Sara Mozelle Centuori

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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.
• Bauman, J. E., Hsu, C. H., Centuori, S., Guillen-Rodriguez, J., Garland, L. L., Ho, E., Padi, M., Bageerathan, V., Bengtson, L., Wojtowicz, M., Szabo, E., & Chow, H. S. (2022). Randomized Crossover Trial Evaluating Detoxification of Tobacco Carcinogens by Broccoli Seed and Sprout Extract in Current Smokers. Cancers, 14(9).
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  Consumption of cruciferous vegetables, rich in the isothiocyanate glucoraphanin, is associated with reduced risk of tobacco-related cancers. Sulforaphane, released by hydrolysis of glucoraphanin, potently induces cytoprotective phase II enzymes. Sulforaphane decreased the incidence of oral cancer in the 4NQO carcinogenesis model. In residents of Qidong, China, broccoli seed and sprout extracts (BSSE) increased detoxification of air pollutants benzene and acrolein, also found in tobacco smoke. This randomized, crossover trial evaluated detoxification of tobacco carcinogens by the BSSE Avmacol in otherwise healthy smokers. Participants were treated for 2 weeks with both low and higher-dose BSSE (148 µmol vs. 296 µmol of glucoraphanin daily), separated by a 2-week washout, with randomization to low-high vs. high-low sequence. The primary endpoint was detoxification of benzene, measured by urinary excretion of its mercapturic acid, SPMA. Secondary endpoints included bioavailability, detoxification of acrolein and crotonaldehyde, modulation by genotype, and toxicity. Forty-nine participants enrolled, including 26 (53%) females with median use of 20 cigarettes/day. Low and higher-dose BSSE showed a mean bioavailability of 11% and 10%, respectively. Higher-dose BSSE significantly upregulated urinary excretion of the mercapturic acids of benzene ( = 0.04), acrolein ( < 0.01), and crotonaldehyde ( = 0.02), independent of genotype. Retention and compliance were high resulting in early study completion. In conclusion, BSSE significantly upregulated detoxification of the tobacco carcinogens benzene, acrolein, and crotonaldehyde in current tobacco smokers.
• Centuori, S. M., & Bauman, J. E. (2022). c-Met Signaling as a Therapeutic Target in Head and Neck Cancer. Cancer journal (Sudbury, Mass.), 28(5), 346-353.
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  Despite a dearth of activating driver mutations in head and neck squamous cell carcinoma (HNSCC), aberrant activation of the oncogenes, epidermal growth factor receptor (EGFR), and c-Met is near-universal in human papillomavirus (HPV)-negative disease. Although EGFR activation drove the successful development of the anti-EGFR monoclonal antibody cetuximab in HNSCC, no c-Met-targeting therapy has gained regulatory approval. Inhibition of the c-Met pathway may subvert oncogenesis within the tumor-intrinsic compartment, blocking tumoral proliferation, invasion, migration, and metastasis, or the tumor-extrinsic compartment, modulating the immunosuppressive tumor microenvironment. This review discusses the rationale and current drug development strategies for targeting c-Met or its exclusive ligand hepatocyte growth factor (HGF) in HNSCC.
• Centuori, S. M., & Bhattacharya, D. (2022). Locally produced autoantibodies in cancer. Cell, 185(7), 1110-1111.
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  The function and antigen-specificities of tumor-infiltrating B cells are mostly unknown. In a new study by Mazor et al., matrix metalloproteinase 14 (MMP14), a self-antigen that is overexpressed by ovarian cancers, is shown to drive B cell activation and autoantibody production in tertiary lymphoid structures (Mazor et al., 2022).
• Parsons, J. K., Pinto, P. A., Pavlovich, C. P., Uchio, E., Nguyen, M. N., Kim, H. L., Gulley, J. L., Sater, H. A., Jamieson, C., Hsu, C. H., Wojtowicz, M., House, M., Schlom, J., Donahue, R. N., Dahut, W. L., Madan, R. A., Bailey, S., Centuori, S., Bauman, J. E., , Parnes, H. L., et al. (2022). A Phase 2, Double-blind, Randomized Controlled Trial of PROSTVAC in Prostate Cancer Patients on Active Surveillance. European urology focus.
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  There is an unmet clinical need for interventions to prevent disease progression in patients with localized prostate cancer on active surveillance (AS).
• 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.
• Dickinson, S. E., Khawam, M., Kirschnerova, V., Vaishampayan, P., Centuori, S. M., Saboda, K., Calvert, V. S., Petricoin, E. F., & Curiel-Lewandrowski, C. (2021). Increased PD-L1 Expression in Human Skin Acutely and Chronically Exposed to UV Irradiation. Photochemistry and photobiology, 97(4), 778-784.
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  Overexpression of PD-L1 (CD274) on tumor cells may represent a hallmark of immune evasion, and overexpression has been documented in several tumors including cutaneous squamous cell carcinoma (cSCC). While PD-L1/PD-1 activity in the skin has been primarily described in inflammatory models, our goal was to examine PD-L1 expression in human keratinocytes exposed to UV irradiation. We assessed PD-L1 expression in human sun-protected (SP) and sun-damaged (SD) skin, actinic keratosis (AK), and cSCC using IHC and protein microarray. Both methods found low baseline levels of PD-L1 in SP and SD skin and significantly increased expression in cSCC. Next, we examined PD-L1 expression in acute models of UV exposure. In human SP skin exposed to 2-3 MED of UV (n = 20), epidermal PD-L1 was induced in 70% of subjects after 24 h (P = 0.0001). SKH-1 mice exposed to acute UV also showed significant epidermal PD-L1 induction at 16, 24 and 48 h. A time- and dose-dependent induction of PD-L1 was confirmed in cultured human keratinocytes after UV, which was markedly reduced in the presence of MEK/ERK, JNK or STAT3 inhibitors. These findings suggest that UV induces upregulation of PD-L1 through established, pharmacologically targetable stress-signaling pathways in keratinocytes.
• Geiger, J. L., Cedars, E. D., Zang, Y., Daniel, N. P., Li, H., Grandis, J. R., Centuori, S. M., Daniel, J. E., & Bauman, J. E. (2021). Clinical trials optimizing investigator and self‐collection of buccal cells for RNA yield. Laryngoscope Investigative Otolaryngology.
• Tapia, E., Villa-Guillen, D. E., Chalasani, P., Centuori, S., Roe, D. J., Guillen-Rodriguez, J., Huang, C., Galons, J. P., Thomson, C. A., Altbach, M., Trujillo, J., Pinto, L., Martinez, J. A., Algotar, A. M., & Chow, H. S. (2021). A randomized controlled trial of metformin in women with components of metabolic syndrome: intervention feasibility and effects on adiposity and breast density. Breast cancer research and treatment, 190(1), 69-78.
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  Obesity is a known risk factor for post-menopausal breast cancer and may increase risk for triple negative breast cancer in premenopausal women. Intervention strategies are clearly needed to reduce obesity-associated breast cancer risk.
• Sweeney, N. W., Gomes, C. J., De Armond, R., Centuori, S. M., Parthasarathy, S., & Martinez, J. D. (2019). Hypoxia Suppresses High Fat Diet-Induced Steatosis And Development Of Hepatic Adenomas. Hypoxia (Auckland, N.Z.), 7, 53-63.
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  Nonalcoholic fatty liver disease (NAFLD) is considered the most common form of silent liver disease in the United States and obesity is associated with increased risk of NAFLD. Obstructive sleep apnea (OSA) which is common in obese individuals is associated with a greater incidence of NAFLD, which in turn, increases the risk for hepatocellular carcinoma (HCC). It is unclear how obesity, OSA and NAFLD interrelate nor how they collectively contribute to an increased risk for developing HCC.
• Centuori, S. M., Gomes, C. J., Kim, S. S., Putnam, C. W., Larsen, B. T., Garland, L. L., Mount, D. W., & Martinez, J. D. (2018). Double-negative (CD27IgD) B cells are expanded in NSCLC and inversely correlate with affinity-matured B cell populations. Journal of translational medicine, 16(1), 30.
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  The presence of B cells in early stage non-small cell lung cancer (NSCLC) is associated with longer survival, however, the role these cells play in the generation and maintenance of anti-tumor immunity is unclear. B cells differentiate into a variety of subsets with differing characteristics and functions. To date, there is limited information on the specific B cell subsets found within NSCLC. To better understand the composition of the B cell populations found in NSCLC we have begun characterizing B cells in lung tumors and have detected a population of B cells that are CD79ACD27IgD. These CD27IgD (double-negative) B cells have previously been characterized as unconventional memory B cells and have been detected in some autoimmune diseases and in the elderly population but have not been detected previously in tumor tissue.
• Gomes, C. J., Harman, M. W., Centuori, S. M., Wolgemuth, C. W., & Martinez, J. D. (2018). Measuring DNA content in live cells by fluorescence microscopy. Cell division, 13, 6.
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  Live-cell fluorescence microscopy (LCFM) is a powerful tool used to investigate cellular dynamics in real time. However, the capacity to simultaneously measure DNA content in cells being tracked over time remains challenged by dye-associated toxicities. The ability to measure DNA content in single cells by means of LCFM would allow cellular stage and ploidy to be coupled with a variety of imaging directed analyses. Here we describe a widely applicable nontoxic approach for measuring DNA content in live cells by fluorescence microscopy. This method relies on introducing a live-cell membrane-permeant DNA fluorophore, such as Hoechst 33342, into the culture medium of cells at the end of any live-cell imaging experiment and measuring each cell's integrated nuclear fluorescence to quantify DNA content. Importantly, our method overcomes the toxicity and induction of DNA damage typically caused by live-cell dyes through strategic timing of adding the dye to the cultures; allowing unperturbed cells to be imaged for any interval of time before quantifying their DNA content. We assess the performance of our method empirically and discuss adaptations that can be implemented using this technique.
• Gomes, C. J., Centuori, S. M., Harman, M. W., Putnam, C. W., Wolgemuth, C. W., & Martinez, J. D. (2017). The induction of endoreduplication and polyploidy by elevated expression of 14-3-3γ. Genes & cancer, 8(11-12), 771-783.
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  Several studies have demonstrated that specific 14-3-3 isoforms are frequently elevated in cancer and that these proteins play a role in human tumorigenesis. 14-3-3γ, an isoform recently demonstrated to function as an oncoprotein, is overexpressed in a variety of human cancers; however, its role in promoting tumorigenesis remains unclear. We previously reported that overexpression of 14-3-3γ caused the appearance of polyploid cells, a phenotype demonstrated to have profound tumor promoting properties. Here we examined the mechanism driving 14-3-3γ-induced polyploidization and the effect this has on genomic stability. Using FUCCI probes we showed that these polyploid cells appeared when diploid cells failed to enter mitosis and subsequently underwent endoreduplication. We then demonstrated that 14-3-3γ-induced polyploid cells experience significant chromosomal segregation errors during mitosis and observed that some of these cells stably propagate as tetraploids when isolated cells were expanded into stable cultures. These data lead us to conclude that overexpression of the 14-3-3γ promotes endoreduplication. We further investigated the role of 14-3-3γ in human NSCLC samples and found that its expression is significantly elevated in polyploid tumors. Collectively, these results suggests that 14-3-3γ may promote tumorigenesis through the production of a genetically unstable polyploid intermediate.
• Centuori, S. M., Gomes, C. J., Trujillo, J., Borg, J., Brownlee, J., Putnam, C. W., & Martinez, J. D. (2016). Deoxycholic acid mediates non-canonical EGFR-MAPK activation through the induction of calcium signaling in colon cancer cells. Biochimica et biophysica acta, 1861(7), 663-70.
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  Obesity and a western diet have been linked to high levels of bile acids and the development of colon cancer. Specifically, increased levels of the bile acid deoxycholic acid (DCA), an established tumor promoter, has been shown to correlate with increased development of colorectal adenomas and progression to carcinoma. Herein we investigate the mechanism by which DCA leads to EGFR-MAPK activation, a candidate mechanism by which DCA may promote colorectal tumorigenesis. DCA treated colon cancer cells exhibited strong and prolonged activation of ERK1/2 when compared to EGF treatment alone. We also showed that DCA treatment prevents EGFR degradation as opposed to the canonical EGFR recycling observed with EGF treatment. Moreover, the combination of DCA and EGF treatment displayed synergistic activity, suggesting DCA activates MAPK signaling in a non-canonical manner. Further evaluation showed that DCA treatment increased intracellular calcium levels and CAMKII phosphorylation, and that blocking calcium with BAPTA-AM abrogated MAPK activation induced by DCA, but not by EGF. Finally we showed that DCA-induced CAMKII leads to MAPK activation through the recruitment of c-Src. Taken together, we demonstrated that DCA regulates MAPK activation through calcium signaling, an alternative mechanism not previously recognized in human colon cancer cells. Importantly, this mechanism allows for EGFR to escape degradation and thus achieve a constitutively active state, which may explain its tumor promoting effects.
• Centuori, S. M., Garland, L. L., Gomes, C. J., Kim, S., Martinez, J. D., Mount, D. B., & Putnam, C. W. (2015).

  Abstract 1299: Tumor-infiltrating B cells are predictive of human lung squamous cell survival

  . Immunology, 75(15_Supplement), 1299-1299. doi:10.1158/1538-7445.am2015-1299
• Trad, M., Gautheron, A., Fraszczak, J., Alizadeh, D., Larmonier, C., LaCasse, C. J., Centuori, S., Audia, S., Samson, M., Ciudad, M., Bonnefoy, F., Lemaire-Ewing, S., Katsanis, E., Perruche, S., Saas, P., & Bonnotte, B. (2015). T Lymphocyte Inhibition by Tumor-Infiltrating Dendritic Cells Involves Ectonucleotidase CD39 but Not Arginase-1. BioMed research international, 2015, 891236.
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  T lymphocytes activated by dendritic cells (DC) which present tumor antigens play a key role in the antitumor immune response. However, in patients suffering from active cancer, DC are not efficient at initiating and supporting immune responses as they participate to T lymphocyte inhibition. DC in the tumor environment are functionally defective and exhibit a characteristic of immature phenotype, different to that of DC present in nonpathological conditions. The mechanistic bases underlying DC dysfunction in cancer responsible for the modulation of T-cell responses and tumor immune escape are still being investigated. Using two different mouse tumor models, we showed that tumor-infiltrating DC (TIDC) are constitutively immunosuppressive, exhibit a semimature phenotype, and impair responder T lymphocyte proliferation and activation by a mechanism involving CD39 ectoenzyme.
• Young, G. M., Radhakrishnan, V. M., Centuori, S. M., Gomes, C. J., & Martinez, J. D. (2015). Comparative analysis of 14-3-3 isoform expression and epigenetic alterations in colorectal cancer. BMC cancer, 15, 826.
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  The 14-3-3 family is a group of intracellular proteins found in all eukaryotic organisms. Humans have seven isoforms that serve as scaffolds to promote interactions of regulatory phospho-proteins involved in many vital cellular processes and previous studies have shown that disturbances in native 14-3-3 levels can contribute significantly to the development of various cancers.
• Centuori, S. M., & Martinez, J. D. (2014). Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer. Digestive diseases and sciences, 59(10), 2367-80.
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  A high-fat diet coincides with increased levels of bile acids. This increase in bile acids, particularly deoxycholic acid (DCA), has been strongly associated with the development of colon cancer. Conversely, ursodeoxycholic acid (UDCA) may have chemopreventive properties. Although structurally similar, DCA and UDCA present different biological and pathological effects in colon cancer progression. The differential regulation of cancer by these two bile acids is not yet fully understood. However, one possible explanation for their diverging effects is their ability to differentially regulate signaling pathways involved in the multistep progression of colon cancer, such as the epidermal growth factor receptor (EGFR)-mitogen-activated protein kinase (MAPK) pathway. This review will examine the biological effects of DCA and UDCA on colon cancer development, as well as the diverging effects of these bile acids on the oncogenic signaling pathways that play a role in colon cancer development, with a particular emphasis on bile acid regulation of the EGFR-MAPK pathway.
• Mount, D. W., Putnam, C. W., Centouri, S. M., Manziello, A. M., Pandey, R., Garland, L. L., & Martinez, J. D. (2014). Using logistic regression to improve the prognostic value of microarray gene expression data sets: application to early-stage squamous cell carcinoma of the lung and triple negative breast carcinoma. BMC medical genomics, 7, 33.
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  Numerous microarray-based prognostic gene expression signatures of primary neoplasms have been published but often with little concurrence between studies, thus limiting their clinical utility. We describe a methodology using logistic regression, which circumvents limitations of conventional Kaplan Meier analysis. We applied this approach to a thrice-analyzed and published squamous cell carcinoma (SQCC) of the lung data set, with the objective of identifying gene expressions predictive of early death versus long survival in early-stage disease. A similar analysis was applied to a data set of triple negative breast carcinoma cases, which present similar clinical challenges.
• Centuori, S. M., Trad, M., LaCasse, C. J., Alizadeh, D., Larmonier, C. B., Hanke, N. T., Kartchner, J., Janikashvili, N., Bonnotte, B., Larmonier, N., & Katsanis, E. (2012). Myeloid-derived suppressor cells from tumor-bearing mice impair TGF-β-induced differentiation of CD4+CD25+FoxP3+ Tregs from CD4+CD25-FoxP3- T cells. Journal of leukocyte biology, 92(5), 987-97.
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  MDSCs and Tregs play an essential role in the immunosuppressive networks that contribute to tumor-immune evasion. The mechanisms by which tumors promote the expansion and/or function of these suppressive cells and the cross-talk between MDSC and Treg remain incompletely defined. Previous reports have suggested that MDSC may contribute to Treg induction in cancer. Herein, we provide evidence that tumor-induced gr-MDSCs, endowed with the potential of suppressing conventional T Lc, surprisingly impair TGF-β1-mediated generation of CD4(+)CD25(+)FoxP3(+) iTregs. Furthermore, gr-MDSCs impede the proliferation of nTregs without, however, affecting FoxP3 expression. Suppression of iTreg differentiation from naïve CD4(+) cells by gr-MDSC occurs early in the polarization process, requires inhibition of early T cell activation, and depends on ROS and IDO but does not require arginase 1, iNOS, NO, cystine/cysteine depletion, PD-1 and PD-L1 signaling, or COX-2. These findings thus indicate that gr-MDSCs from TB hosts have the unanticipated ability to restrict immunosuppressive Tregs.
• Janikashvili, N., LaCasse, C. J., Larmonier, C., Trad, M., Herrell, A., Bustamante, S., Bonnotte, B., Har-Noy, M., Larmonier, N., & Katsanis, E. (2011). Allogeneic effector/memory Th-1 cells impair FoxP3+ regulatory T lymphocytes and synergize with chaperone-rich cell lysate vaccine to treat leukemia. Blood, 117(5), 1555-64.
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  Therapeutic strategies combining the induction of effective antitumor immunity with the inhibition of the mechanisms of tumor-induced immunosuppression represent a key objective in cancer immunotherapy. Herein we demonstrate that effector/memory CD4(+) T helper-1 (Th-1) lymphocytes, in addition to polarizing type-1 antitumor immune responses, impair tumor-induced CD4(+)CD25(+)FoxP3(+) regulatory T lymphocyte (Treg) immunosuppressive function in vitro and in vivo. Th-1 cells also inhibit the generation of FoxP3(+) Tregs from naive CD4(+)CD25(-)FoxP3(-) T cells by an interferon-γ-dependent mechanism. In addition, in an aggressive mouse leukemia model (12B1), Th-1 lymphocytes act synergistically with a chaperone-rich cell lysate (CRCL) vaccine, leading to improved survival and long-lasting protection against leukemia. The combination of CRCL as a source of tumor-specific antigens and Th-1 lymphocytes as an adjuvant has the potential to stimulate efficient specific antitumor immunity while restraining Treg-induced suppression.
• LaCasse, C. J., Janikashvili, N., Larmonier, C. B., Alizadeh, D., Hanke, N., Kartchner, J., Situ, E., Centuori, S., Har-Noy, M., Bonnotte, B., Katsanis, E., & Larmonier, N. (2011). Th-1 lymphocytes induce dendritic cell tumor killing activity by an IFN-γ-dependent mechanism. Journal of immunology (Baltimore, Md. : 1950), 187(12), 6310-7.
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  Dendritic cells (DCs) encompass a heterogeneous population of cells capable of orchestrating innate and adaptive immune responses. The ability of DCs to act as professional APCs has been the foundation for the development and use of these cells as vaccines in cancer immunotherapy. DCs are also endowed with the nonconventional property of directly killing tumor cells. The current study investigates the regulation of murine DC cytotoxic function by T lymphocytes. We provide evidence that CD4(+) Th-1, but not Th-2, Th-17 cells, or regulatory T cells, are capable of inducing DC cytotoxic function. IFN-γ was identified as the major factor responsible for Th-1-induced DC tumoricidal activity. Tumor cell killing mediated by Th-1-activated killer DCs was dependent on inducible NO synthase expression and NO production. Importantly, Th-1-activated killer DCs were capable of presenting the acquired Ags from the killed tumor cells to T lymphocytes in vitro or in vivo. These observations offer new possibilities for the application of killer DCs in cancer immunotherapy.
• Cantrell, J., Larmonier, C., Janikashvili, N., Bustamante, S., Fraszczak, J., Herrell, A., Lundeen, T., J LaCasse, C., Situ, E., Larmonier, N., & Katsanis, E. (2010). Signaling pathways induced by a tumor-derived vaccine in antigen presenting cells. Immunobiology, 215(7), 535-44.
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  We have previously reported on the anti-tumoral potential of a chaperone-rich cell lysate (CRCL) vaccine. Immunization with CRCL generated from tumors elicits specific T and NK cell-dependent immune responses leading to protective immunity in numerous mouse tumor models. CRCL provides both a source of tumor antigens and danger signals leading to dendritic cell activation. In humans, tumor-derived CRCL induces dendritic cell activation and CRCL-loaded dendritic cells promote the generation of cytotoxic T lymphocytes in vitro. The current study was designed to identify the signaling events and modifications triggered by CRCL in antigen presenting cells. Our results indicate that tumor-derived CRCL not only promotes the activation of dendritic cells, but also significantly fosters the function of macrophages that thus appear as major targets of this vaccine. Activation of both cell types is associated with the induction of the MAP kinase pathway, the phosphorylation of STAT1, STAT5 and AKT and with transcription factor NF-kappaB activation in vitro and in vivo. These results thus provide important insights into the mechanisms by which CRCL-based vaccines exert their adjuvant effects on antigen presenting cells.

Proceedings Publications

• Vedantham, S., Tseng, H., Centuori, S. M., Garcia, D. O., Chalasani, P., Chiang, J. A., Roe, D., & Chow, H. (2023). Feasibility of quantitative breast density measurements in obese women with dedicated cone-beam breast CT.. In 2023 Program of the 10th International Breast Density & Cancer Risk Assessment Workshop, a21.

Poster Presentations

• Parsons, K. J., Pinto, P., Parnes, H., Pavlovich, C., Uchio, E., Nguyen, M., Kim, H., Gulley, J., Sater, A., Jamieson, C., Hsu, C., Wojtowicz, M., Schlom, J., Donahue, R., Centuori, S. M., Bailey, S., Bauman, J. E., & Chow, H. (2022, February). Immunotherapy to Prevent Progression on Active Surveillance Study (IPASS): A Phase II Randomized, Double Blind, Controlled Trial of PROSTVAC in Prostate Cancer Patients on Active Surveillance. ASCO. Virtual.
• Pinto, L., Centuori, S. M., Guillen-Rodriguez, J., Roe, D., Tapia, E., Chalasani, P., & Chow, S. (2022, November/Fall). Effects of metformin on breast tissue inflammation in premenopausal women with components of metabolic syndrome. SABCS.
• Bauman, J. E., Hsu, C., Centuori, S. M., Jose, G., Garland, L. L., Ho, E., Bengtson, L., Wojtowicz, M., Szabo, E., & Chow, H. (2021, April). Randomized crossover trial evaluating detoxication of tobacco carcinogens by broccoli seed and sprout extract in heavy smokers. American Association for Cancer Research (AACR),. Virtual Interactive 2021: AACR.
• Bauman, J., Saba, N., Roe, D., Bauman, J., Kaczmar, J., Bhatia, A., Muzaffar, J., Julian, R., Wang, S., Bearelly, S., Baker, A., Steuer, C., Giri, A., Burtness, B., Centuori, S. M., Caulin, C., Saboda, K., Obara, S., & Chung, C. (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.
• Field, M., Bauman, J. E., & Centuori, S. M. (2021, June). Implementation and Expansion of Cytek cFluor™ Immunoprofiling Kit, 14 Color to 26 Colors. CYTO. Virtual: ISAC.
• Pinto, L., Tapia, E., Villa Guillen, D., Chalasani, P., Centuori, S. M., Roe, D., Guillen, J., Huang, C., Galons, J., Thomson, C. A., Altbach, M. I., Trujillo, J., Martinez, J. A., Algotar, A., & Chow, H. (2021, November). A randomized controlled trial of metformin in women with components of metabolic syndrome: Intervention feasibility and effects on breast density and adiposity. SABCS.
• Tapia, E., Villa Guillen, D., Chalasani, P., Centuori, S. M., Roe, D., Guillen, J., Huang, C., Cordova, C., Pinto, L., & Chow, H. (2021, November). Effect of metformin on metabolic markers associated with breast cancer risk in a Phase II clinical trial in overweight/obese premenopausal women. SABCS. Virtual: AACR.
• Bauman, J., Roe, D., Saba, N., Bauman, J., Kaczmar, J., Burtness, B., Muzaffar, J., Julian, R., Wang, S., Bearelly, S., Baker, A., Steuer, C., Bhatia, A., Giri, A., Caulin, C., Stabile, L., Centuori, S. M., & Chung, C. (2020, May/Spring). Randomized, phase II study of ficlatuzumab with or without cetuximab in patients with pan-refractory, recurrent/metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).. ASCO.