About

Katharine Griffin Conway is an Associate Professor in the program in Higher & Postsecondary Education at Teachers College, Columbia University, where she has taught since earning her doctorate in 2012. Her scholarly interests include faculty career development, institutional research, and higher education administration. Conway holds a Doctor of Education degree from Teachers College, Columbia University, with a dissertation focused on faculty flourishing and pre-tenure career construction strategies in American research universities. She also holds a Master of Education and a Master of Arts from Teachers College, and a Bachelor of Arts in History from Columbia College, Columbia University. In addition to her academic role, Conway serves as Vice Dean of Administration and Chief Operating Officer at Columbia Business School. Her professional experience includes over a decade at Teachers College in various leadership roles within the Office of the President, most recently as Vice President of Planning and Strategy. She is actively involved in university service, sitting on the Commission on the Status of Women and the Advisory Board for Columbia Community Service.

Research topics

• Genetics
• Cancer research
• Internal medicine
• Biology
• Medicine
• Oncology
• Pathology

Selected publications

• Supplementary Table S3 from Association of Inherited Genetic Variants with Multiple Primary Melanoma

  2025-05-02

  supplementary-materialsOpen access

  <p>Supplementary Table S3 shows the genotype associations with multiple primary melanoma stratified by phenotypic index and back nevi in the GEM study.</p>

  PublisherDOI

• Supplementary Data1 from Tumor miRNA Signatures Associate with Outcomes of Patients with Stage II/III Melanoma

  2025-12-15

  articleOpen access

  <p>Supplementary Tables</p>

  PublisherDOI

• Association of Inherited Genetic Variants with Multiple Primary Melanoma

  Cancer Epidemiology Biomarkers & Prevention · 2025-03-04 · 2 citations

  articleOpen access

  BACKGROUND: Recent genome-wide association studies (GWAS) have identified new susceptibility loci for melanoma, but their associations with multiple primary melanoma (MPM) are unclear. METHODS: We investigated the associations of 69 SNPs in 39 GWAS-identified loci with odds of MPM relative to single primary melanoma in the international, population-based Genes, Environment, and Melanoma study. Per-minor-allele ORs and 95% confidence intervals (CI) for individuals with MPM "cases" (n = 1,205) relative to single primary melanoma "controls" (n = 2,458) were estimated using multivariable logistic regression, and polygenic risk scores (PRS) were calculated and weighted based on a 2020 GWAS meta-analysis (57 of the 68 independent GWAS SNPs available). RESULTS: Thirteen SNPs in 11 gene regions (PARP1, CYP1B1/RMDN3, TERT, RAPGEF5, TYRP1, MTAP, CDKN2A/CDKN2B, KLF4, TYR, SOX6, and ASIP) were statistically significantly associated (P < 0.05) with MPM adjusting for age, sex, age-by-sex interaction, and study center. The highest versus lowest PRS quintile was associated with a 2.81-fold higher odds of MPM (95% CI, 2.10-3.78; P = 7.5 × 10-13); this association was attenuated but remained statistically significant after excluding SNPs individually associated with MPM (OR = 1.75, 95% CI, 1.32-2.31). CONCLUSIONS: Inherited genetic variants spanning 11 gene regions were independently associated with MPM. Nonsignificant SNPs were associated with MPM when aggregated into a PRS, indicating that their cumulative effect may influence MPM risk despite lacking individual statistical significance in our study population. IMPACT: Our findings provide additional evidence that these loci are associated with melanoma risk and estimate the magnitude of their genetic effect on subsequent (multiple) primary melanoma risk.

  PublisherOA PDFDOI

• Supplementary Figures1 from Tumor miRNA Signatures Associate with Outcomes of Patients with Stage II/III Melanoma

  2025-12-15

  articleOpen access

  &lt;p&gt;Supplementary Figures S1-S9&lt;/p&gt;

  PublisherOA PDFDOI

• Data from Association of Inherited Genetic Variants with Multiple Primary Melanoma

  2025-05-02

  preprintOpen access

  &lt;div&gt;AbstractBackground:&lt;p&gt;Recent genome-wide association studies (GWAS) have identified new susceptibility loci for melanoma, but their associations with multiple primary melanoma (MPM) are unclear.&lt;/p&gt;Methods:&lt;p&gt;We investigated the associations of 69 SNPs in 39 GWAS-identified loci with odds of MPM relative to single primary melanoma in the international, population-based Genes, Environment, and Melanoma study. Per-minor-allele ORs and 95% confidence intervals (CI) for individuals with MPM “cases” (&lt;i&gt;n&lt;/i&gt; = 1,205) relative to single primary melanoma “controls” (&lt;i&gt;n&lt;/i&gt; = 2,458) were estimated using multivariable logistic regression, and polygenic risk scores (PRS) were calculated and weighted based on a 2020 GWAS meta-analysis (57 of the 68 independent GWAS SNPs available).&lt;/p&gt;Results:&lt;p&gt;Thirteen SNPs in 11 gene regions (&lt;i&gt;PARP1&lt;/i&gt;, &lt;i&gt;CYP1B1/RMDN3&lt;/i&gt;, &lt;i&gt;TERT&lt;/i&gt;, &lt;i&gt;RAPGEF5&lt;/i&gt;, &lt;i&gt;TYRP1&lt;/i&gt;, &lt;i&gt;MTAP&lt;/i&gt;, &lt;i&gt;CDKN2A/CDKN2B&lt;/i&gt;, &lt;i&gt;KLF4&lt;/i&gt;, &lt;i&gt;TYR&lt;/i&gt;, &lt;i&gt;SOX6&lt;/i&gt;, and &lt;i&gt;ASIP&lt;/i&gt;) were statistically significantly associated (&lt;i&gt;P&lt;/i&gt; &lt; 0.05) with MPM adjusting for age, sex, age-by-sex interaction, and study center. The highest versus lowest PRS quintile was associated with a 2.81-fold higher odds of MPM (95% CI, 2.10–3.78; &lt;i&gt;P&lt;/i&gt; = 7.5 × 10&lt;sup&gt;−13&lt;/sup&gt;); this association was attenuated but remained statistically significant after excluding SNPs individually associated with MPM (OR = 1.75, 95% CI, 1.32–2.31).&lt;/p&gt;Conclusions:&lt;p&gt;Inherited genetic variants spanning 11 gene regions were independently associated with MPM. Nonsignificant SNPs were associated with MPM when aggregated into a PRS, indicating that their cumulative effect may influence MPM risk despite lacking individual statistical significance in our study population.&lt;/p&gt;Impact:&lt;p&gt;Our findings provide additional evidence that these loci are associated with melanoma risk and estimate the magnitude of their genetic effect on subsequent (multiple) primary melanoma risk.&lt;/p&gt;&lt;/div&gt;

  PublisherDOI

• Abstract 6043: Role of Rab11 family interacting proteins in immune recognition of breast cancer

  Cancer Research · 2025-04-21

  article

  Abstract Breast cancer is the second leading cause of death for American women, with the majority of morbidity attributable to metastatic disease. Breast cancer brain metastases (BCBM) account for 30% of breast cancer mortality and treatment options remain limited. While immunotherapy holds great promise, objective response rates for metastatic disease are poor. To improve these outcomes, we must understand the context-specific mechanisms used by cancer cells to suppress and evade the immune system. Successful T cell interaction with cancer cells requires proper surface localization of proteins such as MHC complexes and co-activators, all of which are localized within the cell via endosomal protein trafficking. Immunotherapy also relies on CTLA-4 or PD-1/PD-L1 on the cell surface to remove inhibition of T cells and improve the anti-tumor response. How molecular trafficking controls localization of activating and inhibitory proteins to the surface in order to facilitate cancer-immune cell interaction is a key knowledge gap. We previously showed that Rab11b-mediated endosomal trafficking is required for BCBM. Here we investigate how trafficking-mediated control of the cell surface dictates immune recognition and response. Using a targeted CRISPR screen, we found that Rab11 family interacting proteins Rab11fip2 and Rab11fip3 are required for highly immunogenic ovalbumin (OVA) expressing breast cancer cells to be recognized by OT-I CD8+ T cells. Flow cytometry analysis revealed that the decrease in recognition is not due to surface localization of PD-L1 or the MHC/SIINFEKL complex (SIINFEKL is the OVA peptide presented for OT-I recognition). Knockout of Rab11fip2 or 3 did not change cell proliferation or tumor burden in immunocompromised animals, but led to significantly increased tumor growth in immunocompetent animals. This suggests that non-targeting control cells are partially restrained by the immune system, and knockout of either Rab11fip causes loss of immune recognition to allow faster tumor growth. Immunohistochemical analysis revealed a significant decrease of tumor infiltrating T cells in Rab11fip knockout tumors. Cytotoxic CD8+ T cells exhibited the most extreme decrease in infiltration, with CD4+ helper T cells decreasing in only the Rab11fip3 knockout condition. These results indicate that Rab11 may play a role in immune cell recruitment in addition to recognition and activation. We are currently focused on characterizing Rab11 control of the T cell-cancer cell interaction in human breast cancer cell lines. Dissecting the role of Rab11 in tumor cell antigen presentation, immune cell recruitment, T cell cytotoxicity and activation will help determine if inhibition of Rab11-mediated recycling can be used to increase the efficacy of immunotherapy for patients with BCBM. Citation Format: Oly Khowash, Paras Sahani, Christopher Kywe, Kathleen Conway, Khushi Tekale, Jessica Contreras, Erin Howe. Role of Rab11 family interacting proteins in immune recognition of breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6043.

  PublisherDOI

• Supplementary Table S4 from Association of Inherited Genetic Variants with Multiple Primary Melanoma

  2025-05-02

  supplementary-materialsOpen access

  &lt;p&gt;Supplementary Table S4 shows the estimated effects of SNPs on gene expression in human skin samples.&lt;/p&gt;

  PublisherDOI

• Supplementary Table S1 from Association of Inherited Genetic Variants with Multiple Primary Melanoma

  2025-05-02

  supplementary-materialsOpen access

  &lt;p&gt;Supplementary Table S1 shows SNP information and their associations with MPM relative to SPM in the GEM study.&lt;/p&gt;

  PublisherDOI

• Tumor miRNA Signatures Associate with Outcomes of Patients with Stage II/III Melanoma

  Clinical Cancer Research · 2025-10-20

  article

  PURPOSE: Patients with stage II and resected stage III melanomas have variable clinical outcomes, providing evidence of underlying biological differences in tumors and/or the patients themselves, beyond stage. The approval of adjuvant immunotherapy for stage IIB/C and resected stage III/IV disease (and adjuvant targeted therapy for resected stage III disease) has created a pressing need to develop biomarkers to accurately distinguish patients at low risk versus high risk for recurrence and death from melanoma. miRNAs are promising biomarkers because of their stability in tissues and fluids and their demonstrated functional and prognostic roles in melanoma. We hypothesized that miRNA expression could be integrated into prognostic models that would classify 5-year survival outcomes more accurately than clinical factors alone. EXPERIMENTAL DESIGN: Using a NanoString miRNA Expression Assay, we analyzed 715 primary melanomas from patients with stage II or stage III disease within the InterMEL consortium and examined associations between miRNA expression and melanoma-specific death. RESULTS: When integrated into clinical prognostic models for 5-year melanoma-specific survival, miRNA signatures improved the area under the receiver operating characteristic curve for patients in stage II from 0.71 for a "clinical factors-only" model to 0.81 for a "clinical plus miRNA" model in an independent test set, an improvement of 0.10 with a 95% confidence interval (0.03-0.19). The improvement was more modest for patients in stage III who were included in the analysis. CONCLUSIONS: Incorporating miRNA expression in primary melanomas may enhance the accuracy of clinical prognostic models and potentially aid in the selection of patients with melanoma for adjuvant treatment and clinical trials.

  PublisherDOI

• Supplementary Table S2 from Association of Inherited Genetic Variants with Multiple Primary Melanoma

  2025-05-02

  supplementary-materialsOpen access

  &lt;p&gt;Supplementary Table S2 shows detailed information of 68 independent SNPs identified in the Landi et al. 2020 GWAS.&lt;/p&gt;

  PublisherDOI

Frequent coauthors

• Sharon N. Edmiston

  261 shared

• Robert C. Millikan

  134 shared

• Marianne Berwick

  University of New Mexico

  119 shared

• Melissa A. Troester

  University of North Carolina at Chapel Hill

  119 shared

• Joseph Geradts

  East Carolina University

  115 shared

• Lisa A. Carey

  University of North Carolina at Chapel Hill

  103 shared

• Nancy E. Thomas

  103 shared

• Eloise Parrish

  University of North Carolina at Chapel Hill

  103 shared

Education

• B.A., History

  Columbia College, Columbia University

  2002

• M.A., Higher & Postsecondary Education

  Teachers College, Columbia University

  2006

• Other, Higher & Postsecondary Education

  Teachers College, Columbia University

  2007

• Other, Higher & Postsecondary Education

  Teachers College, Columbia University

  2012