two FDA approved forms of interferon. The first is standard, high-dose interferon, which is given over 12 months. The first month is given intravenously at 20 million units/m2, five consecutive days per week for 4 weeks. The remaining 11 months are given as subcutaneous injections at 10 million units/m2 three times per week. The second form is called pegylated interferon (Sylatron) and is given weekly at 6 mcg/kg/week subcutaneously for eight doses, followed by 3 mcg/kg/week subcutaneously for up to five years. There are several factors involved in choosing between the options, including convenience and length of therapy. If you are considering interferon, it’s also important to talk with your oncologist about clinical trials of medications designed to prevent melanoma from coming back after surgery.
In the United States there are two FDA approved forms of interferon. The first is standard, high-dose interferon, which is given over 12 months. The first month is given intravenously at 20 million units/m2, five consecutive days per week for 4 weeks. The remaining 11 months are given as subcutaneous injections at 10 million units/m2 three times per week. The second form is called pegylated interferon (Sylatron) and is given weekly at 6 mcg/kg/week subcutaneously for eight doses, followed by 3 mcg/kg/week subcutaneously for up to five years. There are several factors involved in choosing between the options, including convenience and length of therapy. If you are considering interferon, it’s also important to talk with your oncologist about clinical trials of medications designed to prevent melanoma from coming back after surgery.
Genetic testing can mean several things. Testing a patient’s melanoma for the presence of a BRAF or C-KIT mutation can be done anytime, although it is important to have those results before starting a BRAF or C-KIT inhibitor. Genetic testing is also being investigated in families where 3 or more members have had melanoma. This type of genetic testing has less of a direct impact on the therapies we choose, but it will, some day, help our understanding of why certain people are at risk for the disease.
Genetic testing can mean several things. Testing a patient’s melanoma for the presence of a BRAF or C-KIT mutation can be done anytime, although it is important to have those results before starting a BRAF or C-KIT inhibitor. Genetic testing is also being investigated in families where 3 or more members have had melanoma. This type of genetic testing has less of a direct impact on the therapies we choose, but it will, some day, help our understanding of why certain people are at risk for the disease.
Yervoy is FDA approved for stage IV melanoma and can be used in patients whose disease cannot be removed by surgery. The biggest benefit of Yervoy is that it improves the average survival of patients compared to other treatments, like chemotherapy. It’s important for patients to talk to their oncologists about the risks and benefits of Yervoy, which, because of the way it interacts with the immune system, can cause some serious side effects.
Yervoy is FDA approved for stage IV melanoma and can be used in patients whose disease cannot be removed by surgery. The biggest benefit of Yervoy is that it improves the average survival of patients compared to other treatments, like chemotherapy. It’s important for patients to talk to their oncologists about the risks and benefits of Yervoy, which, because of the way it interacts with the immune system, can cause some serious side effects.
New answer by
EvanLipsonMD (Physician - Oncology - Hematology/Oncology
(Verified)) in topic(s)
Melanoma Medications,
Drugs,
Stage 4 Melanoma,
Ipilimumab (Yervoy),
Medications,
Melanoma Drugs,
Cancer Medications,
Cancer Drugs,
Melanoma Treatments,
Cancer Treatments,
Melanoma
Currently there are two genetic mutations in melanoma that have treatment options: BRAF mutations and C-KIT mutations. Tumors that have mutations in the BRAF gene often respond to BRAF inhibitors, such as Zelboraf (vemurafenib). Tumors with C-KIT mutations may respond to drugs such as Gleevec (imatinib). Many of these drugs are still in various stages of testing, and some of the most promising are only available on clinical trials.
Currently there are two genetic mutations in melanoma that have treatment options: BRAF mutations and C-KIT mutations. Tumors that have mutations in the BRAF gene often respond to BRAF inhibitors, such as Zelboraf (vemurafenib). Tumors with C-KIT mutations may respond to drugs such as Gleevec (imatinib). Many of these drugs are still in various stages of testing, and some of the most promising are only available on clinical trials.
New answer by
EvanLipsonMD (Physician - Oncology - Hematology/Oncology
(Verified))
This is a very common question. In general, we think of melanoma as being caused by sun (ultraviolet) damage to the skin. For some melanomas this is true, however, for melanomas that start on the soles of the feet, the palms of the hands, under the fingernails, inside the mouth or the nose, or other areas not exposed to the sun, the reason that melanomas form is probably related to other sources of DNA damage. We are just beginning to identify some of the genetic mutations in these types of melanomas, which allows us to design drugs that will stop these cells from growing out of control. (see
http://talkabouthealth.com/what-genetic-mutations-of-melanoma-currently-have-treatment-options-what-are-those-treatments) It’s also important to realize that although some melanomas begin as a mole, other melanomas develop from normal-appearing skin.
This is a very common question. In general, we think of melanoma as being caused by sun (ultraviolet) damage to the skin. For some melanomas this is true, however, for melanomas that start on the soles of the feet, the palms of the hands, under the fingernails, inside the mouth or the nose, or other areas not exposed to the sun, the reason that melanomas form is probably related to other sources of DNA damage. We are just beginning to identify some of the genetic mutations in these types of melanomas, which allows us to design drugs that will stop these cells from growing out of control. (see
http://talkabouthealth.com/what-genetic-mutations-of-melanoma-currently-have-treatment-options-what-are-those-treatments) It’s also important to realize that although some melanomas begin as a mole, other melanomas develop from normal-appearing skin.