Symposium Speaker Spotlight: Dr. Stephen Pandol to discuss How Global Collaboration is Making a Difference

The Hirshberg Foundation is excited to have Dr. Stephen Pandol joining us at the 14th Annual Symposium on Pancreatic Cancer to discuss how medical professionals from around the world are collaborating and making a difference in pancreatic cancer.

Stephen Pandol, MD, is board-certified in internal medicine, and gastroenterology. He leads a multidisciplinary team comprised of molecular and cell biologists, computational chemists, clinical scientists, physicians and population scientists, with the common goal of developing enhanced treatments and improved outcomes for patients with pancreatic cancer, pancreatitis and diabetes.

Dr. Pandol’s research focuses on determining the changes in intracellular signaling and organelle disorders that occur when pancreatitis develops; the mechanisms of cells involved in promoting the growth and metastasis of pancreatic cancer, and how nutrients in the intestine activate gut endocrine cells in diabetes to regulate glucose metabolism and food intake. He has published more than 250 papers, including peer-reviewed articles, reviews and book chapters, and more than 180 abstracts. He is on the editorial boards of American Journal of Physiology Gastrointestinal and Liver Physiology and Gastroenterology and is a Chief Editor on Frontiers in Gastrointestinal Sciences, and a Consulting Editor on Journal of Clinical Investigation.

Dr. Pandol is currently Co-Lead of the Consortium to Study Chronic Pancreatitis, Diabetes, and Pancreatic Cancer and a Counselor for the American Gastroenterology Association. He received the Lifetime Achievement Award from the American Pancreatic Association in 2015.

Dr. Pandol will speak on How Global Collaboration is Making a Difference at the 14th Annual Symposium on Pancreatic Cancer held at UCLA.


Symposium Speaker Spotlight: Panel Discussion – Perspectives from Cancer Survivors and Caregivers

The Hirshberg Foundation is honored to share the stories of pancreatic cancer patients and caregivers from our past three Symposium Patient Panels. These honest and frank discussions give us all perspective, insight and sensitivity to the journey of both patients and loved ones once someone in the family is diagnosed with pancreatic cancer.

Dr. Howard Reber, Dr. Timothy Donahue and Dr. Annette Stanton have moderated our Patient Panels. They are all leaders in their fields and lend their professional experience in guiding these conversations.

Howard Reber, MD is a Distinguished Professor of Surgery Emeritus and Emeritus Chief of the Gastrointestinal and Pancreatic Surgery section at David Geffen School of Medicine at UCLA. He currently serves as Emeritus and Founding Director of the UCLA Agi Hirshberg Center for Pancreatic Diseases.

Timothy Donahue, MD is an Associate Professor of Surgery at the David Geffen School of Medicine at UCLA. He also has a joint appointment in the Department of Molecular and Medical Pharmacology to facilitate his research program. Dr. Donahue is the Chief of Pancreatic Surgery and oversees the pancreatic diseases multi-disciplinary program at UCLA.

Annette L. Stanton, Ph.D., is Professor of Psychology and Psychiatry/Biobehavioral Sciences at the University of California, Los Angeles, senior research scientist at the UCLA Cousins Center for Psychoneuroimmunology, and a member of the Center for Cancer Prevention and Control Research in the Jonsson Comprehensive Cancer Center.

These patient and caregiver perspectives are invaluable to those currently facing a pancreatic cancer diagnosis and we thank all our panelists for sharing their time, their stories and their hope with us.

Watch the 2018 Panel Discussion »

Watch the 2017 Panel Discussion »

Watch Past Panel Discussions »


New research sheds light on pancreatic cancer biology & role of common p53 mutation

New research from Seed Grant recipient, Marina Pasca di Magliano, PhD, from the University of Michigan has deepened our understanding of the biology of pancreatic cancer, crucial to the development of treatment therapies.

The most common form of pancreatic cancer is pancreatic ductal adenocarcinoma, a tumor that starts in the exocrine cells of the pancreas, where digestive enzymes are formed. Nearly all pancreatic cancer tumors show mutations in KRAS and a majority also contain p53 mutations.

The study shows that the p53 mutant protein is responsible for maintaining the biology of the tumor, specifically the way the tumor cells metabolize nutrients to derive energy for their growth. The p53 mutation also showed evidence of mediating malignant potential and cancer cell invasion, giving more insight into how pancreatic cancer spreads.

The pioneering research by Dr. Pasca di Magliano and her lab found that p53 mutation is required for the formation and maintenance of KRAS induced pancreatic cancer precursor lesions. This finding has major implications on the fundamental aspect of tumor biology and the future development of therapy and diagnosis.

As Dr. Pasca di Magliano wrote of her research, “We could never have completed it without the [Hirshberg] Foundation’s support, and I would like to thank you again for supporting us, and for your patience.” We applaud all those involved in this study for their relentless dedication to understanding pancreatic cancer and the work that brings us closer to a cure. Their research instrumental for the development of future treatment options.


The Hirshberg Foundation funds UCLA School of Nursing Project

In a new study conducted by the UCLA School of Nursing, researchers will assess how supportive care can increase the overall quality of life, and potentially survival rates, in pancreatic cancer patients.

It is known that pancreatic cancer patients, and their caregivers, often experience increased levels of depression and a high symptom burden. Furthermore, when patient-reported symptoms are integrated into routine care, there is evidence of increased survival time. We know that supportive care to improve symptoms, reduce hospital stays and preserve quality of life is imperative. This innovative new study will employ online nursing check-ins to track patients’ symptoms and improve supportive care, with the goal to reduce overall pain.

The study will also evaluate how the smartphone app, chemoWave, can increase collaboration with caregivers and improve patient wellbeing by recording and monitoring patients’ physical and emotional states.

By focusing on supportive care for both patients and caregivers, this study hopes to improve overall quality of life, and potentially survival rates for those facing pancreatic cancer.


New study establishes that ATM activity poses a major barrier to the development of cancer in the pancreas by maintaining genomic stability.

A new study published by our 2014-15 Seed Grant recipient, Yiannis Drosos, PhD has uncovered information that can help diagnose and treat pancreatic cancer tumors. 

Research from St. Jude Children’s Research Hospital examined how ATM-deficiency increases genomic instability, which promotes highly metastatic pancreatic cancer.

Approximately 5% of patients with hereditary pancreatic cancer carry genetic alterations in a gene known as ATM. This gene is responsible for synthesizing a protein that is necessary to preserve the stability of the genome as it helps repair DNA damage.

This study reveals that ATM-deficiency leads to persistent DNA damage in both precancerous lesions and primary tumors. The study found that when ATM alterations occurred in combination with Kras mutations (the most common mutation shown in pancreatic cancer patients) highly metastatic pancreatic cancer tumors developed due to un-repaired DNA and genomic instability. However, these tumors showed high sensitivity to low doses of radiation, providing insight into potential treatment option.

This study establishes that ATM activity poses a major barrier to the development of cancer in the pancreas by maintaining genomic stability. The results of this study hold clinical relevance to understanding how pancreatic cancer spreads and potential treatment options. The Hirshberg Foundation is proud to support studies such as this in order to uncover information that will help the diagnosis and/or treatment of pancreatic tumors.

To read the full article: https://www.ncbi.nlm.nih.gov/pubmed/28894253


New two-pronged approach targets pancreatic stellate cells to prevent pancreatic cancer tumor growth

New research conducted at the Ingham Institute for Applied Medical Research in Liverpool, New South Wales, has found a new approach to treating pancreatic cancer. The research, published in Oncotarget, suggests that a combined approach that targets tumor cells with chemotherapy while inhibiting specific pathways that mediate stromal-tumor interactions may represent a novel therapeutic strategy to improve outcomes in pancreatic cancer patients.

This research, funded by the Hirshberg Foundation, aims to find new approaches to treating pancreatic cancer, because targeting cancer cells alone has failed to substantially improve patient outcomes.

It is now acknowledged that the microenvironment surrounding pancreatic cancer cells plays an important role in cancer progression. Pancreatic stellate cells, found in the microenvironment surrounding pancreatic tumors, facilitate pancreatic cancer progression through increased tumor growth and metastasis. This study has shown that a two-pronged approach that combines standard chemotherapy with compounds that cut off the communication between cancer cells and pancreatic stellate cells greatly reduces tumor growth and virtually eliminates tumor spread to distant sites.

Research findings such as this allow us to provide novel treatment options to patients facing pancreatic cancer and provide greater understanding for targeted therapy. As Dr. Apte wrote, “the Hirshberg Seed Grant was absolutely valued and an integral support for us to be able to complete [this] work.”

We thank Dr. Apte & her team for their commitment to Never Give Up in the fight against pancreatic cancer.

Read the complete study here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652738/