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Josh David Lauring, M.D., Ph.D.
Assistant Professor of Oncology
Expertise: Breast Cancer, Medical Oncology
Research Interests: breast cancer
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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
Dr. Lauring and colleagues are building upon the pioneering cancer genetics research completed at the Kimmel Cancer Center that revealed the unique genetic blueprint of breast cancer. He is studying recurrent genetic alterations in cancer cells, including mutations and large-scale chromosomal changes. He has identified mutant genes to which certain types of cancer cells become addicted; that is, the tumors growth and survival is directly tied to these mutant genes. In some cases, these mutant genes are abnormally active and can be successfully targeted with therapy. A well-known example of this in breast cancer is the Her-2 gene. Her-2 is over-expressed in about 15 percent of breast cancers and found to play an important role in the progression of the cancer. As a result, a number of active drugs targeting the Her-2 protein have been developed and have dramatically improved survival for this type of breast cancer. Dr. Lauring is hoping to uncover other targets that may have similar potential for extending survival.
Currently, he is studying mutant genes and chromosomes in human breast cancer cells and cell lines to better understand how the alterations foster abnormal cell growth and the aggressiveness of tumors. These cell lines will serve as model systems to study drugs or other interventions for their ability to selectively inhibit the growth of breast cancers containing that specific mutant gene. Dr. Lauring and team are currently studying a number of altered genes related to the most common type of breast cancer, known as ER-positive or hormone receptor positive breast cancer. This important research is helping to determine if these mutant genes contribute to sensitivity or resistance to widely used hormonal therapies, such as tamoxifen.
Konishi, H.; Karakas, B.; Abukhdeir, A.M.; Lauring, J.; Gustin, J.P.; Garay, J.P.; Konishi, Y.; Gallmeier, E.; Bachman, K.E.; Park, B.H. Knock-in of mutant K-ras in nontumorigenic human epithelial cells as a new model for studying K-ras mediated transformation. Cancer Res. 2007 Sep 15;67(18):8460-8467.
Konishi, H.; Lauring, J.; Garay, J.P.; Karakas, B.; Abukhdeir, A.M.; Gustin, J.P.; Konishi, Y.; Park, B.H. A PCR-based high-throughput screen with multiround sample pooling: application to somatic cell gene targeting. Nat Protoc. 2007;2(11):2865-2874.
Abukhdeir, A.M.; Vitolo, M.I.; Argani, P.; De Marzo, A.M.; Karakas, B.; Konishi, H.; Gustin, J.P.; Lauring, J.; Garay, J.P.; Pendleton, C.; Konishi, Y.; Blair, B.G.; Brenner, K.; Garrett-Mayer, E.; Carraway, H.; Bachman, K.E.; Park, B.H. Tamoxifen-stimulated growth of breast cancer due to p21 loss. Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):288-293.
Lauring, J.; Abukhdeir, A.M.; Konishi, H.; Garay, J.P.; Gustin, J.P.; Wang, Q.; Arceci, R.J.; Matsui, W.; Park, B.H. The multiple myeloma associated MMSET gene contributes to cellular adhesion, clonogenic growth, and tumorigenicity. Blood. 2008 Jan 15;111(2):856-864.
Gustin, J.P.; Karakas, B.; Weiss, M.B.; Abukhdeir, A.M.; Lauring, J.; Garay, J.P.; Cosgrove, D.; Tamaki, A.; Konishi, H.; Konishi, Y.; Mohseni, M.; Wang, G.; Rosen, D.M.; Denmeade, S.R.; Higgins, M.J.; Vitolo, M.I.; Bachman, K.E.; Park, B.H. Knockin of mutant PIK3CA activates multiple oncogenic pathways. Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2835-2840.
Lauring, J.; Cosgrove, D.P.; Fontana, S.; Gustin, J.P.; Konishi, H.; Abukhdeir, A.M.; Garay, J.P.; Mohseni, M.; Wang, G.M.; Higgins, M.J.; Gorkin, D.; Reis, M.; Vogelstein, B.; Polyak, K.; Cowherd, M.; Buckhaults, P.J.; Park, B.H. Knock in of the AKT1 E17K mutation in human breast epithelial cells does not recapitulate oncogenic PIK3CA mutations. Oncogene. 2010 Apr 22;29(16):2337-2345.
Higgins, M.J.; Beaver, J.A.; Wong, H.Y.; Gustin, J.P.;
Lauring, J.D.; Garay, J.P.; Konishi, H.; Mohseni, M.; Wang, G.M.; Cidado, J.; Jelovac, D.; Cosgrove, D.P.; Tamaki, A.; Abukhdeir, A.M.; Park, B.H. PIK3CA mutations and EGFR overexpression predict for lithium sensitivity in human breast epithelial cells. Cancer Biol Ther. 2011 Feb 1;11(3):35-44.