Pam Kreeger

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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 cavityNearly 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.  
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I am examining how two isoforms of Ras (K-Ras and N-Ras) impact apoptosis in the colonPrevious studies suggest that activated K-Ras sensitizes cells to apoptosis, while N-Ras provides an anti-apoptotic signal. This work builds upon previous apoptosis models developed in the Lauffenburger lab and attempts to address two important issues.   
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First, can cue-signal-response models be developed where the ‘cue’ is an intrinsic part of the cell, such as a genetic mutation?  To build such a model, we are utilizing a panel of human colon carcinoma cell lines that have distinct genetic manipulations to both K-Ras and N-Ras. These cell lines show different levels of apoptosis following treatment with TNFalpha, and have differences in both basal and stimulated signaling of key intracellular molecules such as ERK and JNK. Secondly, can cue-signal-response models be developed for more complicated paradigms, especially ''in vivo'' models?  This project will be done in collaboration with the Jacks lab, utilizing their genetic mouse models of human cancer. To correlate to our ''in vitro'' studies, we will generate a dataset of intracellular signaling and apoptosis in the intestinal epithelium of mice with defined K-Ras and N-Ras genotypes.
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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 and invasive behavior of normal OSE and ovarian cancer cells.
 

Revision as of 14:25, 18 August 2006

Lauffenburger Lab

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Pamela K. Kreeger (BE postdoctoral)


Ph.D. Northwestern University, Chemical Engineering, 2005

B.S. Valparaiso University, Chemistry, 2000


I am examining how two isoforms of Ras (K-Ras and N-Ras) impact apoptosis in the colon. Previous studies suggest that activated K-Ras sensitizes cells to apoptosis, while N-Ras provides an anti-apoptotic signal. This work builds upon previous apoptosis models developed in the Lauffenburger lab and attempts to address two important issues.

First, can cue-signal-response models be developed where the ‘cue’ is an intrinsic part of the cell, such as a genetic mutation? To build such a model, we are utilizing a panel of human colon carcinoma cell lines that have distinct genetic manipulations to both K-Ras and N-Ras. These cell lines show different levels of apoptosis following treatment with TNFalpha, and have differences in both basal and stimulated signaling of key intracellular molecules such as ERK and JNK. Secondly, can cue-signal-response models be developed for more complicated paradigms, especially in vivo models? This project will be done in collaboration with the Jacks lab, utilizing their genetic mouse models of human cancer. To correlate to our in vitro studies, we will generate a dataset of intracellular signaling and apoptosis in the intestinal epithelium of mice with defined K-Ras and N-Ras genotypes.


Previous Research

Curriculum Vitae


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