Breast cancer survivor offers wisdom at Faulkner satellite center
Call 877-422-3324 today to make an appointment
Make your appointment or second opinion with Dana-Farber today to meet with an onsite specialist.
Can’t get to Boston? Explore our Online Second Opinion service to get expert advice from Dana-Farber oncologists.
Toll-Free Number866-408-DFCI (3324)
Discover the ways to give and how to get involved to support Dana-Farber.
Poet Richard Fox gains insight – and material – through cancer treatment
A family faces cancer in an unfamiliar city – with help
Choosing mastectomy or not: Studying young women's surgical choices
Jeff's targeted therapy has kept his advanced lung cancer at bay.
Profile, a research project launched by scientists at Dana-Farber Cancer Institute and Brigham and Women's Hospital, is one of the nation's most comprehensive personalized cancer medicine initiatives. Since the project began in 2011, Profile scientists have been analyzing the DNA in tumor tissue from patients coming to Dana-Farber Cancer Institute and Brigham and Women's Hospital for treatment of all types of cancers. Subsequently, Profile testing has expanded to pediatric cancer patients at Boston Children's Hospital.
Every patient's cancer contains a specific pattern of DNA mutations and other alterations — called a "tumor profile" — that can potentially be used to select regimens of cancer therapies for individual patients. With Profile, scientists are creating one of the world's largest databases on the genetic abnormalities that drive the development of tumors, as well as advancing the goals of personalized, precision cancer care.
More than 43,000 patients have consented to have tumor tissue analyzed for the presence of mutations and other cancer-related DNA abnormalities. Since its inception, Profile has completed more than 15,000 genetic profiles of patients' tumors, adding about 400 each month to the database.
In a new phase of Profile, begun in 2013, a technology known as "massively parallel" or "next-generation" sequencing, reads the genetic code of approximately 300 genes in each tumor sample. "Massively parallel" refers to the technology's capacity for sequencing large numbers of genes simultaneously. These genes were chosen because they have been implicated in a variety of cancers.
Called OncoPanel, this advanced sequencing platform is an important update to the original OncoMap platform. OncoPanel can detect not only genetic mutations, but also other critical types of cancer-related DNA alterations. Whereas OncoMap was limited to screening for known mutations, OncoPanel can discover new ones not previously identified.
The genotyping or "genetic profiling" studies are performed on samples of solid tumors, bone marrow, or blood specimens to identify the specific mutations and other DNA alterations driving a patient's cancer. The OncoPanel testing is done at the Center for Advanced Molecular Diagnostics, a CLIA-certified laboratory in the Department of Pathology at Brigham and Women's Hospital.
Profile aims to detect genetic alterations in tumors and potentially identify targeted therapies that are most likely to be effective in individual patients. The databases of tumor genetic profiling data derived from a very large number of patients, and linked to clinical information, make Profile a powerful tool for discovery and personalized cancer medicine. This database, which adheres to emerging IT standards, also supports proposals for new research studies and clinical trials.
To accommodate this constantly evolving field, the Profile program is expected to include germline genotyping and whole-genome sequencing in the future.
Over the past decade, our physicians, researchers, and scientists have been at the forefront of personalized cancer medicine discoveries. As a result, targeted therapies have become the standard of care in multiple types of cancer, including colorectal, lung and breast. These advances include EGFR and ALK discoveries in lung cancer, triple-negative and HER2-positive breast cancer, as well as KRAS, BRAF, and PIK3CA in colorectal cancer.
SYK Inhibition Modulates Distinct PI3K/AKT- Dependent Survival Pathways and Cholesterol Biosynthesis in Diffuse Large B Cell Lymphomas Cancer Cell. 2013 June 10; 23(6):826-838
Targeted therapy boosts lung cancer outcomes
Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1 PNAS. 2013 110(20):8188-8193.
Evolution and Impact of Subclonal Mutations in Chronic Lymphocytic Leukemia Cell. 2013 February 14; 152(4):714–726.
Highly Recurrent TERT Promoter Mutations in Human Melanoma Science. 2013 February 22; 339(6122): 957-959.
Researchers report first success of targeted therapy in most common genetic subtype of non-small cell lung cancer
Sequence analysis of mutations and translocations across breast cancer subtypes Nature. 2012 June 21; 482(7403):405-409.
EGFR mutations are detected comparably in cytologic and surgical pathology specimens of nonsmall cell lung cancer. Cancer Cytopathol. 2009 Feb 25;117(1):67-72
Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med 2010; 363:1693-1703
Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. Cancer Cell. 2010 Jan 19;17(1):77-88
Novel mutant-selective EGFR kinase inhibitors against EGFR T790M. Nature. 2009 Dec 24;462(7276):1070-4
Activating mutations in ALK provide a therapeutic target in neuroblastoma. Nature. 2008 Oct 16;455(7215):975-8.
EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science. 2004;304:1497-500.
Prognostic and predictive value of common mutations for treatment response and survival in patients with metastatic colorectal cancer. Br J Cancer. 2009 Aug 4;101(3): 465-72
Efficacy of neoadjuvant Cisplatin in triple-negative breast cancer. Journal of Clinical Oncology. (JCO June 1, 2010 vol. 28 no. 16 2698-2704
Improving the yield of circulating tumour cells facilitates molecular characterisation and recognition of discordant HER2 amplification in breast cancer. Br J Cancer. 2010 May 11;102(10):1495-502