Week 6: Regan
The vicissitudes of this week were personally testing. I had a major upset with my research when we ran out of our endothelial cell media since it has been backordered from Lonza for weeks now. Without media to feed my cells and keep them alive, I was unable to perform any experiments this week. Instead I turned to focus more on developing my clinical experiences in hematology-oncology.
Firstly, I had the serendipitous opportunity to attend the final Grand Rounds presentation in heme/onc entitled "Genomic Advances in CLL" given by Dr. Andrew Lipsky, MD. The basis of the talk was to outline the current understanding of the rational for treatment order in chronic lymphocytic leukemia. Lipsky covered that CLL is a hematological malignancy found in elderly patients with a lot of variability in the clinical course required. From his talk I learned that all CLLs are cancers of B cells that occur after the B cells encounter antigen. Malignancies in this stage are thought to occur because major gene rearrangements happen after antigen exposure providing for accidentally cancerous genetic mistakes. The two subgroups of CLL are decided by the next post-antigen step: entry into the germinal center. In the healthy state, germinal centers are collections of cells in the lymph nodes that allow for B cells to make better antibodies to recognize antigen. CLLs that have no germinal center exposure tend to be more dangerous than germinal center-experienced CLLs. This distinction is important because it gives clues about how the patient will respond to treatment. In an effort to discover more clues on a patient-by-patient level, doctors and engineers use genomics to understand the cancer on genetic level. This approach can give incites to the potential for progression to Richter's syndrome as well as over all progression of the cancer. On such form of progression, the development of drug resistance, can be noted in a point mutation in the 481 cysteine of Bruton's Tyrosine Kinase (BTK). This mutation can be seen 3-6 months after treatment with Ibrutinib, an irreversible BTK inhibitor. This mutation makes Ibrutinib less effective and warrants the use of other targeted therapies in CLL, especially second generation BTK inhibitors in which effectiveness is not altered by the mutation. Lipsky mentioned that all of this research is possible because of the accessibility of CLL. In order to get a biopsy, a simple blood draw is performed where in solid cancers fine or core needle biopsies would be required but typically more invasive and less justifiable. Because blood samples are so simple to obtain, researchers and physicians are able to get genetic snapshots of how the cancer is responding to treatment and changing over time. These snapshots have allowed the field of CLL research to better characterize CLL on a patient-by-patient level and open up the possibilities of precision medicine. In summary, this talk made me hopeful for the future of cancer research because of the advances make in understanding CLL and the potentials for those understandings to be translated into other cancers like lymphoma, my area of research.
Firstly, I had the serendipitous opportunity to attend the final Grand Rounds presentation in heme/onc entitled "Genomic Advances in CLL" given by Dr. Andrew Lipsky, MD. The basis of the talk was to outline the current understanding of the rational for treatment order in chronic lymphocytic leukemia. Lipsky covered that CLL is a hematological malignancy found in elderly patients with a lot of variability in the clinical course required. From his talk I learned that all CLLs are cancers of B cells that occur after the B cells encounter antigen. Malignancies in this stage are thought to occur because major gene rearrangements happen after antigen exposure providing for accidentally cancerous genetic mistakes. The two subgroups of CLL are decided by the next post-antigen step: entry into the germinal center. In the healthy state, germinal centers are collections of cells in the lymph nodes that allow for B cells to make better antibodies to recognize antigen. CLLs that have no germinal center exposure tend to be more dangerous than germinal center-experienced CLLs. This distinction is important because it gives clues about how the patient will respond to treatment. In an effort to discover more clues on a patient-by-patient level, doctors and engineers use genomics to understand the cancer on genetic level. This approach can give incites to the potential for progression to Richter's syndrome as well as over all progression of the cancer. On such form of progression, the development of drug resistance, can be noted in a point mutation in the 481 cysteine of Bruton's Tyrosine Kinase (BTK). This mutation can be seen 3-6 months after treatment with Ibrutinib, an irreversible BTK inhibitor. This mutation makes Ibrutinib less effective and warrants the use of other targeted therapies in CLL, especially second generation BTK inhibitors in which effectiveness is not altered by the mutation. Lipsky mentioned that all of this research is possible because of the accessibility of CLL. In order to get a biopsy, a simple blood draw is performed where in solid cancers fine or core needle biopsies would be required but typically more invasive and less justifiable. Because blood samples are so simple to obtain, researchers and physicians are able to get genetic snapshots of how the cancer is responding to treatment and changing over time. These snapshots have allowed the field of CLL research to better characterize CLL on a patient-by-patient level and open up the possibilities of precision medicine. In summary, this talk made me hopeful for the future of cancer research because of the advances make in understanding CLL and the potentials for those understandings to be translated into other cancers like lymphoma, my area of research.
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