About

Sarah W.M. George is an Assistant Professor in the Department of Earth, Marine and Environmental Sciences at the University of North Carolina at Chapel Hill. She earned her Ph.D. from the University of Texas at Austin in 2019 and her B.A. from Wellesley College in 2014. Her research group focuses on using the sedimentary record to reconstruct tectonic and climatic processes. She integrates field-based sedimentology and stratigraphy with geochronology, geochemistry, and occasionally geomorphology to study these processes. Most of her research is concentrated in large modern and ancient mountain belts such as the Andes, Himalaya, and Rocky Mountains.

Research topics

• Computer Science
• Artificial Intelligence
• Programming language
• Cell biology
• Genetics
• Biology
• Chemistry
• Cancer research

Selected publications

• Towards Human-AI Collaboration for Misapplication Detection in Programming Exercises

  2025-10-07

  article1st authorCorresponding
  PublisherDOI

• Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer

  UNC Libraries · 2025-07-09

  articleOpen access
  PublisherDOI

• Assistant Dashboard Plus – Enhancing an Existing Instructor Dashboard with Difficulty Detection and GPT-based Code Clustering

  2024-03-18

  articleOpen access1st authorCorresponding

  As interest in programming as a major grows, instructors must accommodate more students in their programming courses. One particularly challenging aspect of this growth is providing quality assistance to students during in-class and out-of-class programming exercises. Prior work proposes using instructor dashboards to help instructors combat these challenges. Further, the introduction of ChatGPT represents an exciting avenue to assist instructors with programming exercises but needs a delivery method for this assistance. We propose a revision of a current instructor dashboard Assistant Dashboard Plus that extends an existing dashboard with two new features: (a) identifying students in difficulty so that instructors can effectively assist them, and (b) providing instructors with pedagogically relevant groupings of students’ exercise solutions with similar implementations so that instructors can provide overlapping code style feedback to students within the same group. For difficulty detection, it uses a state-of-the-art algorithm for which a visualization has not been created. For code clustering, it uses GPT. We present a first-pass implementation of this dashboard.

  PublisherOA PDFDOI

• NotebookGPT – Facilitating and Monitoring Explicit Lightweight Student GPT Help Requests During Programming Exercises

  2024-03-18 · 4 citations

  articleOpen access1st authorCorresponding

  The success of GPT with coding tasks has made it important to consider the impact of GPT and similar models on teaching programming. Students’ use of GPT to solve programming problems can hinder their learning. However, they might also get significant benefits such as quality feedback on programming style, explanations of how a given piece of code works, help with debugging code, and the ability to see valuable alternatives to their code solutions. We propose a new design for interacting with GPT called Mediated GPT with the goals of (a) providing students with access to GPT but allowing instructors to programmatically modify responses to prevent hindrances to student learning and combat common GPT response concerns, (b) helping students generate and learn to create effective prompts to GPT, and (c) tracking how students use GPT to get help on programming exercises. We demonstrate a first-pass implementation of this design called NotebookGPT.

  PublisherOA PDFDOI

• Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer

  UNC Libraries · 2024-08-27 · 24 citations

  articleOpen access
  PublisherDOI

• Data from Rho GTPase Transcriptome Analysis Reveals Oncogenic Roles for Rho GTPase-Activating Proteins in Basal-like Breast Cancers

  2023-03-30

  preprintOpen access

  <div>Abstract<p>The basal-like breast cancer (BLBC) subtype accounts for a disproportionately high percentage of overall breast cancer mortality. The current therapeutic options for BLBC need improvement; hence, elucidating signaling pathways that drive BLBC growth may identify novel targets for the development of effective therapies. Rho GTPases have previously been implicated in promoting tumor cell proliferation and metastasis. These proteins are inactivated by Rho-selective GTPase-activating proteins (RhoGAP), which have generally been presumed to act as tumor suppressors. Surprisingly, RNA-Seq analysis of the Rho GTPase signaling transcriptome revealed high expression of several RhoGAP genes in BLBC tumors, raising the possibility that these genes may be oncogenic. To evaluate this, we examined the roles of two of these RhoGAPs, ArhGAP11A (also known as MP-GAP) and RacGAP1 (also known as MgcRacGAP), in promoting BLBC. Both proteins were highly expressed in human BLBC cell lines, and knockdown of either gene resulted in significant defects in the proliferation of these cells. Knockdown of ArhGAP11A caused CDKN1B/p27-mediated arrest in the G<sub>1</sub> phase of the cell cycle, whereas depletion of RacGAP1 inhibited growth through the combined effects of cytokinesis failure, CDKN1A/p21-mediated RB1 inhibition, and the onset of senescence. Random migration was suppressed or enhanced by the knockdown of ArhGAP11A or RacGAP1, respectively. Cell spreading and levels of GTP-bound RhoA were increased upon depletion of either RhoGAP. We have established that, via the suppression of RhoA, ArhGAP11A and RacGAP1 are both critical drivers of BLBC growth, and propose that RhoGAPs can act as oncogenes in cancer. <i>Cancer Res; 76(13); 3826–37. ©2016 AACR</i>.</p></div>

  PublisherDOI

• Supplementary Figure Legends from Rho GTPase Transcriptome Analysis Reveals Oncogenic Roles for Rho GTPase-Activating Proteins in Basal-like Breast Cancers

  2023-03-30

  preprintOpen access

  <p>Figure Legends for Supplementary Figures S1-S4</p>

  PublisherDOI

• Supplementary Figures from Rho GTPase Transcriptome Analysis Reveals Oncogenic Roles for Rho GTPase-Activating Proteins in Basal-like Breast Cancers

  2023-03-30

  preprintOpen access

  <p>Supplementary Figures S1-S4 Supplementary Figure S1 Western blots showing knockdown of ArhGAP11A or RacGAP1. Supplementary Figure S2 ArhGAP11A and RacGAP1 are both required for proliferation of HER2-enriched and luminal B breast cancer cell lines. Supplementary Figure S3 ArhGAP11A and RacGAP1 regulate cell spreading. Supplementary Figure S4 Constitutively active Rac1 and Cdc42 do not affect BLBC proliferation.</p>

  PublisherDOI

• Supplementary Figures from Rho GTPase Transcriptome Analysis Reveals Oncogenic Roles for Rho GTPase-Activating Proteins in Basal-like Breast Cancers

  2023-03-30

  preprintOpen access

  <p>Supplementary Figures S1-S4 Supplementary Figure S1 Western blots showing knockdown of ArhGAP11A or RacGAP1. Supplementary Figure S2 ArhGAP11A and RacGAP1 are both required for proliferation of HER2-enriched and luminal B breast cancer cell lines. Supplementary Figure S3 ArhGAP11A and RacGAP1 regulate cell spreading. Supplementary Figure S4 Constitutively active Rac1 and Cdc42 do not affect BLBC proliferation.</p>

  PublisherDOI

• Data from Rho GTPase Transcriptome Analysis Reveals Oncogenic Roles for Rho GTPase-Activating Proteins in Basal-like Breast Cancers

  2023-03-30

  preprintOpen access

  <div>Abstract<p>The basal-like breast cancer (BLBC) subtype accounts for a disproportionately high percentage of overall breast cancer mortality. The current therapeutic options for BLBC need improvement; hence, elucidating signaling pathways that drive BLBC growth may identify novel targets for the development of effective therapies. Rho GTPases have previously been implicated in promoting tumor cell proliferation and metastasis. These proteins are inactivated by Rho-selective GTPase-activating proteins (RhoGAP), which have generally been presumed to act as tumor suppressors. Surprisingly, RNA-Seq analysis of the Rho GTPase signaling transcriptome revealed high expression of several RhoGAP genes in BLBC tumors, raising the possibility that these genes may be oncogenic. To evaluate this, we examined the roles of two of these RhoGAPs, ArhGAP11A (also known as MP-GAP) and RacGAP1 (also known as MgcRacGAP), in promoting BLBC. Both proteins were highly expressed in human BLBC cell lines, and knockdown of either gene resulted in significant defects in the proliferation of these cells. Knockdown of ArhGAP11A caused CDKN1B/p27-mediated arrest in the G<sub>1</sub> phase of the cell cycle, whereas depletion of RacGAP1 inhibited growth through the combined effects of cytokinesis failure, CDKN1A/p21-mediated RB1 inhibition, and the onset of senescence. Random migration was suppressed or enhanced by the knockdown of ArhGAP11A or RacGAP1, respectively. Cell spreading and levels of GTP-bound RhoA were increased upon depletion of either RhoGAP. We have established that, via the suppression of RhoA, ArhGAP11A and RacGAP1 are both critical drivers of BLBC growth, and propose that RhoGAPs can act as oncogenes in cancer. <i>Cancer Res; 76(13); 3826–37. ©2016 AACR</i>.</p></div>

  PublisherDOI

Frequent coauthors

• Channing J. Der

  University of North Carolina at Chapel Hill

  28 shared

• Charles M. Perou

  UNC Lineberger Comprehensive Cancer Center

  13 shared

• Nicole M. Baker

  Oakland University

  13 shared

• Prson Gautam

  Institute for Molecular Medicine Finland

  9 shared

• Krister Wennerberg

  University of Copenhagen

  9 shared

• Kirsten L. Bryant

  University of North Carolina at Chapel Hill

  8 shared

• Kent L. Rossman

  8 shared

• Natalia Mitin

  Research Triangle Park Foundation

  8 shared