Quick Links
Agenda
Welcome + Keynote (8:30-9:55)
Session 1: Population Health (9:30-10:20)
Session 2: Clinical Translation (10:50am-12:30pm)
Session 3 Discovery Science (2-3:15)
Poster Abstracts pgs. 9-48
AGENDA
8:00 – 8:30am REGISTRATION AND CONTINENTAL BREAKFAST
WELCOME AND INTRODUCTIONS
Juanita Merchant, MD, PhD Interim Director, Cancer Center
8:30 – 8:40am
8:40 – 9:30am
Associate Director, Basic Sciences, Cancer Center Chief, Division of Gastroenterology and Hepatology, College of Medicine Regents Professor, College of Medicine, The University of Arizona
KEYNOTE
“Avanzando Caminos: Building a Path Forward for Latino Cancer Survivors”
Amelie Ramirez, DrPH Professor and Chair, Department of Population Health Sciences, UT Health San Antonio, Director, Institute for Health Promotion Research
SESSION 1: POPULATION HEALTH
“Hispanic/Latinos and Cancer: Disparities, Paradoxes, and Opportunities to Advance the Science of Resilience”
9:30 – 9:50am
9:50 – 10:00am
10:00 – 10:20am
10:20 – 10:40am
John Ruiz, PhD Professor, Clinical Health Psychology Director, Social Risk and Resilience Factors (SuRRF) Lab Associate Director, IDEA The University of Arizona Cancer Center
“Survival Outcomes for Patients on Statins Receiving AntiHormonal Therapy for Treatment of Hormone Positive Breast Cancer”
Gustavo Miranda poster session speaker, PI: Dr. Jennifer Erdrich
“Tribally-Driven Cancer Research: Increasing the Capacity of Indigenous Youth Knowledge Holders”
Felina Cordova-Marks, DrPH, MPH, MSc Assistant Professor & Director-IndigiWellbeing Health Promotion Sciences Department, Mel + Enid Zuckerman College of Public Health
“Engaging Communities to Develop and Optimize Biobehavioral Interventions”
Rina Fox, PhD, MPH
Assistant Professor in the College of Nursing Co-Director of the UACC Behavioral Measurement and Interventions
Shared Resource, University of Arizona Cancer Center
10:40 – 10:50am BREAK
10:50 – 11:10am
11:10 – 11:20am
SESSION 2: CLINICAL TRANSLATION
“TLR4 Inhibition for Cutaneous Squamous Cell Carcinoma
Prevention: The Power of Team Science”
Clara Curiel-Lewandrowski, MD
Interim Director of Research, The University of Arizona Cancer Center Co-Director Skin Cancer Institute, Chief of Dermatology, College of Medicine Professor, Medicine, College of Medicine (Dermatology) Chief, Division of Dermatology, Department of Medicine
“Cytokine-Induced Memory-Like NK Cells and Tafasitamab Show Efficacy in Treating B-Cell Acute Lymphoblastic Leukemia”
Dimitrios Filioglou Poster session speaker, PI: Dr. Emmanuel Katsanis
“A Designer Transcytotic Paclitaxel Nanovesicle for Enhanced Triple Negative Breast and Pancreatic Cancer Combination Therapies”
Jianqin Lu, PhD
11:20 – 11:40am
11:40am – Noon
Associate Professor, Pharmaceutical Sciences Director Pharmaceutics and Pharmacokinetics Track R. Ken Coit College of Pharmacy Member, Clinical and Translational Oncology Program, University of Arizona Cancer Center
“Expanding Our Understanding of H. Pylori and Gastric Cancer: The NHSP”
Heidi Brown, MPH, PhD Professor, Department of Epidemiology and Biostatistics Mel and Enid Zuckerman College of Public Health Member, Cancer Prevention and Control Program, University of Arizona Cancer Center
Noon – 12:30pm POSTER SESSION PRESENTER LIGHTNING ROUND (9 presenters for 3 min each)
12:30 – 2:00pm LUNCH AND POSTER SESSION
2 – 2:20pm
2:20 – 2:30pm
2:30 – 2:50pm
2:50 – 3:10pm
3:10 – 3:15pm
SESSION 3: DISCOVERY SCIENCE
“Immune Modulation by EGFR-Directed Therapeutics”
Joyce Schroeder, PhD
Professor, Molecular and Cellular Biology Member, Bio5 Institute Member, Cancer Biology Program, The University of Arizona Cancer Center
“RNA Binding Proteins G3BP1/2 Promote Cell Cycle Re-entry and Cell Survival During Recovery from DNA Replication Stress”
Lucas Harrell Poster session speaker, PI: Dr. Ross Buchan
“Assessing HPV16 Productivity vs Tumorigenicity in Oropharyngeal Epithelia”
Rob Jackson, PhD
Department of Immunobiology
The University of Arizona
“Targeting the Kinase-Independent Effects of PIM1 in Solid Tumors”
Noel Warfel, PhD
Associate Professor, Department of Cellular and Molecular Medicine Co-Leader, Experimental Mouse Shared Resource Member, Cancer Biology Program, The University of Arizona Cancer Center
CLOSING REMARKS
Juanita Merchant, MD, PhD
3:15 – 4:30pm RECEPTION
Welcome and Introductions
Juanita Merchant, MD, PhD
Interim Director- Cancer Center
Associate Director- Basic Sciences, Cancer Center
Chief- Division of Gastroenterology and Hepatology, College of Medicine
Regents Professor- College of Medicine
Keynote Speaker
“Avanzando Caminos: Building a Path Forward for Latino Cancer Survivors” 8:30 – 8:40am 8:40 – 9:30am
Amelie Ramirez, DrPH
Professor and Chair- Department of Population Health Sciences UT Health San Antonio, Director, Institute for Health Promotion Research
Amelie Ramirez, DrPH is a health equity pioneer who has achieved national, presidential, and international recognition for her successes in reducing Latino cancer health disparities. As Chair and Full Professor of the Department of Population Health Sciences at UT Health San Antonio, a Hispanic-Serving Institute, Ramirez leads a multidisciplinary team of public health researchers, data scientists, and communication specialists in addressing the cancer experience of Latinos.
As leader of community outreach at the NCI-designated Mays Cancer Center at UT Health San Antonio, Dr. Ramirez has implemented system changes that have enhanced surveillance of the South Texas cancer burden. Dr. Ramirez is a member of the board of directors for the CDC Foundation and an elected member of the National Academy of Medicine. She has been recognized by the Society of Behavioral Medicine, Oprah Winfrey, the Obama White House, Susan G. Komen, and more. Dr. Ramirez is a native of Laredo, Texas. She received her MPH and DrPH degrees from The University of Texas Health Science Center at Houston. Her social media includes LinkedIn and @ SaludAmerica on Twitter, Facebook, YouTube, and Instagram.
9:30 – 9:50am
“Hispanic/Latinos and Cancer: Disparities, Paradoxes, and Opportunities to Advance the Science of Resilience”
John Ruiz, PhD
9:50 – 10:00
“Survival Outcomes for Patients on Statins Receiving Anti-Hormonal Therapy For Treatment of Hormone Positive Breast Cancer” Gustavo
Felina Cordova-Marks, DrPH, MPH, MSc 10:00 – 10:20am
“Tribally-Driven Cancer Research: Increasing the Capacity of Indigenous Youth Knowledge Holders”
Rina Fox, PhD, MPH 10:20 – 10:40am
“Engaging Communities to Develop and Optimize Biobehavioral Interventions”
10:40 – 10:50am
“TLR4 Inhibition for Cutaneous Squamous Cell Carcinoma Prevention: The Power of Team Science”
Clara Curiel-Lewandrowski, MD
Co-Director Skin Cancer Institute
Chief of Dermatology, College of Medicine
Professor, Medicine, College of Medicine (Dermatology)
Chief, Division of Dermatology, Department of Medicine
11:10 – 11:20am
Interim Director of Research, The University of Arizona Cancer Center
POSTER PRESENTATION
“Cytokine-Induced Memory-Like NK Cells and Tafasitamab Show Efficacy in Treating B-Cell Acute Lymphoblastic Leukemia”
Dimitrios Filioglou Poster session speaker, PI: Dr. Emmanuel Katsanis
“A Designer Transcytotic Paclitaxel Nanovesicle for Enhanced Triple Negative Breast and Pancreatic Cancer Combination Therapies”
Jianqin Lu, PhD
Associate Professor Pharmaceutical Sciences Director Pharmaceutics and Pharmacokinetics Track, R. Ken Coit College of Pharmacy Member, Clinical and Tranlational Onocology Program, University of Arizona Cancer Center
10:50 – 11:10am 11:20 – 11:40am 11:40am - Noon
“Expanding Our Understanding of H. Pylori and Gastric Cancer: The NHSP”
Heidi Brown, MPH, PhD
Professor, Department of Epidemiology and Biostatistics Mel and Enid Zuckerman College of Public Health, The University of Arizona Member, Cancer Prevention and Control Program, University of Arizona Cancer Center
Kayla Jones
Fiona Webb
Randy Chou
Juan Contreras II
Keila Espinoza
Elizabeth Borden
Mengyang Chang
Chance Parkinson
LUNCH AND POSTER SESSION
12:30 - 2:00
2:00-2:20pm
“Immune Modulation by EGFR-Directed Therapeutics”
Joyce Schroeder, PhD
Professor, Molecular and Cellular Biology, The University of Arizona Member, Bio5 Institute Member, Cancer Biology Program, University of Arizona Cancer Center
2:20 – 2:30
“RNA Binding Proteins G3BP1/2 Promote Cell Cycle Re-entry and Cell Survival During Recovery from DNA Replication Stress” Lucas Harrell Poster session speaker, PI: Dr. Ross Buchan
“Assessing HPV16 Productivity vs Tumorigenicity in Oropharyngeal Epithelia”
Rob Jackson, PhD
Post Doctoral Fellow- Department of Immunobiology, College of Medicine
2:30-2:50pm 2:50-3:10pm
“Targeting the Kinase-Independent Effects of PIM1 in Solid Tumors”
Noel Warfel, PhD
Associate Professor, Department of Cellular and Molecular Medicine Co-Leader, Experimental Mouse Shared Resource Member, Cancer Biology Program, The University of Arizona Cancer Center
Juanita Merchant, MD, PhD
2 Presenter: Fiona Webb
PI: Rina S. Fox
Usability Testing of a Web Platform to Deliver a Group Stress Management Skills Intervention
Introduction
Conclusions
Citations/Acknowledgements
3 Presenter: Randy Chou
PI: Richard Simpson
Exercise -mobilized lymphocytes have enhanced cytotoxicity against multiple myeloma in combination with with monoclonal antibodies, lenalidomide and dexamethasone
KATSANIS2,3 and Richard J. SIMPSON 1,2,3
Results Randy CHOU1, Grace M. MCKENZIE1, London
Introduction
Multiple Myeloma (MM) is an aggressive incurable malignancy characterized by the infiltration of terminally differentiated plasma cells in the bone marrow, with many patients developing resistance to multiple therapies due to underlying immune dysfunction 2 3
• Several therapeutics exploit the antimyeloma effect of natural killer (NK) cells, such as lenalidomide, dexamethasone combined with monoclonal antibodies designed to increase the antibodydependent cellular cytotoxicity (ADCC), including daratumumab (anti-CD38) and Magrolimab (anti- CD47) Acute exercise is known to redistribute NK-cells between the blood and tissues, which could synergize with current MM therapies to increase efficacy 1 3
• Our primary aim here was to investigate the potential synergy between exercisemobilized immune cells and two MM therapies in an in vitro cytotoxicity assay using the MM 1S cell line We also investigated the effects of two three-drug therapies on the phenotypic and ligand expression on PBMCs and tumor cells, respectively
Methods
• Healthy participants (N=7) completed a 20minute graded cycling protocol from 50% up to 80% VO2max
• Lymphocytes were isolated from blood collected at rest and during the final stage of the graded exercise challenge and cocultured with MM 1S cells at multiple E:T ratios in a 4h flow cytometry-based cytotoxicity assay
Additional cell culture conditions were established to investigate the effects of lenalidomide (R), dexamethasone (d), and either daratumumab (DRd) or magrolimab (MRd) on cytotoxicity
Treatment groups were prepared by adding either DRd or MRd 24 hours prior to the cytotoxicity assay Two treatment strategies were employed: pre-treating target cells only (pre-treatment) and pre-treating both target cells and lymphocytes (co -treatment)
• Exercise-mobilized lymphocytes have enhanced cytotoxicity against MM 1S cells in vitro, which may be enhanced with DRd or MRd treatment
Exercise may synergize with MRd and DRd when used as an adjuvant for adoptive cell therapy (ACT) in multiple myeloma
• DRd-treated lymphocytes seemed to result in higher drop in NK cell population, potentially due to fratricide
• These results highlight the potential benefits of incorporating exercise into treatment regimens for multiple myeloma patients receiving DRd or MRd
References
1 Bigley, A. B., Rezvani, K., Chew, C., Sekine, T., Pistillo, M., Crucian, B., Bollard, C. M., & Simpson, R. J. (2014). Acute exercise preferentially redeploys NK-cells with a highlydifferentiated phenotype and augments cytotoxicity against lymphoma and multiple myeloma target cells. Brain, Behavior, and Immunity, 39, 160–171. https://doi.org/10.1016/j.bbi.2013.10.030
2 Dima, D., Ullah, F., Mazzoni, S., Williams, L., Faiman, B., Kurkowski, A., Chaulagain, C., Raza, S., Samaras, C., Valent, J., Khouri, J., & Anwer, F. (2023). Management of Relapsed–Refractory Multiple Myeloma in the Era of Advanced Therapies: Evidence-Based Recommendations for Routine Clinical Practice. In Cancers (Vol. 15, Issue 7). Multidisciplinary Digital Publishing Institute (MDPI). https://doi.org/10.3390/cancers15072160 3 Dimopoulos, M. A., Oriol, A., Nahi, H., San-Miguel, J., Bahlis N. J., Usmani, S. Z., Rabin, N., Orlowski, R. Z., Komarnicki, M., Suzuki, K., Plesner, T., Yoon, S.-S., ben Yehuda, D., Richardson, P. G., Goldschmidt,
MCDOUGAL 1, Timothy M. KISTNER 2, , John L. SULLIVAN 1, Helena BATATINHA 1, Forrest L. BAKER1,2, Emmanuel
PI: Meghan Skiba
“Cross-sectional analysis of physical health in Hispanic prostate cancer survivors and their caregivers participating in a pilot dyadic exercise program”
Methods:
Recruitment:
We used community outreach, social media advertisement, and clinical referrals to recruit and enroll 16 dyads into Ejercicio Juntos
Background: Hispanic communities experience high burden from prostate cancer; physical activity (PA) can improve health and wellbeing. Limited culturally relevant PA interventions exist for Hispanic men with prostate cancer and their caregivers.
Purpose of Study: Describe enrolled sample of prostate cancer survivors and caregivers participating in Ejercicio Juntos, an adapted, 12-week culturally relevant dyadic remotely delivered strength training intervention for Hispanic men with prostate cancer and their caregivers.
Participation: At baseline, participants completed questionnaires on demographics, body mass index (BMI), and physical activity. Physical function was assessed using a remote short physical performance battery (SPPB).
Results
Age Participants (n=28) averaged at an age of 62.4 ± 12.4
Co nclu sio n: We successfully recruited a sample of Hispanic prostate cancer survivors and their caregivers to Ejercicio Juntos. Both survivors and caregivers reported low levels of physical activity and demonstrated moderate physical function. Pilot testing is currently ongoing.
A ckn ow le d gme nts: We are grateful to our participants, exercise trainers, community partners, and clinical partners including Dr. Alejandro Recio -Boiles, MD and Dr. Juan Chipollini, MD.
by
Juan Contreras II ; Marjorie Barrera BSE, AAS; Bianca SantaMaria, MPH; Terry Badger, PhD RN, FAPOS; Kerri Winters- Stone PhD; Meghan B. Skiba PhD, MS, MPH, RDN
Figure1. Timeline of Participation
D e mogra phi c
Figure 4. RAPA Aerobic Score
Figure 5. RAPA Strength & Flexibility Score
Figure 2. Ethnicity and Origin
Figure
S
Loss of Acid Ceramidase Restores Sphingolipid Composition to
Alleviate Chronic Colitis in IL10 -Deficent Mice
Figure 1: IL10-/-ACMYE mice are protected from parameters of colitis and exhibit reduced expression of
Figure 3: IL10-/-ACMYE mice exhibit reduced infiltration of proinflammatory neutrophils and macrophages, while increasing protective B
CXCL1CXCL2CCL2CCL5IL-1
Figure 2: IL10-/-ACMYE mice retain more ceramides and sphingomyelins, while generating less dhS1P and S1P.
6 Presenter: Elizabeth Borden
PI: Dr. Karen Hastings
IMMUNOEDITING IN TUMORS FROM IMMUNOCOMPETENT PATIENTS
INFILTRATION OF EXHAUSTED CD8+ T CELLS
MUTATIONAL BURDEN IN IMMUNOCOMPETENT PATIENTS
7 Presenter: Mengyang Chang
PI: Wei Wang
8 Presenter: Chance Parkinson
PI: Andrew Paek
Translation control coordinates suppression of the transcription factor p53 in response to
Acknowledgments
9 Presenter: Marija Shahid + Gustavo Miranda
PI: Dr. Jennifer Erdrich
Background:
Statins demonstrate pleiotropic effects, including antineoplastic activities.
●Preclinical and clinical trials show statin interference with cell signaling pathways
●These pathways are also found in cancer proliferation
●In particular, the role of HMG -CoA reductase in carcinogenesis.
Purpose:
This study investigates whether the combination of statins and anti -hormonal therapy is associated with different survival outcomes for patients with hormonepositive breast cancer.
Experimental Design:
Utilizing the SEER-MHOS database for breast cancer patients diagnosed between 2010 -2017, Medicare Part D information was used to extract anti-hormonal therapy and statin use.
PI: Jacob C Schwartz
Understanding the Role of Cytoskeleton Regulator RNA, CYTOR, in HIV Latency
No electronic version provided.
PI: Dr. Alex McGhee
13 Presenter: Amanda Chriswell
PI: Dr. Rina Fox, Dr. Meghan Skiba
Purpose
Applying Innovative Methods to Develop Health Education Text Messages
Rationale
To develop health promotion short message service (SMS) content related to dietary quality, physical activity, and sleep hygiene for cancer survivors and their caregivers
Methods Outcomes
Further refinement of SMS drafts according to stakeholder feedback
Rapid analysis procedure in native language to provide actionable feedback
Virtual Community Engagement Studio (VCES)
References
Existing SMS health behavior interventions for cancer survivors:
• Focus on weight loss4
• Address only single health behaviors
• Do not involve informal caregivers1,3
• Are only available in English2
Generative Artificial Intelligence (AI; ChatGPT 3.5) to develop SMS drafts
SMS Content Generation using generative artificial intelligence (AI) and a Virtual Community Engagement Studio (V-CES) Model12-13
Refined SMS drafts approved by context experts
Chat GPT asked to refine the SMS drafts to clarify and decrease jargon
Translate SMS into Spanish (AI and native speaker)
SMS drafts revised by humans to produce usable messages
Feedback provided by context experts
Acknowledgments
This research was funded by the Arizona Cancer Center Cancer Prevention and Control Program
• > 56 SMS developed for each health behavior in English and Spanish5-11
• Opportunities identified via
• V-CES with 9 diverse stakeholders12,13 (Figure 1)
Positive affirmations
Motivational strategies
Informal/common language
Emphasize evidence
Implications
AI can be an effective tool, but expert human review and revision and community stakeholder feedback are critical
Future work
Test the SMS for feasibility and acceptability among cancer survivor-caregiver dyads
Amanda Chriswell BSN, RN, CEN1, Bianca SantaMaria, MPH1, Terry Badger, PhD, RN,
Figure
14 Presenter: Andrea Hernandez
PI: Dr. Wei Wang
EFFICIENCY ASSESSMENT OF BRD4/PLK1 DUAL DEGRADERS: A PROMISING
APPROACH TO CANCER TREATMENT
Andrea Hern ndez ,2,4 Mengyang Chang2,4 Dr. Wei Wang2,3,4
DICR Intern1, Department of Chemistry and Biochemistry2, Department of Toxicology and Pharmacology University of Arizona , Tucson, AZ 85745
15 Presenter: Christina Lyons
Role of CD36 in Erythroid Differentiation of Human Hematopoietic Stem and Progenitor Cells
16 Presenter: Danielle DiFranco
PI: Joyce Schroeder
A wound that never heals: Drivers of nuclear EGFR
2University
3Molecular
Hypothesis
17 Presenter: Dimitrios Filioglou
PI: Emmanuel Katsanis
of healthy human donors and incubated for 16 hours with IL-12 (10 ng/ml), IL-15 (50 ng/ml) and IL-18 (50 ng/ml) For in vitro cytotoxicity assays, target cells (NALM-6 or RS4:11–B-ALL cell lines) were pre-labeled with CD71-FITC mAb and co-incubated with the effectors (NK or CIMLNK) at 2 5:1 effector: target (E: T) ratio, with or without TAFA (1 μg/ml) for 4 hours PI was added prior to flow cytometric analysis
Degranulation assays were performed to examine mechanistic differences between NK and CIMLNK effectors cells (CD56+) • Blocking assays were also done using 3 μg/ml of unconjugated anti-CD16 mAb to assess whether the effect of CIMLNK + TAFA combination depended on the binding of TAFA with CD16 (FcγR IIIa) For the in vivo experiments: irradiated immunodeficient female NSG mice received 10 000 Nalm6-luc, via teil vein injection (IV) on day 0 On day 1 TAFA was administered at 0 3 - 0 5 mg/kg, IV or intraperitonally (IP) respectively 1 X 106 CIMLNK derived from healthy donors, were injected IV 24h after the tumor injection The luciferase bioluminescence imaging (BLI) system was used to determine leukemia burden Two-way or One-way ANOVA with Tukey’s multiple comparison test were used to detect differences among the culture conditions For the in vivo studies, KaplanMeier survival curves were generated and the GehanBreslow-Wilcoxon test was used to evaluate differences between conditions P-values of < 0 05 were considered significant
CIMLNK + TAFA combination exerts synergistic effects in vitro against B-cell acute lymphoblastic leukemia. Blocking CD16 reduced but did not abolish the TAFA-induced ADCC of CIMLNK
CIMLNK + TAFA combination significantly prolonged survival of mice bearing B-ALL and outperformed all the monotherapies.
Poster Session Home Page
18 Presenter: Erren Ranola
PI: Dr. Jean Wilson
Human Cytomegalovirus Infection of Intestinal Epithelial Cells Compromises Barrier Structure and Signaling
No electronic version provided.
19 Presenter: Fidel Junior Saenz
PI: Geoffrey Gurtner and Kellen Chen
Assessing the Effects of MALAT1 Inhibitor on Proliferation and Invasion in E0771 Breast Cancer Spheroids
No electronic version provided.
Hunter O’Brien1; Wazir Abdullahi, Ph.D.
Lauren Reyes1; Timothy Marlowe, Ph.D. 1
21 Presenter: Jacquanette Slowtalker
PI: Dr. Julie Armin
Jacquanette
Strengthening Native American Cancer-Related Collaborations through Capacity-Building
Slowtalker MPH, Carol Goldtooth-Begay MPH, Julie Armin PhD, Nicolette Teufel-Shone PhD
Native Americans experience poor cancer outcomes and lower chances of survival than other racial groups in the United States. Cancer is the second leading cause of death among Natives in the United States.1
The Partnership for Native American Cancer Prevention (NACP) is a collaboration between The University of Arizona Cancer Center, Northern Arizona University, and the National Cancer Institute. NACP was established to address cancer health disparities in Native American communities.
NACP Outreach and Engagement Core Goal
Strengthen AZ Native Nations’ capacity and infrastructure to provide sustained, community-based cancer education, screening and care services to advance cancer health equity for Native Americans in Arizona.
Two-Eyed Seeing approach2 - integrate Indigenous and non-Indigenous worldviews to leverage community assets to address community needs.
Aim 1 Activities:
Adapt existing curricula and implement training for the 19 tribal Community Health Representative (CHR) programs in cancer education and navigation
Facilitate Partnerships/Program-to-Program
Mentorships for tribal CHR programs
Aim 2 Activities:
Use ECHO (Extension for Community Healthcare Outcomes) to remotely bring together tribes and tribal consortia for connection, learning, and sharing expertise to build and sustain cancer control programming
Conduct grant writing and mentorship
Aim 3 Activities:
Develop and offer the Community Dissemination and Application Training and continue to integrate the Two-Eyed Seeing approach Implement Community Engagement Studios Partners
Acknowledgements
FUNDED BY THE PARTNERSHIP FOR NATIVE AMERICAN CANCER PREVENTION (U54CA143924 AND U54CA143925)
References Cited
22 Presenter: Jesse Altemus
PI: Dr. Jacob Schwartz
Identification and validation of peroxisomal protein interactor hits identified via a novel proteomics method Jesse Altemus1, Rachel Victor, Jacob Schwartz1,2 1Department of Pharmacology, University of Arizona College of Medicine, Tucson, AZ 2University of Arizona Cancer Center, Tucson, AZ
INTRODUCTION
METHODS
REFERENCES
Weihs
24 Presenter: Linda Garland
PI: Forrest Baker, PhD
REFERENCES
1. Salucci, S.; Aramini, B.; Bartoletti-Stella, A.; Versari, I.; Martinelli, G.; Blalock, W.; Stella, F.; Faenza, I. Phospholipase Family Enzymes in Lung Cancer: Looking for Novel Therapeutic Approaches. Cancers 2023, 15, 3245.
2. Zhang T, et al. Up-regulated PLA2G10 in cancer impairs T cell infiltration to dampen immunity. Sci Immunol. 2024 Apr 26;9(94):eadh2334. Epub 2024 Apr 26. PMID: 38669316.
in CD8 T-cell mediated killing of the EGFR mutated cell line H4006 compared to the EGFR wild type A549 (Fig 2), suggesting impaired CD8 T-cell function against NSCLC with higher mRNA expression of sPLA -X. We have found that sPLA2-X and its lipid mediator products are the likely mechanism inhibiting CD8 T-cell migration toward tumor cells. In a modified version of Boyden’s chamber, a model for the study of cell migration through a membrane in response to chemoattractants, we studied the capacity of sPLA2-X to impact T-cell mobility. A porous membrane separated the upper and lower chambers of each well. A combination of chemokines, and the EGFR wildtype (A549) and EGFR mutant (H4006, 400-700-fold more sPLA2-X) cell lines were added to the lower well, and CD8+T cells to the top well. There was a dramatic reduction (~80%) in the number of CD8 T cells that migrated toward the EGFR mutant, H4006, compared to the A549 (Fig 3), suggesting that sPLA2-X could be playing an important role in T-cell mobility. Next, we used a highly selective inhibitor of sPLA2-X activity, KMN-011066 (Cayman Chemical Co.), to determine if CD8 T-cell migration could be restored in the EGFR mutant, H4006 cell line. We found pretreatment (24h) of the EGFR mutant cell line (H4006) with KMN-011066 (1 μg/mL) increased CD8 T-cell migration across the membrane by about ~94% (Fig 4). STUDY
FUTURE STUDIES
These exciting results led us to formulate the following experiments to further investigate sPLA2G-X’s role in altering the tumor microenvironment and KMN011066’s inhibitory and thus pro-T-cell migration properties in vivo and in vitro:
1. (a) Expand on these preliminary findings with the selective sPLA2-X inhibitor, KMN-011066, and utilize the nonspecific pan sPLA inhibitor, Varespladib,
Figure 3
Figure 5
Figure 4
Figure 2
Figure 1
Presenter: Lupita Ramos-Barrera
Goals
Solutions and Methods
Learned and Future Directions
Figure 1. Contents of ICF Review Database
Prooxidant ligand improves the antiproliferative activity of glycoconjugated iron prochelators in ovarian cancer cells
Viability
PI: Elisa Tomat
Madison Grams, Jake Fussell, Elisa Tomat
28 Presenter: Mark Curry
Immune Monitoring Shared Resource
Located within the University of Arizona Cancer Center, this core lab provides comprehensive immune profiling for human and murine blood and tissue samples. This includes consultation, sample preparation, clinical trial support and biorepository services. Our mission is to provide technical expertise to clinical investigators and research scientists who want to characterize the immune system by offering up-todate immune monitoring services for clinical and translational studies, including leading-edge technologies like multispectral flow cytometry and digital spatial profiling. We offer training, assisted, unassisted, and technician operated modalities for all our instruments, and will meet investigators at their desired level of engagement.
https://cancercenter.arizona.edu/researchers/ shared-resources/flow-cytometry iLabs: https://ua.ilab.agilent.com/service_center/sh ow_external/4407?name=flow-cytometryshared-resource
Flow Cytometry Shared Resource
31 Presenter: Michelle Lay
No electronic version provided.
Natascha
Natascha Schippel1, Jing Wei1, Xiaokuang Ma1, Mrinalini
33 Presenter: Ritu Pandey
PI: Ritu Pandey
IMPACT (Individual Molecular Registry of Patients for Accelerated Clinical and Translational medicine), a strategic initiative for genome data analytics of UACC patients to foster precision research.
No electronic version provided.
34 Presenter: Ryan Yellamaty
PI: Shalini Sharma
Biochemical Characterization of UAP56 and its Substrate Selectivity for U1-SL3 RNA
No electronic version provided.
35 Presenter: Sagnik Giri
PI: Carlos Caulin
Crosstalk Between Cancer Cells and Tumor Associated Macrophages in p53 -Mutated Oral Squamous
Manlin Shao1,3, BS, Carlos Caulin2,3, PhD
1Cancer Biology Graduate Program, University of Arizona, Tucson, AZ, USA
2Department of Otolaryngology Head & Neck Surgery, University of Arizona, Tucson, AZ, USA
3University of Arizona Cancer Center, University of Arizona, Tucson, AZ, USA
Oral squamous cell carcinoma (OSCC) is the sixth most common human cancer globally, making up over 90% of all oral malignancies. OSCC is a subtype of human papillomavirus (HPV)-negative Head and Neck SCC (HNSCC), with common risk factors of tobacco and alcohol. TP53 gene makes p53 protein, which acts as a tumor suppressor that regulates cell division and death. The cancer genome atlas network of OSCC indicated many point mutation of TP53 leading to gain-of-function (GOF) mutation. The complex oncogenesis process involves multiple factors including genetic changes, epigenetic influences, and a disrupted tumor microenvironment, which are not yet fully understood. Macrophages play an important role in the tumor microenvironment with the two subtypes: M1 macrophages as proinflammatory, and M2 macrophages as anti -inflammatory contributing to tumor formation and progression. In this study, we hypothesized that the p53R172H mutation promotes the recruitment of tumor-associated macrophages (TAMs) and immune suppressive activities, contributing to OSCC development and progression. To test this hypothesis, I used CRISPR/Cas9 technique to successfully created p53-KO cell lines. Using the orthotopic and immunocompetent animal model, I found that p53-KO injected mice showed plateau or regression in tumor growth in both spontaneous and 4NQO (a carcinogen found in tobacco)-induced cell lines. Immunohistochemistry analysis showed significantly more general and M1 TAMs in p53-mutant injected mice in spontaneous cell lines. With successfully isolated TAM population using F4/80 magnetic bead, we are preparing to send out samples for RNA sequencing soon. This study will elucidate the role of the p53R172H GOF mutation in shaping the TME of OSCC using orthotopic immunocompetent mouse models and quantitative analysis. The findings could form the basis of therapeutic approaches targeting p53 mutations based on the TAM content of the tumors to improve immunotherapy responsiveness in OSCC.
Cell Carcinoma
Tumor Suppression by Mutant p53 Deletion
IHC Analysis of TAM (General, M1, M2)
Conclusions & Future Directions
37 Presenter: Wenpan Li
PI: Jianqin Lu
Cholesterol-modified sphingomyelin chimeric lipid bilayer for improved therapeutic delivery
No electronic version provided.
Methods and Results
of self-assembly and endocytosis/transcytosis process of LinTT1/Camptothesome
LinTT1/Camptothesome-induced transcytosis is Golgi-dependent
LinTT1-decorated
Yanhao Jiang1, Zhiren Wang1, Wenpan Li1, Teng Ma1, Mengwen Li1, Shuang Wu1, Ethan Lin1, Karlie Elizabeth Flader1, Mengjiao Ma1, Mengyang Chang1, Hongmin Li1, Wei Wang1, Jianqin
