Programs and Activities Highlights
- National Association of Veterinary Scientists D.V.M./Ph.D. Colloquium
An ORIP staff member presented a keynote talk, titled “NIH Funding Opportunities for Veterinarian-Scientists,” at the National Association of Veterinary Scientists D.V.M./Ph.D. Colloquium in August 2025. An ORIP staff member also served as a panelist at the D.V.M./Ph.D. Alumni Panel during this meeting.
- Specialized Research Training in Animal Models and Related Resources: Focus Group, Session 2
ORIP held a series of focus groups involving veterinary trainees, early-career scientists, mentors, and training program directors to identify and cultivate opportunities for collaborations and partnerships that address challenges and synergize strategies and resources supporting recruitment and retention of veterinary scientists. In the second session, held May 15, 2025, selected current trainees supported by ORIP T32 grants were invited to discuss the challenges and opportunities that exist in the current program. Additionally, early-career scientists—including ORIP K01 awardees, applicants, and graduates of the T32 program—were invited to discuss challenges faced by early-career scientists.
- T32 and T35 Directors Consortium
The T32 and T35 Directors Consortium was convened on June 2, 2025. ORIP staff presented the latest NIH policies during the meeting. ORIP offers Institutional Research Training Grants through the T32 and T35 mechanisms to encourage veterinarians to consider a career in biomedical research.
- Specialized Research Training in Animal Models and Related Resources: Focus Group, Session 1
ORIP held a series of focus groups involving veterinary trainees, early-career scientists, mentors, and training program directors to identify and cultivate opportunities for collaborations and partnerships that address challenges and synergize strategies and resources supporting recruitment and retention of veterinary scientists. In the first session, held April 11, 2025, selected training program directors and mentors in the ORIP T32 program were invited to discuss the challenges and opportunities that exist in the current program.
- K01 Special Emphasis Research Career Award (SERCA) Guidelines
In April 2025, ORIP updated its K01 SERCA guidelines with new language covering updated ORIP priorities, including new approach methodologies (NAMs) for complementing animal research relevant to human health and diseases. The SERCA is intended to stimulate the development of veterinary scientists with interests in comparative medicine and related research questions.
Read more in the archive.
ORIP-Supported Research Highlights
- Advances in Targeted Autophagy Modulation Strategies to Treat Cancer and Associated Treatment-Induced Cardiotoxicity
Millions of cancer patients and cancer survivors face an increased risk of developing cardiotoxicity and cardiovascular (system encompassing the heart and blood vessels) dysfunction because of cancer progression and cancer treatments. Irregular autophagy causes this increased risk. Autophagy is the breakdown of old, damaged, or abnormal proteins within the cell that are then recycled for use in other proteins. Managing autophagy could protect the cardiovascular system during cancer treatment. This review notes the advances in regulating autophagy and how it could be applied to treat cardiotoxicity while improving cancer treatment outcomes. The researchers highlight in vitro (outside a living organism) models and other tests that are needed to obtain findings that can allow autophagy therapies to be translated into the clinic.
- A STAT3/Integrin Axis Accelerates Pancreatic Cancer Initiation and Progression
In pancreatic ductal adenocarcinoma (PDAC), inflammation and cell stress within the environment surrounding the tumor are known to promote cancer cell growth and increase drug resistance. The signal transducer and activator of transcription 3 (STAT3) pathway directs these responses. Researchers used human cancer cells and mouse models for PDAC (both sexes included) to identify binding sites of STAT3 that regulate gene expression and are linked to poor survival. The results showed that STAT3 interacts with integrin beta 3 to start and grow PDAC tumors. STAT3 also targets 18 genes that are involved in adaptive responses and can be used to identify different survival outcomes. This study highlights a new way to classify PDAC subpopulations for STAT3-targeted therapies.
- Cross-species Protection Suggests Entamoeba histolytica Trogocytosis Enables Complement Resistance Through the Transfer of Negative Regulators of Complement Activation
Amoebae are single-cell organisms that can be parasites to the human body. Entamoeba histolytica, a type of amoeba, causes diarrheal disease when it invades the intestine. E. histolytica spreads through the body using the bloodstream and can evade the immune system. Amoebae eat parts of human cells—an event known as trogocytosis—which allows them to display human proteins and resist being broken down by serum in the blood. Researchers wanted to identify how amoebae resist being broken down. Results showed that amoebae display host proteins that suppress the complement pathway of the immune system, which protects them from being broken down. Other microbes can perform trogocytosis of human cells, so understanding this method of resistance could be relevant to other infections.
- Loss of Hepatocyte-Specific RECK Exacerbates Metabolic Dysfunction–Associated Steatohepatitis
Metabolic dysfunction–associated steatohepatitis (MASH) is a serious liver disease resulting from excess fat buildup. MASH is a major health crisis worldwide due to increases in obesity and insulin resistance, and it is a leading cause for liver transplants in the Western world. The current approach for MASH treatment involves lifestyle changes. Therefore, identifying new ways to treat MASH is critical. Reversion Inducing Cysteine Rich Protein with Kazal Motifs (RECK) is a molecule that regulates the extracellular matrix (ECM). The ECM surrounds a cell, provides structural support, and enhances signaling. The role of RECK in metabolic liver disease is poorly understood. The researchers showed in a previous study that RECK gain-of-function (increased amounts above normal) in liver cells protected mice against diet-induced MASH. In this study, researchers used two mouse models (sex not specified) that depleted RECK in liver cells. They showed that the lack of RECK significantly increased inflammation, cell swelling, and fibrosis (too much ECM). These studies highlight RECK’s potential as a novel therapy for MASH.
- Remdesivir Postexposure Prophylaxis Limits Measles-Induced “Immune Amnesia” and Measles Antibody Responses in Macaques
Measles is a highly contagious viral disease that is a leading cause of childhood illness and death around the world. The measles virus (MeV) replicates considerably in tissue where immune cells are produced and activated. MeV causes the immune system to lose circulating antibodies (a protein that binds to a specific antigen and helps the immune system destroy it) against other pathogens, which leaves the infected child susceptible to other infectious diseases. Researchers wanted to determine whether remdesivir, a broad-spectrum antiviral (a drug that affects a wide range of viruses), can hinder MeV-induced loss of antibodies to other pathogens. They measured antibody reactivity using a MeV rhesus macaque model (both sexes included). Remdesivir given 3–14 days after MeV infection limited the loss of antibodies to non-MeV pathogens. Remdesivir also reduced the immune system’s ability to mount an antibody response to MeV. This study shows that early treatment of measles with remdesivir prevents the loss of antibodies against other pathogens but lessens the response to MeV.
Read more in the archive.
