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Ruben Mesa, MD
RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified) )| Communities: CLL (Chronic Lymphocytic Leukemia) | Answers: 8 |
| Member Since: Jul. 2012 |
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Professional Statement
Professor Mesa grew up in Chicago, IL and obtained his undergraduate work in Nuclear Engineering and Physiology from the University of Illinois in Champaign, Urbana. He subsequently came to Mayo Clinic where he obtained both his medical degree and subsequent training in Internal Medicine and Hematology and Medical Oncology. Dr. Mesa joined the faculty of the Mayo Clinic in Rochester, MN in 2002 as a Consultant Hematologist. His scholarship has focused on advancing the understanding and therapy of the chronic myeloproliferative neoplasms (MPNs) in which he has authored over 300 manuscripts book chapters, editorials, letters, or meeting abstracts. In these disorders, he has been very active in evaluating novel therapeutics, implementing clinical trials, working with quality of life studies and very actively involved with national patient groups. He has been principal investigator or co-principal investigator in 40 clinical trials for patients with MPNs, or other myeloid disorders. He is committed to improving the therapy and quality of life in MPN patients, and is supported by the MPN research Foundation for his work in the MPN QOL International Study Group (www.mpn-qol.org). These latter efforts focus on the assessment of MPN symptoms on the quality of life for MPN patients, and the impact that therapies can have on their burden of illness. He is a frequently invited speaker on the MPNs with over 200 such lectures, and visiting professorships, nationally and internationally. He is an active part, and co-founder, of the International Working Group for Myelofibrosis Research and Treatment (IWG-MRT), and the NCI Funded MPD Research Consortium. He founded the biennial Mayo Clinic Living With a Blood Disease Symposium for patients afflicted with hematologic diseases. He currently sits on the editorial board of the journal Blood, and several other key hematology journals.
Currently, at the Mayo Clinic he transferred to Mayo Clinic in Arizona in 2009 where he is Professor of Medicine and Chair of the Division of Hematology & Medical Oncology. Dr. Mesa also serves as the Deputy Director for Arizona of the Mayo Clinic Cancer Center, an NCI Designated Comprehensive Cancer Center. He has founded an annual national meeting for cancer and hematologic malignancy patients (The Living with Cancer Meeting), held in January annually in Scottsdale, AZ. He divides his time equally between research, patient care, and the organization of clinical trials. He enjoys spending time with his wife and 2 children, and is an avid triathlete.
Currently, at the Mayo Clinic he transferred to Mayo Clinic in Arizona in 2009 where he is Professor of Medicine and Chair of the Division of Hematology & Medical Oncology. Dr. Mesa also serves as the Deputy Director for Arizona of the Mayo Clinic Cancer Center, an NCI Designated Comprehensive Cancer Center. He has founded an annual national meeting for cancer and hematologic malignancy patients (The Living with Cancer Meeting), held in January annually in Scottsdale, AZ. He divides his time equally between research, patient care, and the organization of clinical trials. He enjoys spending time with his wife and 2 children, and is an avid triathlete.
Professional Info
Credential: MD
Primary specialty: Oncology - Hematology/Oncology
Medical school: Mayo Medical School
Residency: Mayo Graduate School of Medicine
Fellowship: Mayo Graduate School of Medicine
Hospital affiliation: Mayo Clinic in Arizona
Practice address:
13400 E. Shea Blvd.
Scottsdale, AZ
85259
Practice phone number: 800-446-2279
RubenMesaMD Activities
I would refer you somewhat to my answer for a previous question (http://talkabouthealth.com/what-factors-determine-if-an-allogeneic-stem-cell-transplant-is-recommended-to-treat-myeloproliferative-neoplasms), but would answer that there are different factors we consider in terms of prognosis. For patients with ET and P vera, important prognostic factors are the age of the patient, whether the bone marrow suggests that the patient has true ET vs. early myelofibrosis. We also recognize that there are prognostic factors in terms of the likelihood of the development of a blood clot or bleeding event, including age over 60, prior blood clotting or bleeding events in the past, and a white count of over 15,000. For individuals with myelofibrosis, I described the prognostic factors in a previous questions (http://talkabouthealth.com/what-factors-determine-if-an-allogeneic-stem-cell-transplant-is-recommended-to-treat-myeloproliferative-neoplasms) with clearly the most significant prognostic factors that we can find is movement towards acute leukemia. The myeloproliferative neoplasms can convert to acute leukemia either from myelofibrosis or, much less commonly, from ET or P vera. This potential for change is important as it is very challenging and difficult to treat and typically can only be corrected with very aggressive sequential chemotherapy followed by stem cell transplantation.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
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9 months ago
A difficult question and a very personalized decision between a patient and their physician. In general, the discussion of bone marrow transplantation is limited to those individuals with myelofibrosis. It has not been thought that the severe risks that can come with bone marrow transplantation are appropriate for those individuals with earlier disease such as P vera and ET. There have been rare exceptions for people with exceeding difficult disease. Amongst patients with myelofibrosis, we typically look at several factors including the age of the patient, is there an available donor and, very importantly, the risk with the disease. What is the expected life expectancy with myelofibrosis and have used the different range of dynamic prognostic scoring models out there, including the DIPSS and the DIPSS plus that look at many factors to get a sense of how life threatening the disease is and we try to balance that against what are the expected outcomes with stem cell transplantation. The prognostic factors which are important are 1) age of the patient, particularly whether they are under or over age 65; whether they have anemia, a hemoglobin of less than 10, particularly whether they need blood transfusions as part of that; a white cell count over 25,000; significant constitutional symptoms, i.e. weight loss greater than 10%, severe bone pain, a low platelet count of less than 100,000, chromosomal changes in the bone marrow or evidence of movement toward acute leukemia. The more of these factors an individual has, the greater concern we have with their myelofibrosis, the stronger the case potentially for considering stem cell transplantation.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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9 months ago
Impact of therapies on myeloproliferative neoplasms is both in the short term and the long term. In the short term we follow three things: 1) How a patient feels. If they had symptoms to begin with, are the symptoms improved, whether this be difficulties with concentration, headaches, fatigue, itching, etc. 2) The size of the spleen. The goal is improving the size of the spleen. We clearly monitor this by physical examination or on clinical trials with imaging. 3) The blood counts. Is it our goal to decrease elevated blood counts as we would in patients with ET or P vera? Is it to improve low blood counts as we might in myelofibrosis? These are all short-term goals. In the long term, we monitor how the patient is doing, their weight, and we can monitor changes in the bone marrow biopsy. Medical treatments, if they impact the appearance of the bone marrow, are typically a slow process that can only be assessed over several months or even a year to two. Changes in the bone marrow biopsy have been most consistent in patients who have successfully received bone marrow transplantation.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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9 months ago
I would say, most accurately, there is not one specific sequence of chemotherapy that one uses to treat MPNs. Treatment must be individualized as patients with ET, P vera and myelofibrosis can be quite heterogeneous. I would say, most accurately, patients with ET and PV, the goals of our therapy typically early on have been to try to decrease the risk of blood clots and bleeding, control symptoms if we can, and the goals of therapy for myelofibrosis, depending upon the severity of myelofibrosis, are to try to alleviate suffering with the disease, improve difficulties associated with the disease or, in appropriate situations, try to cure the disease with bone marrow transplantation. The key for choosing therapy is really dependent upon the goals of therapy and the stage of the disease and how an individual is affected, and can range in patients with ET and P vera, to control of counts to try to decrease the risk of blood clots and bleeding, medicines such as aspirin, phlebotomy to try to control an increase in the red cell count, and appropriate choice of medicine to reduce blood counts – hydroxyurea, anagrelide or interferon (pegylated interferon). In myelofibrosis, goals need to be determined for therapy in sequence of events with the currently only FDA-approved therapy being ruxolitinib, the JAK2 inhibitor, which improves splenomegaly, significant symptoms and potentially even improves survival in patients with advanced myelofibrosis as well as that of bone marrow transplantation, which can cure myelofibrosis, but it is a very involved life altering procedure with the risks that are significant that need to be considered.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
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9 months ago
The myeloproliferative neoplasms are diseases of the bone marrow and to fully understand the disease at the time of diagnosis, we need to be certain where an individual stands in terms of their blood test, how they feel and looking at their bone marrow. It is possible to make an accurate diagnosis of a myeloproliferative neoplasm, particularly P vera, without a bone marrow aspirate and biopsy. That being said, it is essential for us to know where we will begin with a myeloproliferative neoplasm so that we can assess if progression occurs. So, at diagnosis, it is helpful to obtain baseline molecular testing to see whether an individual has the JAK2 mutation, to make certain that the disease is a myeloproliferative neoplasm and not a secondary cause of a change in the blood count. It is important to exclude other bone marrow conditions that can afflict individuals and cause similar blood count changes. It is important to obtain a bone marrow biopsy. There are three pieces of information we learn from the bone marrow aspirate and biopsy we do not learn from the blood; specifically, whether there are any chromosome changes, what is the baseline degree of scarring and is there any movement towards acute leukemia. Other things that can be helpful in the diagnosis process are evaluating to see if the spleen is enlarged by imaging, if not readily able to palpate the spleen at physical examination at the time of diagnosis as well as being certain there are not any other significant illnesses present. We then use the World Health Organization criteria for diagnosing the MPNs, the criteria which were published in 2008, which help us to answer: 1) does the patient have an MPN, and 2) if so, which type.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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9 months ago
Our group here at Mayo Clinic has been very active trying to understand the impact that myeloproliferative neoplasms have upon patients who are affected. We found in 2007, in an internet-based questionnaire of over 1000 patients with MPNs around the world, that patients are quite symptomatic with difficulties of fatigue, night sweats, fevers and weight loss. These symptoms are most problematic in myelofibrosis, but can be present in patients with P vera and ET. We subsequently developed and now have in multiple languages the Myeloproliferative Neoplasm Symptom Assessment Form. Using this form of 27 different questions, we have been able to demonstrate the impact that MPNs have on patients with many common side effects being those associated with the size of the spleen, but many which are independent of the enlargement of the spleen including fatigue, itching, difficulty with sexual function or intimacy, insomnia, pain, weight loss. These instruments both help us identify the impact that the diseases have prior to a therapy and hopefully we can use these instruments or questionnaires to identify benefit that these medicines bring to patients who receive them.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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9 months ago
Currently, our understanding of the causes and progression of the myeloproliferative neoplasms is still partial. We have learned much from 2005 on with the identification of many new mutations in which the JAK2 v617f was only the first. Still many questions remain, including why patients progress, why patients can transform to acute leukemia and how is myelofibrosis different than ET and P vera. With all of these questions, many targeted medicines have been developed. As I answered in a previous answer (http://talkabouthealth.com/what-is-a-jak2-inhibitor-and-what-does-it-have-to-do-with-myeloproliferative-neoplasms), there are a variety of JAK2 inhibitors that are having an impact on MPNs including splenomegaly, a benefit that is seen across most of the JAK2 inhibitors, including improvement in symptoms. There has been variable impact of these medicines in improving anemia. Other targeted therapies are targeting other genetic aspects of the cells afflicted by the myeloproliferative neoplasms, including histone deacetylase inhibitors. This is a medicine that acts on genetic pathways, as well as new medicines that are trying to block the process in the development of myelofibrosis. Many ongoing clinical trials are being used with these agents alone or in combination and many efforts to try to better understand the origin of the MPNs so that we can develop even more effective targeted therapies.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
9 months ago
The myeloproliferative neoplasms include the diseases of myelofibrosis (MF), essential thrombocythemia (ET) and polycythemia vera (PV). These diseases, we believe, are chronic bone marrow diseases that are best thought of as, in part, chronic leukemias. These are genetic diseases, not the genes that we inherit from our parents necessarily, but the genes that control the growth of our blood cells. A certain genetic change was found in 2002 in a key protein called JAK2, a mutation called the JAK2 v617f mutation. This mutation is present in most of the patients with P vera and half of those with ET and myelofibrosis. JAK2 inhibitors are medicines, typically pills, molecules that help to block the increased activity of JAK2 and the pathway in which it is associated in the blood in patients with MPNs. There is currently one JAK2 inhibitor that is approved by the FDA, that is ruxolitinib (Jakafi) made by the company Incyte for patients with intermediate and high-risk myelofibrosis. There are many other JAK2 inhibitors under testing including ruxolitinib for ET and P vera as well as others for myelofibrosis, including CYT387, SAR302503, LY2784544 amongst others.
New answer by RubenMesaMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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9 months ago
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