Audio and slides for this presentation are available on YouTube: http://youtu.be/FyL7sCDc4Zc
Mikael Rinne, MD, PhD, of Dana-Farber Cancer Institute's Center for Neuro-Oncology, discusses the science and genetics behind brain tumors. Rinne covers how scientists can discover DNA alterations in cancer, which alterations are found in brain tumors, and what scientists can do about the alterations.
This talk was originally given at Dana-Farber's "Living with Brain Tumors" forum on Sept. 7, 2013.
For more information, visit the website for Dana-Farber's Center for Neuro-Oncology: http://bit.ly/13nlpEv
ABSTRACT- Lung cancer is the most common cause of cancer related mortality worldwide. The epidermal-growth-factor receptor (EGFR) cascades the signaling pathway that regulates tumor-cell proliferation, invasion, angiogenesis, metastasis, and apoptosis. Since EGFR is often over-expressed in NSCLC and the level of EGFR expression correlates with poor prognosis. EGFR inhibitors have been developed as a novel therapy for non-small-cell lung cancer (NSCLC). Gefitinib is the first molecular targeted agent approved for the treatment of advanced NSCLC. It is a highly effective EGFR TK inhibitor (TKI) selectively blocks the signal transduction pathways implicated in cancer growth. Key-words- Lung Cancer, EGFR, NSCLC, Tyrosine Kinase Inhibitor (TKI)
ABSTRACT- Lung cancer is the most common cause of cancer related mortality worldwide. The epidermal-growth-factor receptor (EGFR) cascades the signaling pathway that regulates tumor-cell proliferation, invasion, angiogenesis, metastasis, and apoptosis. Since EGFR is often over-expressed in NSCLC and the level of EGFR expression correlates with poor prognosis. EGFR inhibitors have been developed as a novel therapy for non-small-cell lung cancer (NSCLC). Gefitinib is the first molecular targeted agent approved for the treatment of advanced NSCLC. It is a highly effective EGFR TK inhibitor (TKI) selectively blocks the signal transduction pathways implicated in cancer growth. Key-words- Lung Cancer, EGFR, NSCLC, Tyrosine Kinase Inhibitor (TKI)
Audio and slides for this presentation are available on YouTube: http://youtu.be/e_KVYJX2GTs
Have you ever wondered about your genetic predisposition to cancer? How cancer evolves in families? Or how cancer cells differ from normal cells in your body? Join Judy Garber, MD, MPH, director of the Center for Cancer Genetics and Prevention at Dana-Farber Cancer Institute, as she explores the basics of cancer genetics, DNA mutations, genetic screening, management, and more.
Microsatellite instability testing is an important part in diagnostics in Metastatic cancer settings after the FDA has given approval for tissue agnostic indications in almost all solid cancers. MSI by PCR and MMR status by IHC is also helpful for evaluation of genetic risk in Colon and Endometrial cancers
Audio and slides for this presentation are available on YouTube: http://youtu.be/e_KVYJX2GTs
Have you ever wondered about your genetic predisposition to cancer? How cancer evolves in families? Or how cancer cells differ from normal cells in your body? Join Judy Garber, MD, MPH, director of the Center for Cancer Genetics and Prevention at Dana-Farber Cancer Institute, as she explores the basics of cancer genetics, DNA mutations, genetic screening, management, and more.
Microsatellite instability testing is an important part in diagnostics in Metastatic cancer settings after the FDA has given approval for tissue agnostic indications in almost all solid cancers. MSI by PCR and MMR status by IHC is also helpful for evaluation of genetic risk in Colon and Endometrial cancers
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Commonly thought of as a childhood cancer, leukemia is actually much more common in adults. While symptoms of the disease are consistent among each, researchers are beginning to understand more about underlying biological factors that influence the different ways leukemia develops in children and adults. What are other differences and similarities?
An overview of Clinical Trials for Metastatic HER2-positive Breast Cancer by Dr. Ian Krop, MD, PhD, Chief and Clinical Research Director, Breast Oncology Center at Susan F. Smith Center for Women's Cancers at Dana-Farber Cancer Institute
Overview of clinical trials for metastatic triple-negative breast cancer by Sara M. Tolaney, MD, MPH, Associate Director and Associate Director of Clinical Research at Susan F. Smith Center for Women's Cancers at Dana-Farber Cancer Institute.
Research increasingly shows that “energy balance” is important in breast cancer. Learn why exercise, weight, and diet are important for breast cancer patients.
Prostate cancer is a disease in which cancer forms in the tissues of the prostate, a male gland just below the bladder and in front of the rectum. Prostate cancer is rare in men younger than 50 years of age, and the chance of developing prostate cancer increases as men get older. In the United States, a man has a one in five chance of being diagnosed with prostate cancer in his lifetime.
There are many different pediatric brain tumor types and classifications based upon the tumor’s cell structure, composition, rate of growth, location, and other characteristics. A child’s tumor may have the same microscopic appearance to an adult tumor, but the mutations that cause its growth are completely different.
Soft tissue sarcoma refers to cancer that begins in the muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. View the slideshow to learn more about signs and symptoms of this cancer, as well as risk factors.
Cancer-related fatigue is one of the most common problems patients face. Patients often report feeling wiped out during cancer treatments like chemotherapy and radiation, and for many, feeling tired or worn out continues into life after cancer treatment.
Here are 10 tips for alleviating treatment-related fatigue, through methods such as energy preservation and exercise – the latter of which is now known to be an effective strategy for combating this prevalent side effect.
There are more than 120 different types of brain tumors that may occur in adults. Learn about the five most common types.
For more on brain tumors, visit www.dana-farber.org/braintumor
Multiple myeloma is a type of cancer that begins in plasma cells, white blood cells that produce antibodies. It is also called Kahler's disease, myelomatosis or plasma cell myeloma.
Integrative therapies range from individual treatments, such as acupuncture, massage, and Reiki, to group programs for movement, meditation, and creative arts, as well as exercise and nutritional consultations.
Research conducted by Dana-Farber investigators and others has shown that, when used in conjunction with traditional cancer care, integrative therapies can help ease cancer-related symptoms and improve your quality of life.
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Sustainability has become an increasingly critical topic as the world recognizes the need to protect our planet and its resources for future generations. Sustainability means meeting our current needs without compromising the ability of future generations to meet theirs. It involves long-term planning and consideration of the consequences of our actions. The goal is to create strategies that ensure the long-term viability of People, Planet, and Profit.
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The Basic Science of Brain Tumors
1. The “Basic” Science
Mikael Rinne, M.D., Ph.D.
Dana-Farber Cancer Institute
Center for Neuro-Oncology
September 7, 2013
of Brain Tumors
2. What is Cancer?
DNA directs the functions of cells
Adaptedfromwww.scienceprogress.org
Alterations in the DNA can disrupt cellular function
(mutation, amplification, deletion)
Certain specific alterations can cause cells to:
- divide constantly
- divide indefinitely
- ignore signals to stop growing
- resist cell death
- invade / spread to other sites
- recruit blood vessels
3. What is Cancer?
DNA directs the functions of cells
“Hallmarks” of Cancer:
(Cell 2011)
Adaptedfromwww.scienceprogress.org
Alterations in the DNA can disrupt cellular function
(mutation, amplification, deletion)
Certain specific alterations can cause cells to:
- divide constantly
- divide indefinitely
- ignore signals to stop growing
- resist cell death
- invade / spread to other sites
- recruit blood vessels
4. What is Cancer?
DNA directs the functions of cells
“Hallmarks” of Cancer:
(Cell 2011)
Adaptedfromwww.scienceprogress.org
Alterations in the DNA can disrupt cellular function
(mutation, amplification, deletion)
Certain specific alterations can cause cells to:
- divide constantly
- divide indefinitely
- ignore signals to stop growing
- resist cell death
- invade / spread to other sites
- recruit blood vessels
The result is Cancer
Cancer is caused by a series
of DNA alterations
5. What causes these changes in DNA?
DNA alterations occur at random
Most result from normal “everyday” life in the cell:
- errors copying or separating DNA
- cellular by-products reacting with DNA
6. What causes these changes in DNA?
DNA alterations occur at random
Most result from normal “everyday” life in the cell:
- errors copying or separating DNA
- cellular by-products reacting with DNA
DNA alterations can also result from specific exposures:
- tobacco smoke – [lung cancer]
- ultraviolet light – [melanoma]
- radiation – [leukemias]
- chemicals (asbestos) – [mesothelioma]
- oncoviruses (HPV) – [cervical cancer]
7. What causes these changes in DNA?
DNA alterations occur at random
Random accumulation of specific mutations leads to cancer
Most result from normal “everyday” life in the cell:
- errors copying or separating DNA
- cellular by-products reacting with DNA
DNA alterations can also result from specific exposures:
- tobacco smoke – [lung cancer]
- ultraviolet light – [melanoma]
- radiation – [leukemias]
- chemicals (asbestos) – [mesothelioma]
- oncoviruses (HPV) – [cervical cancer]
Majority of DNA changes have no effect on cell function
Most alterations are either corrected or trigger cell death
…and do not cause cancer
8. How can cancer cell growth be stopped?
Chemotherapy & Radiation damage DNA to trigger cell death
Greatest effect seen in rapidly dividing cells (not cancer-specific)
An increasing understanding of alterations “driving” cancer growth
9. How can cancer cell growth be stopped?
(NEJM 2004)
(NEJM 2010)
(NEJM 2010)
Chemotherapy & Radiation damage DNA to trigger cell death
Greatest effect seen in rapidly dividing cells (not cancer-specific)
An increasing understanding of alterations “driving” cancer growth
Recent trials have shown that successfully targeting
cancer “drivers” can lead to significant tumor responses:
- CML with Bcr-Abl fusion: Imatinib
- Breast Cancer with Her-2 amplification: Trastuzumab
- Lung Cancer with EGFR mutation: Gefitinib
- Lung Cancer with EML4-ALK fusion: Crizotinib
- Melanoma with BRAF mutation: Vemurafenib
10. How can cancer cell growth be stopped?
(NEJM 2004)
(NEJM 2010)
(NEJM 2010)
Chemotherapy & Radiation damage DNA to trigger cell death
Greatest effect seen in rapidly dividing cells (not cancer-specific)
An increasing understanding of alterations “driving” cancer growth
Recent trials have shown that successfully targeting
cancer “drivers” can lead to significant tumor responses:
- CML with Bcr-Abl fusion: Imatinib
- Breast Cancer with Her-2 amplification: Trastuzumab
- Lung Cancer with EGFR mutation: Gefitinib
- Lung Cancer with EML4-ALK fusion: Crizotinib
- Melanoma with BRAF mutation: Vemurafenib
11. How can cancer cell growth be stopped?
(NEJM 2004)
(NEJM 2010)
(NEJM 2010)
(JCO 2011)
Significant interest in discovering DNA alterations in cancers
Chemotherapy & Radiation damage DNA to trigger cell death
Greatest effect seen in rapidly dividing cells (not cancer-specific)
An increasing understanding of alterations “driving” cancer growth
Recent trials have shown that successfully targeting
cancer “drivers” can lead to significant tumor responses:
- CML with Bcr-Abl fusion: Imatinib
- Breast Cancer with Her-2 amplification: Trastuzumab
- Lung Cancer with EGFR mutation: Gefitinib
- Lung Cancer with EML4-ALK fusion: Crizotinib
- Melanoma with BRAF mutation: Vemurafenib
12. How can we discover the DNA alterations in Cancer?
Advances in DNA sequencing technology has made it
possible to sequence entire cancer genomes
www.tcga.org
Broad Institute
Large part of this effort carried out in Boston…
The Cancer Genome Atlas (TCGA)
Comprehensive evaluation of 25 Cancer types
Glioblastoma was the 1st tumor studied
Approximately 500 GBMs characterized in depth
Low Grade Glioma project ongoing
Numerous brain tumor types analyzed / being analyzed:
Glioblastoma
Low Grade Glioma
Meningioma
Brain Metastases
Medulloblastoma
13.
14. What about DNA alterations in Individual Tumors?
Every tumor can have different alterations
Potential for different “drivers” of tumor growth
Certain alterations are more common
Revealed by studying many tumors
To translate these findings to individual patients,
we need to know which alterations are present
in an individual patient’s tumor
15. What about DNA alterations in Individual Tumors?
Every tumor can have different alterations
Potential for different “drivers” of tumor growth
www.dana-farber.org
Goal is to personalize treatment: “Precision Medicine”
Certain alterations are more common
Revealed by studying many tumors
To translate these findings to individual patients,
we need to know which alterations are present
in an individual patient’s tumor
Technology pioneered at Dana-Farber Cancer Institute
allows evaluation of individual patient tumors
- OncoMap / OncoPanel
- DFCI/BWH Neuropathology Tissue Bank
16. What are the DNA alterations in Brain Tumors?
Initial results discovered significantly
amplified or deleted genes
(Nature Genetics 2013)
(PNAS 2007)
17. What are the DNA alterations in Brain Tumors?
(MutSigCV v0.9, Broad Institute)
Initial results discovered significantly
amplified or deleted genes
(Nature Genetics 2013)
(PNAS 2007)
(MutSigCV v2.0, Broad Institute)
Ongoing efforts to discover other alterations…
More recent discovery of recurrent mutations
18. What are the implications of these alterations?
Results show frequent common alterations
in several common “pathways”
19. What are the implications of these alterations?
Results show frequent common alterations
in several common “pathways”
20. What are the implications of these alterations?
Results show frequent common alterations
in several common “pathways”
Constant Division
Ignore Stop
Signals
Resist Cell Death
Indefinite Division
∞
Recruit Blood Vessels Invasion
Additional research has revealed
alterations responsible for:
- indefinite division
- invading / spreading to other sites
- recruiting blood vessels
These pathways are responsible for:
- constant division
- ignoring signals to stop growing
- resisting cell death
21. Indefinite Division
∞
Recruit Blood Vessels Invasion
What can we do about these alterations?
Constant Division
Ignore Stop
Signals
Resist Cell Death
A number of drugs have been developed to
target many of these alterations / pathways
Significant ongoing research to:
- Identify targets within these pathways
- Design drugs to inhibit these targets
22. Indefinite Division
∞
Recruit Blood Vessels Invasion
What can we do about these alterations?
Constant Division
Ignore Stop
Signals
Resist Cell Death
A number of drugs have been developed to
target many of these alterations / pathways
Many current clinical trial agents
target these pathways
Significant ongoing research to:
- Identify targets within these pathways
- Design drugs to inhibit these targets
23. Indefinite Division
∞
Recruit Blood Vessels Invasion
What can we do about these alterations?
Constant Division
Ignore Stop
Signals
Resist Cell Death
A number of drugs have been developed to
target many of these alterations / pathways
Continued significant effort to initiate
clinical trials focused on the most
promising targets
Many current clinical trial agents
target these pathways
Significant ongoing research to:
- Identify targets within these pathways
- Design drugs to inhibit these targets