Carlos Caulin

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Scholarly Contributions

Journals/Publications

• Bauman, J. E., Saba, N. F., Roe, D., Bauman, J. R., Kaczmar, J., Bhatia, A., Muzaffar, J., Julian, R., Wang, S., Bearelly, S., Baker, A., Steuer, C., Giri, A., Burtness, B., Centuori, S., Caulin, C., Klein, R., Saboda, K., Obara, S., & Chung, C. H. (2023). Randomized Phase II Trial of Ficlatuzumab With or Without Cetuximab in Pan-Refractory, Recurrent/Metastatic Head and Neck Cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 41(22), 3851-3862.
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  Primary or acquired resistance to cetuximab, an antiepidermal growth factor receptor monoclonal antibody (mAb), minimizes its utility in recurrent/metastatic head and neck squamous cell carcinoma (HNSCC). Aberrant hepatocyte growth factor/cMet pathway activation is an established resistance mechanism. Dual pathway targeting may overcome resistance.
• Yan, H., Ma, Y., Zhou, X., He, Y., Liu, Y., Caulin, C., Wang, L., Xu, H., & Luo, H. (2023). Spontaneous Murine Model of Anaplastic Thyroid Cancer. Journal of visualized experiments : JoVE.
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  Anaplastic thyroid cancer (ATC) is a rare but lethal malignancy with a dismal prognosis. There is an urgent need for more in-depth research on the carcinogenesis and development of ATC, as well as therapeutic methods, since standard treatments are essentially depleted in ATC patients. However, low prevalence has hampered thorough clinical studies and the collection of tissue samples, so little progress has been achieved in creating effective treatments. We used genetic engineering to create a conditionally inducible ATC murine model (mATC) in a C57BL/6 background. The ATC murine model was genotyped by TPO-cre/ERT2; Braf; Trp53 and induced by intraperitoneal injection with tamoxifen. With the murine model, we investigated the tumor dynamics (tumor size ranged from 12.4 mm to 32.5 mm after 4 months of induction), survival (the median survival period was 130 days), and metastasis (lung metastases occurred in 91.6% of mice) curves and pathological features (characterized by Cd8, Foxp3, F4/80, Cd206, Ki67, and Caspase-3 immunohistochemical staining). The results indicated that spontaneous mATC possesses highly similar tumor dynamics and immunological microenvironment to human ATC tumors. In conclusion, with high similarity in pathophysiological features and unified genotypes, the mATC model resolved the shortage of clinical ATC tissue and sample heterogeneity to some extent. Therefore, it would facilitate the mechanism and translational studies of ATC and provide an approach to investigate the treatment potential of small molecular drugs and immunotherapy agents for ATC.
• Luo, H., Xia, X., Huang, L. B., An, H., Cao, M., Kim, G. D., Chen, H. N., Zhang, W. H., Shu, Y., Kong, X., Ren, Z., Li, P. H., Liu, Y., Tang, H., Sun, R., Li, C., Bai, B., Jia, W., Liu, Y., , Zhang, W., et al. (2022). Pan-cancer single-cell analysis reveals the heterogeneity and plasticity of cancer-associated fibroblasts in the tumor microenvironment. Nature communications, 13(1), 6619.
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  Cancer-associated fibroblasts (CAFs) are the predominant components of the tumor microenvironment (TME) and influence cancer hallmarks, but without systematic investigation on their ubiquitous characteristics across different cancer types. Here, we perform pan-cancer analysis on 226 samples across 10 solid cancer types to profile the TME at single-cell resolution, illustrating the commonalities/plasticity of heterogenous CAFs. Activation trajectory of the major CAF types is divided into three states, exhibiting distinct interactions with other cell components, and relating to prognosis of immunotherapy. Moreover, minor CAF components represent the alternative origin from other TME components (e.g., endothelia and macrophages). Particularly, the ubiquitous presentation of endothelial-to-mesenchymal transition CAF, which may interact with proximal SPP1 tumor-associated macrophages, is implicated in endothelial-to-mesenchymal transition and survival stratifications. Our study comprehensively profiles the shared characteristics and dynamics of CAFs, and highlight their heterogeneity and plasticity across different cancer types. Browser of integrated pan-cancer single-cell information is available at https://gist-fgl.github.io/sc-caf-atlas/ .
• Budden, T., Gaudy-Marqueste, C., Craig, S., Hu, Y., Earnshaw, C. H., Gurung, S., Ra, A., Akhras, V., Shenjere, P., Green, R., Jamieson, L., Lear, J., Motta, L., Caulín, C., Oudit, D., Furney, S. J., & Virós, A. (2021). Female Immunity Protects from Cutaneous Squamous Cell Carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 27(11), 3215-3223.
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  Cancer susceptibility and mortality are higher in males, and the mutational and transcriptomic landscape of cancer differs by sex. The current assumption is that men are at higher risk of epithelial cancers as they expose more to carcinogens and accumulate more damage than women. We present data showing women present with less aggressive primary cutaneous squamous cell carcinoma (cSCC) and early strong immune activation.
• Centuori, S. M., Caulin, C., & Bauman, J. E. (2021). Precision and Immunoprevention Strategies for Tobacco-Related Head and Neck Cancer Chemoprevention. Current treatment options in oncology, 22(6), 52.
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  To date, there is no FDA-approved chemoprevention approach for tobacco-related HNSCC. Effective chemoprevention approaches validated in sufficiently powered randomized trials are needed to reduce the incidence and improve survival. In this review, we recap the challenges encountered in past chemoprevention trials and discuss emerging approaches, with major focus on green chemoprevention, precision prevention, and immunoprevention. As our current depth of knowledge expands in the arena of cancer immunotherapy, the field of immunoprevention is primed for new discoveries and successes in cancer prevention.
• Centuori, S., Bauman, J., & Caulin, C. (2020). Precision and immunoprevention strategies for tobacco-related head and neck cancer chemoprevention. Current Treatment Options in Oncology.
• Luo, H., Xia, X., Kim, G. D., Liu, Y., Xue, Z., Zhang, L., Shu, Y., Yang, T., Chen, Y., Zhang, S., Chen, H., Zhang, W., Li, R., Tang, H., Dong, B., Fu, X., Cheng, W., Zhang, W., Yang, L., , Peng, Y., et al. (2021). Characterizing dedifferentiation of thyroid cancer by integrated analysis. Science advances, 7(31).
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  Understanding of dedifferentiation, an indicator of poo prognosis for patients with thyroid cancer, has been hampered by imprecise and incomplete characterization of its heterogeneity and its attributes. Using single-cell RNA sequencing, we explored the landscape of thyroid cancer at single-cell resolution with 46,205 cells and delineated its dedifferentiation process and suppressive immune microenvironment. The developmental trajectory indicated that anaplastic thyroid cancer (ATC) cells were derived from a small subset of papillary thyroid cancer (PTC) cells. Moreover, a potential functional role of on ATC development was revealed by integrated analyses of copy number alteration and transcriptional regulatory network. Multiple genes in differentiation-related pathways (e.g., EMT) were involved as the downstream targets of CREB3L1, increased expression of which can thus predict higher relapse risk of PTC. Collectively, our study provided insights into the heterogeneity and molecular evolution of thyroid cancer and highlighted the potential driver role of in its dedifferentiation process.
• Luo, H., Xia, X., Kim, G., Liu, Y., Zhang, L., Yang, T., Zhang, S., Li, R., Tang, H., Dong, B., Fu, X., Cheng, W., Zhang, W., Yang, L., Peng, Y., Dai, L., Hu, H., Jiang, Y., Gong, C., , Hu, Y., et al. (2020). Characterizing de-differentiation of thyroid cancer by integrated analysis. Science Advances.
• Wang, J., Hu, Y., Escamilla-Rivera, V., Gonzalez, C. L., Tang, L., Wang, B., El-Naggar, A. K., Myers, J. N., & Caulin, C. (2021). Epithelial Mutant p53 Promotes Resistance to Anti-PD-1-Mediated Oral Cancer Immunoprevention in Carcinogen-Induced Mouse Models. Cancers, 13(6).
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  Oral squamous cell carcinoma (OSCC) develops through the multistep malignant progression of squamous epithelium. This process can be prevented by PD-1 blockade in a mouse model for oral carcinogenesis. OSCCs exhibit a high incidence of mutations that confer oncogenic gain-of-function (GOF) activities that promote resistance to standard therapies and poor clinical outcomes. To determine whether epithelial mutations modulate anti-PD-1-mediated oral cancer immunoprevention, we generated mouse models for oral carcinogenesis by exposing mice carrying epithelial-specific mutations to the carcinogen 4NQO. Consistent with the oncogenic functions of mutant , mice with OSCCs expressing the GOF mutation developed higher metastasis rates than mice with loss-of-function (LOF) deletion or with wild-type . Throughout oral cancer progression, pre-invasive and invasive lesions showed a gradual increase in T-cell infiltration, recruitment of immunosuppressive regulatory T-cells (Tregs), and induction of PD-1/PD-L1 immune checkpoint proteins. Notably, while PD-1 blockade prevented the development of OSCCs in mice with wild-type or deletion, GOF abrogated the immunopreventive effects of anti-PD-1, associated with upregulation of IL17 signaling and depletion of exhausted CD8 cells in the microenvironment of the tumors. These findings sustain a potential role for profiling in personalized oral cancer immunoprevention.
• Amit, M., Takahashi, H., Dragominr, P., Lindemann, A., Gleber-Netto, F., Picketing, P., Anfossi, S., Osman, A., Cai, Y., Wang, R., Knutsen, E., Shmizu, M., Ivan, C., Rao, X., Siverman, D., Tam, S., Zhao, M., Caulin, C., Zinger, A., , Tasciotti, E., et al. (2020). Loss of p53 drives neuron reprogramming in head and neck cancer. Nature.
• Chari, N. S., Ivan, C., Le, X., Li, J., Mijiti, A., Patel, A. A., Osman, A. A., Peterson, C. B., Williams, M. D., Pickering, C. R., Caulin, C., Myers, J. N., Calin, G. A., & Lai, S. Y. (2020). Disruption of TP63-miR-27a* feedback loop by mutant TP53 in head and neck cancer. Journal of the National Cancer Institute.
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  Alterations in the epidermal growth factor receptor (EGFR) and PI3K pathways in head and neck squamous cell carcinomas (HNSCC) are frequent events that promote tumor progression. Ectopic expression of the EGFR-targeting microRNA (miR), miR-27a* (miR-27a-5p) inhibits tumor growth. We sought to identify mechanisms mediating repression of miR-27a* in HNSCC, which have not been previously identified.
• Hu, Y., Song, Z., Chen, J., & Caulin, C. (2020). Overexpression of MYB in the Skin Induces Alopecia and Epidermal Hyperplasia. The Journal of investigative dermatology.
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  Skin homeostasis is controlled by a complex interplay between tightly regulated transcription factors and signaling pathways. MYB is a transcription factor expressed in hair follicle progenitor cells and found overexpressed in adnexal skin tumors. However, the biological consequences of deregulated MYB expression in the skin remain poorly understood. To address this, we generated transgenic mice that overexpress MYB in epidermal and follicular keratinocytes. These mice exhibited a normal hair coat after birth but gradually developed alopecia, accompanied by altered follicular differentiation, disrupted hair cycle, and a marked depletion of hair follicle stem cells. Additionally, transgenic mice developed massive epidermal hyperplasia and hyperkeratosis. Global expression profiling not only confirmed that the skin of these mice exhibited transcriptomic features of alopecia and epidermal differentiation, but also revealed features of psoriasis and the inflammatory response. The latter was further confirmed by the increased T-cell infiltration found in the skin of transgenic mice. Overall, these results suggest that tight regulation of MYB expression in the skin is critical to maintain skin homeostasis.
• Wang, J., Xei, T., Wang, B., William, W. N., Heymach, J. V., El-Naggar, A. K., Myers, J. N., & Caulin, C. (2018). PD-1 blockade prevents the development and progression of carcinogen-induced oral premalignant lesions.. Cancer Prevention Research, 10(12), 684-693. doi:10.1158/1940-6207
• Foy, J. P., Tortereau, A., Caulin, C., Le Texier, V., Lavergne, E., Thomas, E., Chabaud, S., Perol, D., Lachuer, J., Hong, W. K., Goudot, P., Lippman, S. M., Bertolus, C., & Saintigny, P. (2016). The dynamics of gene expression changes in a mouse model of oral tumorigenesis may help refine prevention and treatment strategies in patients with oral cancer. Oncotarget, 7(24), 35932-35945.
• Li, Z., Gonzalez, C. L., Wang, B., Zhang, Y., Mejia, O., Katsonis, P., Lichtarge, O., Myers, J. N., El-Naggar, A. K., & Caulin, C. (2016). Cdkn2a suppresses metastasis in squamous cell carcinomas induced by the gain-of-function mutant p53R172H. J Pathol, 240(2), 224-34. doi:10.1002/path
• Mitani, Y., Liu, B., Rao, P., Borra, V., Zafereo, M., Weber, R. S., Kies, M. S., Lozano, G., Futreal, A., Caulin, C., & El-Naggar, A. K. (2016). Novel MYBL1 gene rearrangements with recurrent MYBL1-NFIB fusions in salivary adenoid cystic carcinomas lacking t(6;9) translocations. Clin Cancer Res, 22, 725-33.
• Neskey, D. M., Osman, A. A., Ow, T., Katsonis, P., McDonald, T. O., Hicks, S. C., Hsu, T., Pickering, C. R., Ward, A., Patel, A. A., Yordy, J. S., Skinner, H. D., Giri, Y., Sano, D., Story, M. D., Beadle, B. M., El-Naggar, A. K., Kies, M. S., William, W. N., , Caulin, C., et al. (2015). Evolutionary action score of TP53 (EAp53) identifies high risk mutations associated with decreased survival and increased distant metastases in head and neck cancer. Cancer Research, 75(7), 1527-36.
• Osman, A. A., Monroe, M. M., Ortega Alves, M. V., Patel, A. A., Katsonis, P., Fitzgerald, A. L., Neskey, D. M., Frederick, M. J., Woo, S. H., Caulin, C., Hsu, T., Ow, T., McDonald, T. O., Kimmel, M., Meyn, R. E., Lichtarge, O., & Myers, J. N. (2015). Wee-1 kinase inhibition overcomes cisplatin resistance associated with high risk TP53 mutations in head and neck cancer through mitotic arrest followed by senescence. Mol Cancer Ther, 14(2), 608-19.
• Savar, A., Acin, S., Gonzalez, C. L., El-Sawy, T., Mejia, O., Li, Z., Esmaeli, B., Lacy-Hulbert, A., El-Naggar, A. K., McCarthy, J. H., & Caulin, C. (2015). Loss of epithelial p53 and av integrin cooperate through Akt to induce squamous cell carcinoma yet prevent remodeling of the tumor microenvironment. Oncogene, 34(4), 516-24.
• Tanaka, N., Patel, A. A., Wang, J., Frederick, M. J., Kalu, N. N., Zhao, M., Fitzgerald, A. L., Xie, T. X., Silver, N. L., Caulin, C., Zhou, G., Skinner, H. D., Johnson, F. M., Myers, J. N., & Osman, A. A. (2015). Wee-1 kinase inhibition sensitizes high-risk HPV+ HNSCC to apoptosis accompanied by downregulation of MCI-1 and XIAP antiapoptotic proteins. Clin Cancer Research, 21(21), 4831-44.
• Li, X., Moses, R. E., Jing, J., Cao, W., & Caulin, C. (2014). Stresses, again and age-related disorders. Oxidative Medicine and Cellular Longevity. doi:10.1155/2014/320564
• Mitani, Y., Rao, P. H., Maity, S. N., Lee, Y. C., Ferraotto, R., Post, J. C., Licitra, L., Lippman, S. M., Kies, M. S., Weber, R. S., Caulin, C., Lin, S. H., & El-Naggar, A. K. (2014). Alterations associated with androgen receptor gene activation in salivary duct carcinoma of both sexes. Clin Cancer Res, 20(24), 6570-81.
• Pickering, C. R., Zhou, J. H., Lee, J. J., Drummond, J. A., Peng, S. A., Saade, R. E., Tsai, K. Y., Curry, J. L., Tetzlaff, M. T., Lai, S. Y., Yu, J., Muzny, D. M., Doddapaneni, H., Shinbrot, E., Covington, K. R., Zhang, J., Seth, S., Caulin, C., Clayman, G. L., , El-Naggar, A. K., et al. (2014). Mutational landscape of aggressive cutaneous squamous cell carcinoma. Clin Cancer Res, 20(24), 6582-92.
• Zhou, G., Wang, J., Zhao, M., Sano, D., Xie, T. X., Tanaka, N., Sano, D., Pate, A. A., Ward, A. M., Sandulache, V., Jasser, S., Skinner, H. D., Fitzgerald, A. L., Osman, A. A., Wei, Y., Xia, X., Songyang, Z., Mills, G. G., Hung, M. C., , Caulin, C., et al. (2014). Gain-of-function mutant P53 promotes cell growth and cancer cell metabolism via inhibition of AMPK activation. Mol Cell, 54(6), 960-74.
• Ali, A., Wang, Z., Fu, J., Ji, L., Liu, J., Li, L., Wang, H., Chen, J., Caulin, C., Myers, J. N., Zhang, P., Xiao, J., Zhang, B., & Li, X. (2013). Differential regulation of the REGy-proteasome pathway by p53/TGF-B signaling and mutant p53 in cancer cells. Nat Commun, 4, 2667.
• Zhang, L., Mitani, Y., Caulin, C., Rao, P. H., Kies, M. S., Saintingny, O., Zhang, B., Weber, R. S., Lippman, S. M., & El-Naggar, A. K. (2013). Detailed genome wide SNP analysis of major salivary carcinomas localizes subtype-specific chromosome sites and oncogenes of potential clinical significance. Am J Pathol, 2048-5.

Presentations

• Caulin, C. (2006, August). Activation of the gain-of-function p53R172H allele predisposes to oral cancer progression. AHNS Annual Meeting & Research Workshop on Biology, Prevention and Treatment of Head & Neck Cancer. Chicago, IL.
• Caulin, C. (2006, June). Oncogenic role for a gain-of-function p53 mutations in skin cancer progression. MMHCC Steering Committee Meting. Seattle, WA.
• Caulin, C. (2008, July). The role of p53 mutations in mouse models for oral cancer. 7th International Conference on Head and Neck Cancer. San Francisco, CA.
• Caulin, C. (2010, October). Oral cancer progression induce by mutant p53 in response to chemotherapy. AHNS Research Workshop on Biology, Prevention and Treatment of Head and Neck Cancer. Arlington, VA: American Head and Neck Society.
• Caulin, C. (2017, April). PD-1 blockade prevents the development of oral squamous cell carcinoma from carcinogen-induced premalignant lesions. AHNS Annual Meeting. San Diego, CA: AHNS.
• Caulin, C. (2021, August). Immunoprevention of carcinogen-induced oral cancer. University of Arizona Cancer Center Grand Rounds. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2021, January). Immune checkpoint blockade for oral cancer prevention. University of Arizona Cancer Center. Head & Neck Research/Translational Research Team Meeting. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2021, May). Targeting CDK4/6 in mouse oral premalignant lesions. University of Arizona Cancer Center CP-CTNet. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2021, October). p53 mutations in oral carcinogenesis and response to immune checkpoint inhibitors.. Department of Basic Medical Sciences at the UA College of Medicine – Phoenix.. Phoenix, AZ: UA College of Medicine – Phoenix.
• Caulin, C. (2020, April). CDK 4/6 inhibition in p16- oral premalignant lesions. University of Arizona Cancer Center CP-CTNet. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2020, April). Role of Genetic Alterations in Head and Neck Cancer Development and Response to Therapy. University of Arizona Cancer Center CBIO Data Blitz. Tucson, AZ: University of Arizona Cancer Center.
• Hu, Y., Zhu, X., Luo, H., & Caulin, C. (2020, April). MYB and the MYB-NFIB fusion induce adenoid cystic carcinoma. AACR 2020 Meeting, 2020. April 24-29, 2020.
• Caulin, C. (2019, March). Transgenic Mouse Models for Adenoid Cystic Carcinoma. Advances in Adenoid Cystic Carcinoma Translational Research.. Boston, MA.
• Caulin, C. (2019, October). Oncogenic Drivers of Adenoid Cystic Carcinoma. University of Arizona Cancer Center Grand Rounds. Tucson, AZ..
• Caulin, C. (2018, July). Mouse models for molecular drivers and preclinical studies in head and neck cancer. University of Arizona Cancer Center Scientific Leadership Council. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2018, October). Immunoprevention in mouse models for oral cancer. University of Arizona Cancer Center, Cancer Prevention Program. Tucson, AZ: University of Arizona Cancer Center, Cancer Prevention Program.
• Caulin, C. (2018, October). Molecular drivers of head and neck cancer progression and resistance to therapy. University of Arizona College of Medicine. Tucson, AZ: University of Arizona College of Medicine.
• Caulin, C. (2018, October). Overcoming the resistance of head and neck cancer to immune checkpoint inhibitors. UACC CBP/TDP Drug Development Symposium, University of Arizona Cancer Center.. Tucson, AZ: University of Arizona Cancer Center.
• Caulin, C. (2018, September). Modeling genetic alterations for head and neck cancer development and response to therapy.. University of Arizona. Cancer Biology Graduate Interdisciplinary Program.. Tucson, AZ: University of Arizona Cancer Biology Graduate Interdisciplinary Program..
• Caulin, C. (2018, September). p53 mutations in head and neck cancer progression and resistance to immunoprevention. University of Arizona. Department of Otolaryngology Grand Rounds. Tucson, AZ: University of Arizona Department of Otolaryngology.
• Caulin, C. (2017, August). PD-1 blockade prevents the development and progression of carcinogen-induced oral premalignant lesions. NIH Head & Neck/Thyroid SPORE Workshop. Rockville, MD: NCI.
• Caulin, C. (2017, February). Defining molecular drivers of head and neck cancers in mouse models. Ohio State University. Columbus, OH: Ohio State University.
• Caulin, C. (2017, February). Modeling molecular drivers of head and neck cancers in mice. University of Arizona. Tucson, AZ: University of Arizona.
• Caulin, C. (2017, October). Mouse model for adenoid cystic carcinoma. 4th International Conference on Malignant Salivary Tumors. Gainesville, FL.
• Caulin, C. (2017, September). Mouse models for genetic drivers and preclinical studies in head and neck cancer. Rutgers New Jersey Medical School-Rutgers Cancer Institute of New Jersey. Newark, NJ: New Jersey Medical School.
• Wang, J., Wang, B., Zhu, X., Xie, T., El-Naggar, A. K., Myers, J. N., & Caulin, C. (2017, Fall). PD-1 blockade prevents the development of oral squamous cell carcinoma from carcinogen-induced premalignant lesions. AHNS Annual Meeting. San Diego, CA: AHNS.
• Wang, J., Zhang, Y., Wang, B., El-Naggar, A. K., Myers, J. N., & Caulin, C. (2017, Fall). Mutant p53 promotes progression and metastasis of mouse oral tumors induced by 4NQO associated with specific immune infiltrates. AACR Annual Meeting. Washington, DC: AACR.
• Caulin, C. (2016, April). Modeling adenoid cystic carcinoma in mice. Center for Genetics and Genomics. Houston, TX: MD Anderson Cancer Center.
• Caulin, C. (2015, February). Mutant p53 in squamous cell carcinoma progression and metastasis. University of New Mexico, Department of Genetics. Albuquerque, NM: University of New Mexico.
• Caulin, C. (2015, July). Mutant p53 in squamous cell carcinoma progression and metastasis. Head and Neck Cancer Research Seminar. Houston, TX: MD Anderson Cancer Center.
• Caulin, C. (2013, July). Transgenic mouse model for Myb Overexpression in adenoid cystic carcinoma. International Myb Conference. Albuquerque, NM: University of New Mexico Cancer Center.
• Caulin, C. (2012, September). Modeling squamous cell carcinoma development and malignant progression in mice. Sao Paulo Advanced School of Comparative Oncology. Sao Paulo Brasil: Sao Paulo Advanced School of Comparative Oncology.
• Caulin, C. (2009, November). Inducible mouse models for skin and oral cancers. X National Congress of SBMCTA Brazilian Society of Environmental Mutagenesis. Ouro Preto, Brazil: National Congress of SBMCTA.

Poster Presentations

• Caulin, C. (2021). Randomized phase II trial of ficlatuzumab with or without cetuximab in pan-refractory, advanced head and neck squamous cell carcinoma (HNSCC).. 2021 ASCO Annual Meeting.
• Chung, C., Obara, S., Saboda, K., Caulin, C., Centuori, S. M., Burtness, B., Giri, A., Steuer, C., Baker, A., Bearelly, S., Wang, S., Julian, R., Muzaffar, J., Bhatia, A., Kaczmar, J., Bauman, J., Roe, D., Saba, N., & Bauman, J. (2021, May/Spring). Randomized, phase II study of ficlatuzumab with or without cetuximab in pan-refractory, advanced head and neck squamous cell carcinoma (HNSCC).
  . ASCO.
• Amit, M., Takahashi, H., Dragominr, P., Lindemann, A., Gleber-Netto, F., Picketing, P., Anfossi, S., Osman, A., Cai, Y., Wang, R., Knutsen, E., Shmizu, M., Ivan, C., Rao, X., Siverman, D., Tam, S., Zhao, M., Caulin, C., Zinger, A., , Tasciotti, E., et al. (2021, April). Cancer takes a nerve: Loss of p53 drives neuron reprogramming in head and neck cancer. AACR 2021 Meeting. Virtual: AACR.

Others

• Foy, J., Tortereau, A., Caulin, C., Lavergne, E., Chabaud, S., Perol, D., Lang, W., Lippman, S. M., Goudot, P., Ki Hong, W. K., Bertolus, C., & Saintigny, P. (2014, September). The dynamics of gene expression changes observed in a murine model of oral carcinogenesis is associated with specific patterns of pathway activation and drug sensitivity profiles. 13th Annual AACR International Conference on Frontiers in Cancer Prevention Research, Sheraton New Orleans.
• Caulin, C. (2013, June). Disssecting the role of p53 mutations in mouse models for squamous cell carcinoma. University of New Mexico Cancer Center.
• Li, Z., Mejia, O., & Caulin, C. (2013, Fall). Deletion of Cdkn2a induces EMT and promotes metastasis in skin carcinomas induced by mutant p53. 6th International Mutant p53 Workshop, Toronto Canada.
• Caulin, C. (2010, January). Dissecting the role of p53 mutations in mouse models for skin cancer. University of Texas MD Anderson Cancer Center.
• Caulin, C. (2009, June). Mouse models for oral cancer. MD Anderson Surgical Grand Rounds.
• Caulin, C. (2008, July). Oncogenic role of p53 mutations in mouse squamous cell carcinomas. NIH, NIDCR, Bethesda MD.
• Caulin, C. (2008, November). Inducible mouse models for cancers of the oral cavity. Workshop on Salivary Gland Tumor Research, NIDCR (NIH).