American Pancreatic Association Foundation

The APA Foundation’s mission is to cure pancreatic diseases through research,collaboration, and advocacy.

About APAF

The APA Foundation is a 501(c)3 organization accepting tax deductible donations to support efforts of the APA in fostering clinical and basic science research needed to cure diseases of the pancreas. The APAF supports awards for young investigators and travel grants promoting research opportunities.

The APA Foundation mission is to cure pancreatic diseases through research, collaboration and advocacy.

The APAF is proud to offer the Young Investigator in Pancreatology Grant on an annual basis.The purpose of the grant is to attract and retain the next generation of scientists in the field of basic and clinical pancreatology.  CLICK HERE for additional information.

Donate or make a pledge through our online form.

Please contact us at apa@apapancreas.org if you have any questions.

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The APA is a Non-Profit Organization with a 501c3 designation. Your kind donations will be used to support research efforts towards finding cures for diseases of the pancreas. Donations are tax-deductible to the extent allowed by law.

  

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Donor Wall

The APA Foundation thanks the following donors for their generosity.

DIAMOND
$50,000+

⦿ Vay Liang & Frisca Yan Go
⦿ Agi Hirshberg
⦿ Barbara Kenner PhD
⦿ Manju & Ashok K. Saluja
⦿ Betty & Paul Webster III, MD

GOLD
$20,000 – $49,999

⦿ William Go & Fiona Wong
⦿ Fred Gorelick
⦿ Stephen and Marnell Pandol

SILVER
$10,000 – $19,999

⦿ Anonymous Donor
⦿ Edward Bradley III
⦿ Suresh Chari
⦿ Fan & William Chey
⦿ T. Kurata
⦿ Joan Lowry
⦿ Janina Voss

BRONZE
$5,000 – $9,999

⦿ Christopher Forsmark
⦿ Min Lee
⦿ Howard Reber
⦿ Aliye Uc

CONTRIBUTORS | Under $5,000

Thank you to all our contributors

TheBenevityCommunityImpactFund/ Ameriprise Financial, Inc.
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Grants

American Pancreatic Association Foundation

Young Investigator in Pancreatology Grants

The prestigious American Pancreatic Association Foundation Young Investigator in Pancreatology Grant program represents the pinnacle of funding opportunities aimed at fostering groundbreaking research in the field of pancreatology. The APAF prioritizes projects in basic and translational research specifically focused on pancreatitis or pancreatic cancer. With a successful application, recipients are granted $100,000 to directly support the costs of their independent research projects, empowering the next generation of researchers towards the ultimate goal of eradicating pancreatic diseases.Your contribution to the APA Foundation directly fuels these impactful grants, allowing young investigators to push the boundaries of pancreatic research. Together, we can make a significant impact on the future of healthcare and bring us one step closer to a world without pancreatic disease.

2025 Winners

Yang Chen, PhD

MD Anderson Cancer Center

Unraveling the Role of TREM2 in Pancreatitis and Pancreatic Cancer

Samuel Han, MD, MS

Mayo Clinic

Improving Smoking Cessation in Acute Recurrent Pancreatitis and Chronic Pancreatitis

Gyuwon Jeong, PhD

Stanford

Decoding Intercellular Crosstalk in Chronic Pancreatitis Induced by Autophagy Dysfunction

Abdul Rasheed, PharmD

AIG Hospitals

Evaluation of the Relationship Between Neural Sensitisation and Neuropsychological Alterations in Patients With Painful Chronic Pancreatitis

2024 Winners

Mahya Faghih MD

Johns Hopkins

A Pilot Study of Scrambler Therapy for Painful Chronic Pancreatitis

Mate Sandor MD

University of California, Los Angeles

TRPV6 Channelopathy of the Pancreas Promotes Trypsin-Dependent Pancreatitis

Jonathan Baldan MD

Vrije Universiteit Brussel

Subpopulation Profiling of Acinar Cells with Increased Risk for Cancer Initiation

Zhijun Zhou MD

The University of Oklahoma Health Sciences Center

Metabolic Reprogramming Promotes Muscle Wasting and Immune Evasion in Pancreatic Cancer

2023 Winners

Anoop Narayana Pillai

Mayo Clinic, Arizona

Role of Amphipathic Liponecrosis in Severe Acute Pancreatitis

Michelle Cooley PhD

University of Wisconsin

The Role of D52 in Pancreatic Acinar Paligenosis

Carmen Mota Reyes MD

Klinikum rechts der Isar | Germany

Neuroimmune Crosstalk Regulates Anti-Tumor Immune Responses in Pancreatic Cancer

Christopher Halbrook PhD

University of California Irvine | United States

Targeting Metabolism to Elimate Immune Suppression in Pancreatic Cancer

2022 Winners

Laura Antonucci PhD

University of California San Diego

Linking pancreatitis, oxidative stress, and lipid metabolism in pancreatic cancer progression: a new avenue to early intervention

Jiale Wang MD

Mayo Clinic

CRISPR-based Gene Therapy for Human Hereditary Pancreatitis

Cory Wyatt PhD

Oregon Health and Science University

Early Detection of Necrosis in Acute Pancreatitis using Magnetic  Resonance Fingerprinting

2021 Winners

Murli Manohar

Stanford University School of Medicine Department of Pediatrics

Understanding local and systemic immune responses during mild acute pancreatitis, severe acute pancreatitis, and recovery

Sonja Woermann

MD Andeson Cancer Center, University of Texas, Houston

Role of APOBEC3A in pancreatitis and inflammation triggered carcinogenesis

Sun Xingshen

University of Iowa

Early Pathogenesis of SPINK1 Deficiency in a Ferret Model

2020 Winners

Mario A. Shields PhD

Feinberg School of Medicine at Northwestern University

Par3 deficiency promotes fatty replacement in chronic pancreatitis

Andrea Geisz PhD

Boston University Henry M. Goldman School of Dental Medicine

Impact of Sentinel Attack of Acute Pancreatitison Severity of Subsequent Episodes in Mice

Guru Trikudanathan MD

University of Minnesota – Twin Cities

Role of genes on pain and diabetes outcomes after TPIAT in POST (GenPOST)

2019 Winners

Julie Sneddon PhD

University of California

Natalia Khalaf MD, MPH

Baylor College of Medicine

2018 Winners

Subhankar Dolai MD

University of Toronto

Role of SNARE proteins in dysregulated autophagy in alcoholic pancreatitis

Mohammad Tarique PhD

University of Miami

2017 Winners

Scott Messenger PhD

University of Wisconsin

Trypsinogen trafficking is regulated by CAPS2

Anna Evans Phillips MD MS

University of Pittsburgh School of Medicine

The Role of Quantitative Sensory Testing in Painful Chronic Pancreatitis

Update on Researches

Andrea Geisz

Update on Research:In the first part of the funding period we finished experiments under Specific aim 1 to investigate whether a sentinel acute pancreatitis attack has any impact on the severity of subsequent episodes in C57BL/6N mice. Acute recurrent pancreatitis C57BL/6N in mice. We induced 1-­3 acute pancreatitis attacks in C57BL/6N mice with 10 hourly injections of cerulein and sacrificed them 1 hour or 7 days after the last injection. Histologic evaluation and scoring of pancreatic tissue indicated that relative to the initial attack, edema and inflammatory cell infiltration were significantly increased in the second and third episodes (not shown). Quantitative scoring also revealed that necrosis was increased in mice with acute pancreatitis compared to the saline treated animals, however this was not further augmented in mice with two or three acute pancreatitis episodes (not shown). Pancreas weight was significantly increased in mice with two and three attacks compared to mice with a single acute pancreatitis episode (Figure 1). As expected, plasma amylase activities were significantly increased in mice with two and three acute pancreatitis attacks relative to mice with one acute pancreatitis episode. Similarly, measurement of pancreas MPO content indicated increased neutrophil infiltration in the groups with two and three episodes compared with mice with a single attack (Figure 2). Thus, all parameters of acute pancreatitis indicated that the extent of pancreatic injury was increased during subsequent attacks.

Update on Research:
Over the past 6 months we made progress in Aim 1. We utilized two different models of AP, namely that of mild to moderate AP that recovers over time (cerulein) (Figure 1A); and a severe form of AP that is associated with high mortality (choline deficient DL-ethionine-induced, CDE) (Figure 2A). We performed kinetic studies where we isolated leukocytes from the periphery (blood) and tissues (pancreas) as the mice recovered or continued to progress towards severe disease as occurs in subsets of AP patients. In-depth profiling of pancreatic leukocytes identified variety of immune cells as represented in UMAP plot (Figure 1B) during AP and recovery. Volcano plot showing differential abundance analysis of different immune cells revealed that monocytes (Ly6C+, inflammatory) were the top altered immune cells compared across all time points (0h, 12h, 24h, 48h, 168h) and between 0h (control) and 12h (AP) (Figure 1C, 1D). We also observed significantly decreased CD206+ macrophages in a pairwise comparison between 0h and 12h (Figure 1D). UMAP revealed dynamic changes in monocyte and CD206+ macrophage clusters represented by blue and red dotted circles respectively (Figure 1B, 1E). The frequency of monocytes peaked at 24h and normalized to baseline at 48h/168h (recovery phases) (Figure 1E, 1F). The frequency of CD206+ macrophages was significantly reduced at 12h (AP) and recovered at 48h (Figure 1E, 1G). These findings indicate that disease induction and recovery is associated with dynamic shifts in pancreatic monocytes and CD206+ macrophages.Update on funding and what positions you have held since award:
We have utilized $ 31,704.55 during the first period of progress report from 07/01/2021 -12/31/2021 towards salary, fringe and travel support (see attached official budget report).  We are expecting to use remaining $ 68,295.45 in next six months from 01/01/2022 to 06/30/ 2022 towards, CyTOF data analysis, RNA seq, flowcytometry, supplies (antibodies, reagents, chemicals, kits), animals, PBMCs and salary support etc.

Update on Research:
We set out to investigate whether A3A changes the immune cell infiltration (Immune profile) and severity (ADM, PanIN formation, fibrosis) of human chronic pancreatitis. We successfully developed a multiplex OPAL staining platform in human chronic pancreatitis samples which will allow us to decipher immune cell composition (Figure 1) and ADM formation (Figure 4) in a quantitative and spatial manner. In addition, we prepared HE staining to quantify and grade pre-cancerous lesions (Figure 4) and we were able to correlate high A3A expression with severe fibrosis (Figure 2) in CP patients. Utilizing targeted sequencing, we observed higher C>T and C>G mutations rates in important tumor suppressor genes/ oncogenes (CDKN2A, TP53, HRAS, ALK, KIT) suggesting that A3A might enhance the inflammation triggered mutagenesis in a pre-cancerous disease (Figure 6 A-C). Overall, our data shows, that A3A might aggravate the course of the disease by enhancing fibrosis, inflammatory response and could facilitate inflammation induced mutagenesis in human chronic pancreatitis. We next investigated the role of A3A in acute cerulein induced pancreatitis employing our novel A3A GEMM models. We found that WT but less mutant (deaminase deficient) A3A significantly aggravates the course of the disease. Edema at 8h and 24h, necrosis and apoptosis (cleaved caspase 3+ cells) at 24h were significantly increased (Figure 5) in A3A WT mice compared to non-A3A littermate controls. Furthermore, we observed an upregulation of the inflammatory response as seen by infiltrating immune cells (CD45+ cells), increased cytokines and inflammatory pathway activation (Figure 3). Overall, our data suggest, that A3A when present during acute cerulein pancreatitis significantly aggravates the inflammatory response and severity of the disease. More detailed studies will follow in the next funding period to better decipher the role A3A in acute and chronic pancreatitis on a phenotypic and mechanistic level.

Update on Research:BACKGROUND & AIMMutations in the serine protease inhibitor Kazal type 1 (SPINK1) are associated with an increased risk for chronic pancreatitis (CP). It is presumed that loss of SPINK1 expression or function results in intrapancreatic trypsin activation and progressive pancreatitis. However, a published mouse model did not recapitulate the human disease. Homozygous mice died shortly after birth and heterozygous mice did not show any phenotype. 
METHODSWe generated SPINK1–/–(KO) ferrets and collected pancreata from neonatal (2-4 weeks), weaning (6-8 weeks), and adult (> 6 months) KO ferrets and age-matched controls, and monitored their pancreatic disease development and progression using histopathology, immunocytochemistry (IHC), immunofluorescence (IF), and pancreatic trypsin activity measurements.
RESULTSWhen compared to wild-type ferrets at 2-4 weeks of age, KO ferrets had no difference in weight gain or pancreatic fecal elastase; they had intact pancreatic architecture, minimal inflammation, and normal intrapancreatic trypsin activity. Beginning at 6-7 weeks, KO ferrets demonstrated slower weight gain and required chow supplemented with pancreatic enzymes for survival. At 6-7 weeks, the KO ferret pancreas had increased trypsin activity with acinar cell loss, dilated ducts, inflammatory cell infiltration that showed diffuse myeloperoxidase positive staining, mild fibrosis, but normal pancreatic mass (early CP). The adult KO pancreata showed severe loss of parenchyma, fatty infiltration, extensive fibrosis containing scattered ducts, and acini with markedly reduced pancreatic mass (late CP).
CONCLUSIONThis is the first viable SPINK1-deficient animal model that spontaneously develops a progressive pancreatic disease that is similar to what has been observed in humans. The pathology is likely driven by the activation of trypsin within the pancreas.

Update on Research:
We have recruited 10 patients with acute pancreatitis within 48 hours of hospital admission. This is out of the proposed 30 patients. Recruitment has ramped up substantially in the last few months, with 9 of the 10 patients recruited in the last 4 months. Initial results have demonstrated increased T1, T2, and T1rho relaxation times in and outside of the pancreas. We are now working on finishing image processing on our current subjects and correlating the results to their CT and bloodwork results. For training, I am still planning to attend PancreasFest and the annual meeting of the APA. Additionally, I have attended all meeting of the TPIAT surgical committee and have plans to attend a whipple surgery.Update on funding and what positions you have held since award:
We have used a similar sequence in a recently funded U01 application, in which I am a co-investigator. I’m also planning to submit for a larger R21 or R01 grant using the data from this work.

Update on Research:
Despite a relatively advanced understanding of the etiology and pathogenesis of Pancreatic ductal adenocarcinoma (PDAC), and the achievement of 5-year relative survival rate for 11.5% of cases (SEER Cancer Statistics Review (CSR) 1975-2018), the therapeutic approaches to this malignancy are often insufficient, and it is still unknown how stress and tissue injury trigger pancreatic intraepithelial neoplasia (PanIN) to PDAC progression. We found that pancreatic tissue injury and oxidative stress activate the transcription factor NRF2 to induce the polycomb protein and lysine methylase EZH2. Whereas normal pancreatic cells exhibit transient EZH2 induction, cells harboring oncogenic KRAS and stabilized NRF2 display enduring EZH2 upregulation that renders them malignant PDAC precursors. During the early stages of pancreatic intraepithelial neoplasia (PanIN) to PDAC progression EZH2 mediates transcriptional silencing of key acinar-identity genes, correlating with histone H3K27 trimethylation of their promoters/enhancers, while activating genes that control fatty acid and cholesterol biosynthesis and cell proliferation, independently.

Update on Research:
Paligenosis is a cellular process by which mature, differentiated cells are recruited back into the cell cycle to proliferate and replenish lost cells after large-scale tissue injury. As the exocrine pancreas lacks a dedicated source of stem cells, pancreatic acinar cells can undergo paligenosis to restore the gland after pancreatitis. In acini, paligenosis manifests in discrete stages including 1) enhanced lysosomal degradation of organelles to downscale secretory function (i.e. dedifferentiation), 2) acquisition of ductal and mucinous progenitor-like characteristics (i.e. acinar-to-ductal metaplasia or ADM), and 3) proliferation. Experimentally, acinar cell paligenosis can be induced by in vivo pancreatitis or modeled by suspension culture-induced dedifferentiation of isolated acini in vitro. We previously reported that the endolysosomal system is lost during pancreatitis, and that expression of the endolysosomal protein Tumor Protein D52 (TPD52 or D52) maintains both the endolysosomal system and acinar secretion in culture. Preliminary data for this project indicates that D52 plays a role in maintaining acinar differentiation, secretory function and polarity, and that inducible, acinar-specific deletion of D52 in mice results in spontaneous paligenosis.The goals for this project are to characterize the stages of paligenosis with the loss of D52, and how this state impacts tissue recovery during pancreatitis. We have completed a time course of acinar-specific D52 deletion and are currently assessing markers of paligenosis over 14 days. Additionally, assessment of aged (1 year post-deletion) D52 knockout mouse pancreas suggests an arrest of paligenosis and enhanced tissue senescence compared to controls, which we hypothesize may be a protective mechanism to prevent multiple rounds of proliferation. Interestingly, preliminary data of D52 knockout mice subject to cerulein-induced in vivo pancreatitis suggests a mild protective effect that we are working to elucidate further. No changes in the proposed experimental approaches have been necessary nor are anticipated at this time.I fully intend and look forward to reporting the results of this project at the APA conference coming up in December 2024.