Northwestern Events Calendar

Jan
31
2022

Pharmacology Research Works in Progress: Carly Weddle & Kaitlyn DeMeulenaere

When: Monday, January 31, 2022
4:00 PM - 5:00 PM CT

Where: Online

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

Contact: Lexi Smith   (312) 503-4893

Group: Department of Pharmacology Seminars

Category: Lectures & Meetings

Description:

Carly Weddle
PhD Candidate in the Laboratory of Paul Burridge, PhD

Modeling breast cancer with patient-specific human induced pluripotent stem cells
Existing patient-derived models of breast cancer fail to recapitulate important aspects of breast tumorigenesis, notably the intra-and inter-tumoral heterogeneity of human breast tumors. Human induced pluripotent stem cells (hiPSCs) are an appealing tool for modeling cancer because they provide a scalable source of patient-derived cells that retain key features of underlying cancer cells, including mutational burdens and drug sensitivities. However, no study to date has examined the potential of hiPSCs to model breast tumorigenesis. We demonstrate for the first time that primary breast cancer cells can be reprogrammed into hiPSCs and re-differentiated into mammary epithelial cells to model breast tumorigenesis.

Kaitlyn DeMeulenaere 
PhD Candidate in the Laboratory of Murali Prakria, PhD

"Sex-specific regulation of neuropathic pain by microglial Orai1 channels"
Store-operated Orai1 channels are implicated in initiating inflammatory responses in many immune cells and contribute to an array of cellular functions, including gene expression and exocytosis. Spinal microglia play a central role in directing inflammatory responses that underlie neuropathic pain, but specific checkpoints for this process remain unknown. We aim to uncover the role of Orai1 in microglia during neuropathic pain and its alterations to cellular mechanisms. Our experiments indicate that Orai1 is a critical checkpoint in neuropathic pain processing and cytokine production in the spinal cord after injury, but these results reveal a sex specific phenotype due to deletion of Orai1 in microglia. My work focuses on the mechanistic contribution of microglial Orai1 channels to neuropathic pain and the basis for the observed sex differences.

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