Northwestern Events Calendar

Feb
10
2020

Pharmacology Research Works-in-Progress: Rokana Taftaf and Rummi Ganguly

When: Monday, February 10, 2020
4:00 PM - 5:00 PM CT

Where: Ward Building, 5-230, 303 E. Chicago Avenue, Chicago, IL 60611 map it

Audience: Faculty/Staff - Student - Post Docs/Docs - Graduate Students

Contact: Liz Murphy   (312) 503-4892

Group: Department of Pharmacology Seminars

Category: Lectures & Meetings

Description:

Please join the Department of Pharmacology for a Works-in-Progress presentations

Rokana Taftaf, MD
PhD Candidate in the Laboratory of Huiping Liu, MD, PhD

ICAM1 Promotes Breast Cancer Stemness and Metastasis
Cancer stem cell (CSC) properties are essential for metastasis. However, the cellular heterogeneity and molecular mechanisms underlying CSC-mediated metastasis have yet to be elucidated. Using single cell RNA sequencing, we compared the tumor cells from breast tumors to those in early lung metastases of patient-derived breast tumor xenograft, and found a 60-fold increase of Intercellular Adhesion Molecule 1 (ICAM1) expression in the lung metastases, along with other stemness genes. I hypothesize that ICAM1 initiates metastasis with enhanced stemness and serves as a novel therapeutic target for breast cancer metastasis.


Rummi Ganguly
PhD Candidate in the Laboratory of Alfred George, MD

Impact of Developmentally-Regulated Alternative Splicing on Functional Consequences of SCN2A Mutation Associated with Epileptic Encephalopathy
Mutations in genes encoding voltage‑gated sodium channels (NaV), including SCN2A (NaV1.2), are associated with epilepsy of a wide range of clinical severity, age‑of‑onset, and pharmacoresponsiveness. Determining the functional properties of mutant NaV1.2 channels is valuable for establishing molecular mechanisms and genotype‑phenotype relationships. Because epilepsies associated with NaV1.2 mutations have variable age of onset of symptoms, we examined the effects of developmentally‑regulated alternative splicing of SCN2A on the biophysical properties of the recurrent mutation SCN2A-R853Q. From these studies, we are developing computational models of each channel variant to be integrated into live-recordings of excitatory neurons derived from induced pluripotent stem cells (iPSCs) to simulate the mutant’s effects on neuronal excitability. 

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