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Josh David Lauring, M.D., Ph.D.
Assistant Professor of Oncology
Expertise: Breast Cancer, Medical Oncology
Research Interests: Cancer genetics; precision oncology
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Johns Hopkins Sidney Kimmel Comprehensive Cancer Center
Appointment Phone: 410-955-8964
401 N. Broadway
Baltimore, MD 21231 map
Dr. Lauring and his colleagues are working to hone in on the genetic changes that drive cancer growth. Finding these “driver” mutations is the first step toward identifying therapeutic targets for drug development, ultimately improving outcomes for patients with breast cancer.
Beyond identifying genetic mutations responsible for the development and spread of breast cancer, Dr. Lauring’s laboratory is actually creating a way to model a common and particularly complex type of genetic change that occurs in cancer, known as chromosomal amplification.
“We have succeeded in actually being able to create these amplifications in human cancer cell lines in the lab. If we can make them amplify the regions we want, the idea is that we could figure out the drivers [of certain forms of breast cancer],” Dr. Lauring explains.
In the twenty years that Dr. Lauring has been at Hopkins in research and patient care, he has seen incredible progress. Two decades ago, the benefit of chemotherapy had only recently been established for breast cancer. Now, clinicians treat certain forms of breast cancer with drugs to specifically target a given cancer’s genetic makeup.
Dr. Lauring points to HER2-positive breast cancer as an excellent example of a type of cancer for which a particular drug, Herceptin, has been found effective in both the cancer’s early stages as well as when it has metastasized. “Taking one of the [originally] worst prognostic groups, now we almost hope to find HER-2 on a pathology report because we’ve got so many drugs we can use against that target. Even in the metastatic setting, we’re much more hopeful about extending life,” he says.
Dr. Lauring acknowledges that the genetic complexity of cancer poses challenges to future drug development and treatment. The relationship between a mutation in a cancer and the response or resistance to targeted therapies is still poorly understood. Dr. Lauring is using cell line models to investigate this relationship and inform the use of gene mutations to select patients for targeted therapy.
“It is going to take a lot of effort by many investigators to reap the benefits of our new understanding of cancer genetics. But clearly, you can see that the field as a whole is moving along. There are a lot of people chipping away at it,” he says.
- Assistant Professor of Oncology
- MD, Johns Hopkins University School of Medicine (2000)
- Johns Hopkins University School of Medicine / Internal Medicine (2003)
- Johns Hopkins University School of Medicine / Oncology (2008)
- American Board of Internal Medicine / Medical Oncology (2005, 2017)
Research & Publications
Selected PublicationsView all on Pubmed
Lauring J, Abukhdeir AM, Konishi H, Garay JP, Gustin JP, Wang Q, Arceci RJ, Matsui W, and Park BH. The multiple myeloma-associated MMSET gene contributes to cellular adhesion, clonogenic growth, and tumorigenicity. Blood. 2008 Jan 15; 111 (2): 856-64. PMCID: PMC2200833
Lauring J, Cosgrove DP, Fontana S, Gustin JP, Konishi H, Abukhdeir AM, Garay JP, Mohseni M, Wang GM, Higgins M, Gorkin D, Reis M, Vogelstein B, Polyak K, Cowherd M, Buckhaults P, and Park BH. Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations. Oncogene. 2010 Apr 22;29(16):2337-45. Epub 2010 Jan 25. PMCID: PMC3042798.
Yi KH, Axtmayer J, Gustin JG, Rajpurohit A, Lauring J. Functional analysis of non-hotspot AKT1 mutants found in human breast cancers identifies novel driver mutations: implications for personalized medicine. Oncotarget. 2013 Jan;4(1):29-34. PMCID: PMC3702205.
Beaver JA, Gustin JP, Yi KH, Rajpurohit A, Thomas M, Gilbert SF, Rosen DM, Park BH, Lauring J. PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system. Clinical Cancer Research. 2013:19:5413-22. PMCID: PMC3805128.
Springer S, Yi KH, Park J, Rajpurohit A, Price AJ, Lauring J. Engineering targeted chromosomal amplifications in human breast epithelial cells. Breast Cancer Res Treat. 2015 Jul:152(2):313-321. PMCID: PMC4491111.