- University of Delaware
- Cornell University
- Yale University
- University of California
Awards & Honors
- Magna cum laude, University of Delaware
- NIH Predoctoral Fellowship (1971-1976)
- Fellow of the Howard Hughes Medical Institute, University of California, San Francisco (1977-1981)
- Women on the Move, Main Line Today (2008)
Despite several promising advances, the main treatments used today to treat cancer (e.g., surgery, radiation therapy, chemotherapy) reduce tumor burden but do not cure about half of cancer patients. Over half a million Americans continue to die from cancer every year. Most of these patients die because the cancer spreads throughout the body (metastasizes).
Successful treatment of metastatic disease is a great challenge because tumors can develop elsewhere in the body, requiring administration of therapy to the entire patient rather than just to the tumor. Surgery is not always an option, or if used, may not remove every cancer cell. Alternatively, effective radiation and chemotherapy not only kill cancer cells but also many healthy cells, leading to a high level of toxicity for the patient. Therefore, there is a great need for more effective and targeted methods to destroy cancer cells.
Dr. Sawicki's Research
Dr. Sawicki’s laboratory is developing new therapeutic strategies that hold great promise for improving the treatment of metastatic cancer. These strategies are based on the delivery of genetic material, specifically, DNA and siRNA, exclusively to tumor cells, thus protecting healthy cells from damage. Indeed, she was among the first to explore the use of non-viral vectors for the in vivo delivery of DNA.
To carry the genetic material inside cancer cells, Dr. Sawicki and her collaborators at MIT, Robert Langer and Daniel Anderson, explored the use of extremely small particles called nanoparticles.
Nanoparticle research currently is an area of intense scientific research because of its wide variety of potential biomedical applications. Dr. Sawicki identified therapeutic targets and evaluated therapeutic efficacy of many nanoparticle formulations in various cancer mouse models.
HuR research. Dr. Sawicki is currently working with Thomas Jefferson University’s Jonathan Brody, an expert on the role of a protein called HuR in pancreatic cancer. Their studies have contributed to an understanding of the role that HuR plays in regulating the expression of genes that help pancreatic cancer cells survive. Their work, which may lead to new targets for effective treatment of this deadly disease, draws on Dr. Sawicki’s extensive experience with gene regulation and animal models for pancreatic cancer.
Her recent work with Robert Getts at Genisphere, uses a DNA dendrimer nanocarrier platform called 3DNA® to suppress ovarian tumor growth and overcome drug resistance. In a recent study, tumor growth was suppressed in the absence of non-specific toxicity to healthy tissue following systemic administration of tumor-targeted 3DNA®-delivery of siHuR to ovarian tumors in mice. This work takes a significant step forward in the field of cancer therapeutics and advances the potential use of 3DNA® technology in the clinic.
Stem cells. The significance of her interest in identifying stem cells in normal developmental processes and the gene-expression profiles of these cells has grown as the field of cancer stem cells/tumor-initiating cells has gained importance. These studies lay the groundwork for identifying potential new therapeutics that target cancer stem cells and lead to more enduring cancer treatments.
Mouse models. Dr. Sawicki is also known for her expertise in generating transgenic mice. Using this technology, she has developed several cancer mouse models useful for her lab’s studies, as well as those of other researchers investigating the role of selected genes in cancer initiation and progression.
Dr. Sawicki has been funded by multiple awards from the National Institutes of Health and the U.S. Department of Defense, as well as from foundations.
Dr. Sawicki's Lab
Dr. Sawicki’s lab focuses on translational studies designed to validate the utility of novel DNA and siRNA cancer therapeutics. Nucleic acid molecules are conjugated to a nanocarrier called 3DNA® (Genisphere). The 3DNA® is also conjugated to molecules that target delivery and uptake of the therapeutic to tumor cells following systemic administration, thus sparing healthy cells from deleterious effects. Mouse cancer models are used to test efficacy and safety of these new therapeutics. Different imaging modalities, including bioluminescence, ultrasound and microCT, are routinely used to measure tumor response to treatment with 3DNA® formulations. These pre-clinical studies are designed to meet requirements for FDA approval and entry into clinical trials.
- Weidan Peng, PhD, Research Assistant Professor
- Elevated HuR in Pancreas Promotes a Pancreatitis-like Inflammatory Microenvironment that Facilitates Tumor Development. Peng W, Furuuchi N, Aslanukova L, Huang YH, Brown SZ, Jiang W, Addya S, Vishwakarma V, Peters E, Brody JR, Dixon DA, Sawicki JA. Mol Cell Biol. 2017 Nov 13. doi: 10.1128/MCB.00427-17.
- Insights from HuR biology point to potential improvement for second-line ovarian cancer therapy. Huang YH, Peng W, Furuuchi N, DuHadaway JB, Jimbo M, Pirritano A, Dunton CJ, Daum GS, Leiby BE, Brody JR, Sawicki JA. Oncotarget. 2016 Mar 2.
- Delivery of Therapeutics Targeting the mRNA-Binding Protein HuR Using 3DNA Nanocarriers Suppresses Ovarian Tumor Growth. Huang YH, Peng W, Furuuchi N, Gerhart J, Rhodes K, Mukherjee N, Jimbo M, Gonye GE, Brody JR, Getts RC, Sawicki JA. Cancer Res. 2016 Mar 15;76(6):1549-59. Epub 2016 Feb 26.
- The mRNA-binding protein HuR promotes hypoxia-induced chemoresistance through posttranscriptional regulation of the proto-oncogene PIM1 in pancreatic cancer cells. Blanco FF, Jimbo M, Wulfkuhle J, Gallagher I, Deng J, Enyenihi L, Meisner-Kober N, Londin E, Rigoutsos I, Sawicki JA, Risbud MV, Witkiewicz AK, McCue PA, Jiang W, Rui H, Yeo CJ, Petricoin E, Winter JM, Brody JR. Oncogene. 2015 35(19):2529-41.
- HuR Contributes to TRAIL Resistance by Restricting Death Receptor 4 Expression in Pancreatic Cancer Cells. Romeo C, Weber MC, Zarei M, DeCicco D, Chand SN, Lobo AD, Winter JM, Sawicki JA, Sachs JN, Meisner-Kober N, Yeo CJ, Vadigepalli R, Tykocinski ML, Brody JR. Mol Cancer Res. 2016 14(7):599-611.
- The RNA-binding protein HuR facilitates proliferation and metastasis in human pancreatic ductal adenocarcinoma; M Jimbo, FF Blanco, B Screnci, G Cosma, V Alexeev, YH Huang, Cancer Research 75 (15 Supplement), 5133-5133
- Inhibition of HuR effectively suppresses ovarian tumor growth in mice; JA Sawicki, YH Huang, JR Brody, RC Getts, K Rhodes, J Gerhart, Cancer Research 75 (15 Supplement), 3542-3542
- MUC1 Promoter–Driven DTA as a Targeted Therapeutic Strategy against Pancreatic Cancer; RM Tholey, S Lal, M Jimbo, RA Burkhart, FF Blanco, JA Cozzitorto, Molecular Cancer Research 13 (3), 439-448
- Targeting the mRNA-binding protein HuR impairs malignant characteristics of pancreatic ductal adenocarcinoma cells. Jimbo M, Blanco FF, Huang YH, Telonis AG, Screnci BA, Cosma GL, Alexeev V, Gonye GE, Yeo CJ, Sawicki JA, Winter JM, Brody JR, Oncotarget. 2015 Sep 29;6(29):27312-31.
- Abstract B06: Abi1 levels regulate prostate tumor progression in mice downstream from Pten inactivation; A Chorzalska, X Xiong, A Lunardi, JR White, JA Sawicki, G Bratslavsky, Molecular Cancer Research 12 (11 Supplement), B06-B06
- Systemic administration of DNA nanoparticles containing the diphtheria toxin gene reduces pancreatic tumor load in mice; JA Sawicki, W Peng, K Rhodes, R Getts Cancer Research 74 (19 Supplement), 700-700
- Normal estrogen, but low dehydroepiandrosterone levels, in women with pulmonary Mycobacterium avium complex. A preliminary study; J Danley, R Kwait, DD Peterson, J Sendecki, B Vaughn, K Nakisbendi, Annals of the American Thoracic Society 11 (6), 908-914
- TP53 supports basal-like differentiation of mammary epithelial cells by preventing translocation of deltaNp63 into nucleoli; PM Munne, Y Gu, M Tumiati, P Gao, S Koopal, S Uusivirta, J Sawicki, GH Wdi, SG Kuznetsov. Sci Rep. 2014 Apr 11;4:4663.
- HuR posttranscriptionally regulates WEE1: implications for the DNA damage response in pancreatic cancer cells; S Lal, RA Burkhart, N Beeharry, V Bhattacharjee, ER Londin, Cozzitorto JA, Romeo C, Jimbo M, Norris ZA, Yeo CJ, Sawicki JA, Winter JM, Rigoutsos I, Yen TJ, Brody JR. Cancer Research 74 (4), 1128-1140.