Pam Kreeger

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The objective of my research is to develop quantitative models of how normal and neoplastic OSE behave.  In particular, I seek to identify how EGF signaling impacts proliferation of normal OSE and early lesions, and address the hypothesis that mutations in the Kras signaling pathway lead to the rapid metastasis of ovarian cancer.
The objective of my research is to develop quantitative models of how normal and neoplastic OSE behave.  In particular, I seek to identify how EGF signaling impacts proliferation of normal OSE and early lesions, and address the hypothesis that mutations in the Kras signaling pathway lead to the rapid metastasis of ovarian cancer.
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[[Media:KreegerCV.pdf]]
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[[Media:KreegerCV.pdf |Curriculum Vitae]]
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Revision as of 15:37, 20 December 2005

Lauffenburger Lab

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Pamela Kreeger (BE postdoctoral)


Ph.D. Northwestern University, Chemical Engineering, 2005

B.S. Valparaiso University, Chemistry, 2000


Ovarian cancer is the deadliest of all gynecological cancers, with a mortality rate of nearly 60%. Currently, ovarian cancer is associated with a poor prognosis as the majority of patients are diagnosed only after the disease has spread into the abdominal cavity. Nearly 90% of ovarian tumors originate in the ovarian surface epithelium (OSE), a thin layer of cells covering the ovary that has no known major function. Importantly, there is limited understanding of the precursor lesion and tumor progression, inhibiting the development of diagnostic tests and effective treatments.

The objective of my research is to develop quantitative models of how normal and neoplastic OSE behave. In particular, I seek to identify how EGF signaling impacts proliferation of normal OSE and early lesions, and address the hypothesis that mutations in the Kras signaling pathway lead to the rapid metastasis of ovarian cancer.

Curriculum Vitae

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