Cancer Metabolism and Microenvironment Program Archives - Sanford Burnham Prebys

Tag: Cancer Metabolism and Microenvironment Program

Institute News

Curebound awards two grants to Sanford Burnham Prebys scientists

AuthorGreg Calhoun
Date

February 12, 2025

split photo of Brooke Emerling and Michael Jackson
Brooke Emerling, PhD, is director of the Cancer Metabolism and Microenvironment Program. Michael Jackson, PhD, is senior vice president for Drug Discovery and Development in the Conrad Prebys Center for Chemical Genomics.

The San Diego-based philanthropic organization has awarded $43 million in cancer research to date

Curebound recently announced the awarding of 17 grants in December 2024 for a total of $8.25 million in funding to advance cancer research in 2024.

Two new grants will support cancer research conducted by scientists at Sanford Burnham Prebys. Since 2014, 32 Curebound grants have supported projects that included scientists at the institute.

A workaround for a tricky target

The TP53 gene contains the blueprint for constructing a protein called tumor protein p53. This protein is considered a tumor suppressor because it helps cells grow in a controlled manner.

When cell growth goes awry, however, the TP53 gene is a common culprit as the most frequently mutated gene in cancers. While this ubiquity has placed a bullseye on the mutated tumor protein p53 for aspiring drug developers, it has proven tricky to target directly.

Brooke Emerling, PhD, director of the Cancer Metabolism and Microenvironment Program, and her collaborators have shown that the growth of cancer cells with a mutated TP53 gene is dependent on lipid enzymes called phosphatidylinositol-5-phosphate 4-kinases (PI5P4K). Emerling and her collaborators have identified compounds that break down these enzymes.

The researchers have demonstrated the ability of these compounds to target and eliminate cancer cells with a mutated TP53 gene without harming normal cells. Curebound will support the team’s ongoing efforts to work around the difficult-to-target tumor protein p53 by instead targeting PI5P4K.

Next, the group plans to optimize the compounds that break down PI5P4K to develop cancer drugs that are strong candidates for future clinical trials.

Curebound collaborators: Patrick Kearney, PhD, director of Medicinal Chemistry in the Conrad Prebys Center for Chemical Genomics, and Eric Wang, PhD, assistant professor in the Cancer Molecular Therapeutics Program.

Boosting the immune system against lung cancer

The immune system is one of the main defenses of the human body to fend off harmful pathogens and invasive cells such as cancer. Among all white blood cells, a particular cell type, called a T cell, can directly kill cancer cells and therefore plays an essential role in building anti-tumor immune responses.

Immunotherapies that boost the anti-cancer capabilities of T cells have revolutionized the way we treat cancer, especially in blood cancers such as leukemia, lymphoma and myeloma. More recently, immunotherapies are rapidly advancing to become mainstream treatments for solid cancers as well.

Currently, however, less than a third of patients with lung cancer benefit from immunotherapies. Pandurangan Vijayanand, MD, PhD, the William K. Bowes Distinguished Professor at the La Jolla Institute for Immunology, discovered that certain T cells called cytotoxic T lymphocytes have molecular features associated with a robust immune response against lung cancer tumors. His work has identified new targets for lung cancer immunotherapy.

Curebound will support Vijayanand’s collaboration with Michael Jackson, PhD, senior vice president for Drug Discovery and Development in the Conrad Prebys Center for Chemical Genomics, to use this research to identify agents to boost tumor immune responses.

The research team’s work has the potential to identify a new class of immunotherapy drugs for patients with lung cancer.

Curebound collaborator: Changlu Liu, PhD, director of Receptor Pharmacology in the Conrad Prebys Center for Chemical Genomics.

Pandurangan Vijayanand

Pandurangan Vijayanand, MD, PhD, is the William K. Bowes Distinguished Professor at the La Jolla Institute for Immunology.

Institute News

Protein superfamily crucial to the immune system experiences Broadway-style revival

AuthorGreg Calhoun
Date

November 19, 2024

Tumor necrosis factor-α (TNF), shown in pink and tan, is depicted in a complex with an antibody called golimumab, pictured in slate gray
Tumor necrosis factor-α (TNF), shown in pink and tan, is part of a large family of signaling proteins known to play a key role in developing and coordinating the immune system. Here, TNF is depicted in a complex with an antibody called golimumab, pictured in slate gray. Golimumab is used as a drug to treat rheumatoid arthritis and other autoimmune disorders, which it does by smothering the receptors on TNF that initiate inflammation.

More than 25 years after targeting a member of this superfamily of proteins led to groundbreaking treatments for several autoimmune diseases including rheumatoid arthritis and Crohn’s disease, San Diego scientists note a resurgence of interest in research to find related new drug candidates.

In 1998, the same year “Footloose” debuted on Broadway, REMICADE® (infliximab) was approved by the FDA for the treatment of Crohn’s disease. This was the first monoclonal antibody ever used to treat a chronic condition, and it upended the treatment of Crohn’s disease.

Research published in February 2024 demonstrated better outcomes for patients receiving infliximab or similar drugs right after diagnosis rather than in a “step up” fashion after trying other more conservative treatments such as steroids.

Infliximab and ENBREL® (etanercept) — also approved in 1998 to treat rheumatoid arthritis — were the first FDA-approved tumor necrosis factor-α (TNF) inhibitors. TNF is part of a large family of signaling proteins known to play a key role in developing and coordinating the immune system.

The early success of infliximab and etanercept generated excitement among researchers and within the pharmaceutical industry at the possibility of targeting other members of this protein family. They were interested in finding new protein-based (biologics) drugs to alter inflammation that underlies the destructive processes in autoimmune diseases.

As “Footloose” made it back to Broadway in 2024 for the first time since its initial run, therapies targeting the TNF family are in the midst of their own revival. Carl Ware, PhD, a professor in the Immunity and Pathogenesis Program at Sanford Burnham Prebys, and collaborators at the La Jolla Institute for Immunology and biotechnology company Inhibrx, report in Nature Reviews Drug Discovery that there is a resurgence of interest and investment in these potential treatments.

“Many of these signaling proteins or their associated receptors are now under clinical investigation,” said Ware. “This includes testing the ability to target them to treat autoimmune and inflammatory diseases, as well as cancer.”

Today, there are seven FDA-approved biologics that target TNF family members to treat autoimmune and inflammatory diseases. There also are three biologics and two chimeric antigen receptor (CAR)-T cell-based therapies targeting TNF members for the treatment of cancer. This number is poised to grow as Ware and his colleagues report on the progress of research and many clinical trials to test new drugs in this field and repurpose currently approved drugs for additional diseases.

“The anticipation levels are high as we await the results of the clinical trials of these first-, second- and — in some cases — third-generation biologics,” said Ware.

Ware and his coauthors also weighed in on the challenges that exist as scientists and drug companies develop therapies targeting the TNF family of proteins, as well as opportunities presented by improvements in technology, computational analysis and clinical trial design.

Portrait of Carl Ware

Carl Ware, PhD, is a professor in the Immunity and Pathogenesis Program at Sanford Burnham Prebys.

“There are still many hurdles to get over before we truly realize the potential of these drugs,” noted Ware. “This includes the creation of more complex biologics that can engage several different proteins simultaneously, and the identification of patient subpopulations whose disease is more likely to depend on the respective proteins being targeted.

“It will be important for researchers to use computational analysis of genetics, biomarkers and phenotypic traits, as well as animal models that mimic these variables. This approach will likely lead to a better understanding of disease mechanisms for different subtypes of autoimmune conditions, inflammatory diseases, and cancer, enabling us to design better clinical trials where teams can identify the appropriate patients for each drug.”

Institute News

The implastic nature of plastic culture

AuthorScott LaFee
Date

November 4, 2024

Cultured cancer cells from the “immortal” HeLa human line. Image courtesy of Matthew Daniels, Wellcome Collection.
Cultured cancer cells, like these from the “immortal” HeLa human line, have proven crucial to basic cancer research. But do they accurately capture the look and behavior of living tumor cells? Kevin Tharp says no, hindering effective drug development. Image courtesy of Matthew Daniels, Wellcome Collection.

There is an art (and science) to creating cell culture models that reflect the complexities of disease. Such models have long been indispensable to parsing the underlying mechanisms of pathology and to preclinical drug discovery.

But art, writes Kevin Tharp, PhD, assistant professor in the Cancer Metabolism and Microenvironment Program, doesn’t always imitate life — at least not when it comes to finding effective cancer therapeutics.

“Just like a machine-learning algorithm trained on irrelevant datasets, efforts to discover anticancer therapeutics are limited by the models we use,” Tharp writes in the British Journal of Pharmacology. “Our drug discovery pipeline works incredibly well but is applied to models that poorly recapitulate in vivo physiology. This may be why drug discovery approaches efficiently identify drugs that work in the context tested and yet often fail to translate into clinical success.”

It’s a case of there’s no place like home. Cancer cell models are cultured on plastic in two-dimensions with limited or no diversity of neighbors. Cancer cells in vivo reside in three dimensions, with dynamic and complex interactions with neighboring cells and surroundings, i.e., the tumor microenvironment.

It’s like growing up on Disneyland’s Main Street versus a real-world urban city. Cultured cancer cells simply don’t look or behave exactly the same as cancer cells in an actual  tumor. Nor do the investigational molecules being tested as potential therapies.

Tharp suggests a multi-pronged approach: Initially culture target cells using conventional methods, then transfer the cells to new culture formats that enforce distinct, non-genomic cytoskeleton architectures and expression patterns that more closed mimic real life.

Institute News

Raising awareness of breast cancer research at Sanford Burnham Prebys

AuthorGreg Calhoun
Date

October 31, 2024

Kelly Kersten, PhD, and Kevin Tharp, PhD

The October Science Connect Series event was themed around Breast Cancer Awareness Month and featured two cancer research experts.

The Sanford Burnham Prebys Wellness Ambassadors hosted a Science Connect event on Wednesday, October 30, 2024, featuring two faculty experts discussing their breast cancer research and its implications.

The Science Connect Series provides a forum for Sanford Burnham Prebys principal investigators to share their research with administrative personnel. Faculty members gain experience in communicating their science to a lay audience, and administrators gain a better understanding of research conducted at the institute so they can become better advocates and ambassadors of the shared mission to translate science into health.

Kelly Kersten, PhD, an assistant professor in the Cancer Metabolism and Microenvironment Program, opened the event by focusing on the importance of finding new treatments —such as immunotherapies — for the one-third of breast cancer patients that are diagnosed after the early stages of the disease when surgery is less effective.

The immune system is one of the main defenses of the human body to fend off harmful pathogens and invasive cells, such as cancer. Among all white blood cells, a particular cell type, called a T cell, can directly kill cancer cells and therefore plays an essential role in building anti-tumor immune responses.

Many types of cancer are confronted and infiltrated by T cells, only to be suppressed by the local tumor environment.

“While immunotherapies that boost the immune system have revolutionized the way we treat cancer, many patients do not respond to the treatments, and the mechanisms of resistance remain largely unclear,” said Kersten.

Kersten’s goal is to understand why T cells enter a state known as exhaustion and lose their tumor-killing capacity. This knowledge will help her team find potential future therapies that could prevent T-cell exhaustion and improve immunotherapies for cancer patients.

Kevin Tharp, PhD, also an assistant professor in the Cancer Metabolism and Microenvironment Program, shared that his lab’s focus is on how cancer cells adapt their metabolism to generate the energy needed to spread to other tissues through metastasis. He presented his team’s work with the Kersten lab on another aspect of potential resistance to immunotherapy in breast cancer.

Tharp and Kersten are studying the hypothesis that part of the reason why these therapies fail is due to tumor-associated fibrosis, the creation of a thick layer of fibrous collagen (like scar tissue) that acts as a barrier against the anti-tumor immune response. They published a paper on June 3, 2024, in Nature Cancer,  discussing how tumor-associated macrophages, a type of immune cell found abundantly in the tumor microenvironment, respond to the physical properties of fibrosis.

By synthesizing injury-associated collagens that facilitate wound closure, TAMs experience metabolic changes and generate metabolic byproducts that suppress the anti-tumor function of immune cells.

“The metabolic changes in the microenvironment present more of a challenge to anti-tumor responses than the physical barrier,” said Tharp. “Our study provides an alternative explanation for why anti-tumor immunity is impaired in fibrotic solid tumors.”

To follow up on these results, Tharp is collaborating with Sarah Blair, MD, a professor of surgery at the University of California San Diego, to fund and initiate a clinical trial testing the potential of dietary supplements to counteract the suppressive effects of TAM metabolic byproducts as an adjunct therapy to surgery.

Institute News

Two Sanford Burnham Prebys scientists selected for American Cancer Society postdoctoral fellowships

AuthorGreg Calhoun
Date

October 18, 2024

combined photos of Alicia Llorente Lope and Ambroise Manteau
Alicia Llorente Lope, PhD, is a postdoctoral associate in the lab of Brooke Emerling, PhD, director of the Cancer Metabolism and Microenvironment Program at Sanford Burnham Prebys. Ambroise Manceau, PhD, is a postdoctoral associate in the lab of Cosimo Commisso, PhD, interim director and deputy director of the institute’s NCI-Designated Cancer Center.

Funds will support Alicia Llorente Lope and Ambroise Manceau who study breast and pancreatic cancer

Alicia Llorente Lope, PhD, and Ambroise Manceau, PhD, were awarded 2024 Postdoctoral Fellowships from the American Cancer Society (ACS). These prestigious awards provide more than $65,000 per year for up to three years to support early career scientists studying cancer.

“I was so excited when I heard the news,” said Llorente. “It is a privilege to have this award, and it feels very validating to know that someone saw enough potential in my research to deem it worthy of funding.”

Tackling treatment-resistant breast cancer

Llorente joined the lab of Brooke Emerling, PhD, director of the Cancer Metabolism and Microenvironment Program at Sanford Burnham Prebys, nearly three years ago after beginning her breast cancer research career as a doctoral student.

“I was first interested in breast cancer because my grandmother died of the disease, and I wanted to contribute to finding new therapeutic opportunities for cancer patients,” said Llorente. Llorente’s ACS-funded research project focuses on HER2-positive (HER2+) breast cancer.

Roughly one in five breast cancer tumors have elevated levels of the HER2 protein. While these tumors tend to grow quickly, drugs targeting the HER2 protein are usually effective at first. However, HER2+ tumors often are able to adapt and develop resistance to these drugs over time, leaving patients with few if any remaining treatments options.

Llorente has found evidence that a form of the protein phosphatidylinositol-5-phosphate 4-kinase (PI5P4K) plays a role in breast cancer tumors becoming resistant to HER2 drugs.

Brooke Emerling

Brooke Emerling, PhD

“We’ve revealed a strong connection between elevated levels of PI5P4K gamma and reduced survival rates in patients with HER2+ breast cancer,” explained Llorente. “I plan to explore whether targeting both HER2 and PI5P4K gamma in breast cancer cells may provide a path to overcoming treatment resistance.” Llorente also will study the functions of PI5P4K gamma in breast cancer cells to see why these cells cease to respond to HER2-targeting drugs.

“I am incredibly proud of Alicia for spearheading this groundbreaking project targeting the lipid kinase PI5P4K gamma,” said Emerling. “Her insightful analysis of breast cancer datasets, which uncovered a correlation between elevated expression of PI5P4K gamma and worse outcomes in HER2+ patients, has set the stage for vital research aimed at overcoming the significant challenge of resistance to targeted therapies in HER2+ tumors.”

Cosimo Commisso headshot

Cosimo Commisso, PhD

Powering down pancreatic cancer

Manceau is in the second year of his postdoctoral training in the lab of Cosimo Commisso, PhD, interim director and deputy director of the institute’s NCI-Designated Cancer Center. During his doctoral program, Manceau studied how abnormal cells die in a programmed series of steps called apoptosis, a process known to go awry in cancer and neurodegenerative diseases.

“It began as a basic science project about the molecular processes around cell death, and over time it led to possible therapeutic implications,” said Manceau. “I learned that I like to study fundamental biology and then try to find an application for it, and I saw in the Commisso lab an opportunity to do just that in pancreatic cancer.”

Manceau’s fellowship project focuses on pancreatic ductal adenocarcinoma (PDAC) — the most common form of pancreatic cancer with only a 13% five-year survival rate — and its ravenous pursuit of energy. Because of PDAC cells’ constant need for fuel to sustain their rampant growth, they adapt by reshaping the surface of their cells to snatch extra nutrients from the jelly-like substance between cells.

Commisso and others have shown that cutting off the extra power supplied by this process — known as macropinocytosis — reduces tumor growth. Manceau has studied the contents taken by contorted pancreatic cell surfaces in pockets called macropinosomes. By analyzing every single protein in this scooped goop, he found that calcium transporter proteins present in macropinosomes also are required for macropinocytosis.

“During the fellowship, I will work to understand how these transporter proteins affect macropinocytosis,” said Manceau. “These proteins have never been targeted before in pancreatic cancer, so our long-term goal is to use this strategy to cut the nutrient supply to tumors and see if we can inhibit tumor growth.”

“By disrupting the cancer cells’ ability to feed themselves through macropinocytosis, we can potentially starve tumors and inhibit their growth,” added Commisso. “Ambroise’s research aims to target key proteins involved in this process, opening up new possibilities for treatments that could significantly improve outcomes for patients battling pancreatic cancer.”

Institute News

How a protein component of nuclear pore complexes regulates development of blood cells and may contribute to myeloid disorders

AuthorCommunications
Date

June 5, 2024

A computer graphic depicts a nuclear pore in a eukaryotic cell. Nuclear pores are large protein complexes that span the nuclear membrane and allow the movement of molecules, such as proteins, RNAs, and other molecules between the nucleus and the cell’s cytoplasm. Image courtesy of M. Towler and J. Aitken, Wellcome Collection.
Computer graphic depicts a nuclear pore in a eukaryotic cell. Nuclear pores are large protein complexes that span the nuclear membrane & allow the movement of molecules, such as proteins, RNAs, & other molecules between the nucleus & the cell’s cytoplasm.

Nuclear pore complexes (NPCs) are channels composed of multiple proteins that ferry molecules in and out of the nucleus, regulating many critical cellular functions, such as gene expression, chromatin organization and RNA processes that influence cell survival, proliferation, and differentiation.

In recent years, new studies, including work by Maximiliano D’Angelo, PhD, associate professor in the Cancer Metabolism and Microenvironment Program at Sanford Burnham Prebys, have noted that NPCs in cancer cells are different, but how these alterations contribute to malignancy and tumor development—or even how NPCs function in normal cells—is poorly understood.

In a new paper, published June 5, 2024 in Science Advances, D’Angelo with first author Valeria Guglielmi, PhD, and co-author Davina Lam, uncover Nup358, one of roughly 30 proteins that form the NPCs, as an early player in the development of myeloid cells, blood cells that if not formed or working properly leads to myeloid disorders such as leukemias.

The researchers found that when they eliminated Nup358 in a mouse model, the animals experienced a severe loss of mature myeloid cells, a group of critical immune cells responsible for fighting pathogens that are also responsible for several human diseases including cancer. Notably, Nup358 deficient mice showed an abnormal accumulation of early progenitors of myeloid cells referred as myeloid-primed multipotent progenitors (MPPs).

“MPPs are one of the earliest precursors of blood cells,” said D’Angelo. “They are produced in the bone marrow from hematopoietic stem cells, and they differentiate to generate the different types of blood cells.

Maximiliano D’Angelo and Valeria Guglielmi

“There are different populations of MPPs that are responsible for producing specific blood cells and we found that in the absence of Nup358, the MPPs that generate myeloid cells, which include red blood cells and key components of the immune system, get stuck in the differentiation process.”

Fundamentally, said Gugliemi, Nup358 has a critical function in the early stages of myelopoiesis (the production of myeloid cells). “This is a very important finding because it provides insights into how blood cells develop, and can help to establish how alterations in Nup358 contribute to blood malignancies.”

The findings fit into D’Angelo’s ongoing research to elucidate the critical responsibilities of NPCs in healthy cells and how alterations to them contribute to immune dysfunction and the development and progression of cancer.

“Our long-term goal is to develop novel therapies targeting transport machinery like NPCs,” said D’Angelo, who recently received a two-year, $300,000 Discovery Grant from the American Cancer Society to advance his work.

This research was supported in part by a Research Scholar Grant from the American Cancer Society (RSG-17-148-01), the Department of Defense (grant W81XWH-20-1-0212) and the National Institutes of Health (AI148668).

The study’s DOI is 10.1126/sciadv.adn8963.

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Maximiliano D’Angelo

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Pancreatic cancer symposium celebrates 10th anniversary in San Diego

AuthorGreg Calhoun
Date

May 22, 2024

From left to right, co-hosts Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging and Regeneration Program; and Cosimo Commisso, Ph.D., director of, and associate professor in, the Cancer Metabolism and Microenvironment Program.
From left to right, co-hosts Pamela Itkin-Ansari, Ph.D., adjunct professor in the Development, Aging and Regeneration Program; and Cosimo Commisso, Ph.D., director of, and associate professor in, the Cancer Metabolism and Microenvironment Program.

The 2024 PancWest Symposium brought more than 120 scientists to the Sanford Burnham Prebys campus in San Diego to discuss the latest advances in pancreatic cancer research.

More than 120 pancreatic cancer researchers from the West Coast traveled to San Diego from as far as Vancouver to attend the 2024 PancWest Symposium on May 17. The PancWest Symposium was founded in 2014 to regularly bring the scientific community studying pancreatic cancer together to discuss advances in the field and foster new collaborations.

The PancWest Symposium is held every two years in a different city to showcase expert scientists who are making important contributions to the field of pancreatic cancer research, including tumorigenesis, tumor progression and the discovery of novel therapeutic paradigms, such as immunomodulation and metabolic targeting.

The 2024 event was held on the Sanford Burnham Prebys campus in the Fishman Auditorium and was hosted by Cosimo Commisso, Ph.D., director of, and associate professor in, the Institute’s Cancer Metabolism and Microenvironment Program; and Pamela Itkin-Ansari, Ph.D., adjunct professor in the Institute’s Development, Aging and Regeneration Program.

“While pancreatic cancer accounts for only three percent of cancer cases, it has the highest mortality rate among major cancers and is the third leading cause of cancer-related death in the U.S.,” says Commisso.

PancWest Symposium poster presentations in Chairmen's Hall

The symposium’s events included a keynote address, 12 featured speakers, a poster session and a series of “power talks” providing attendees a chance to hear two-minute oral presentations from selected poster presenters.

“Unless we find ways to better diagnose and treat this disease, it is projected to become the second most deadly cancer in less than 20 years,” adds Itkin-Ansari. “That is why events such as PancWest are so important to enhance innovation and foster collaboration.”

Rosalie C. Sears, Ph.D., professor of Molecular and Medical Genetics, co-director of the Brenden-Colson Center for Pancreatic Care and Krista L. Lake Chair in Cancer Research at Oregon Health & Science University in Portland, gave the symposium’s keynote address.

Additional events at the symposium included 12 featured speakers, a poster session and a series of “power talks” providing attendees a chance to hear two-minute oral presentations from selected poster presenters.

“Being a part of PancWest has been a transformative experience,” shares Itkin-Ansari. “The exchange of groundbreaking research and innovative ideas among leading experts advanced our scientific understanding.”

“It also paved the way for new therapeutic strategies, ultimately offering hope and improved outcomes for patients battling pancreatic cancer,” adds Commisso.

More information about the symposium and featured speakers is available on the event’s webpage.

Institute News

The “Eph” system may pave the way for novel cancer therapies

AuthorSusan Gammon
Date

November 27, 2023

Elena Pasquale, PhD, Sanford Burnham Prebys

Over the past three decades, researchers have been investigating an important cell communication system called the “Eph system,” and the evidence implicating the system in cancer is staggering.

The Eph system is comprised of multiple Eph receptors and their ligands—ephrins—and are involved in contact-dependent communication between cells. They play essential roles in regulating various cellular processes.

Modern studies have shed light on the Eph system’s role in tumor expansion, invasiveness, metastasis, cancer stem cell maintenance and therapy resistance.

This month, Elena Pasquale, PhD, published a review in Nature Reviews Cancer that summarizes the current state of research on the Eph system and its links to cancer progression and drug resistance.

“The Eph system has many critical functions during the development of tissues and organs, but it also has the capacity to either promote or suppress cancer progression and malignancy” says Pasquale. “In cancer, the activities of the Eph system can differ depending on the circumstances—for example, which Eph receptors and ligands are present in a tumor cell, the types of tumor cells in which they function, and the characteristics of these cells.”

“It’s this remarkable versatility that makes the Eph system a compelling but also challenging target for potential therapies,” says Pasquale.

“The aims of this review were to comprehensively survey the large body of data regarding various aspects related to Eph signaling in tumors and to highlight potential strategies for therapeutic targeting,” says Pasquale. “Overall, while significant progress has been made in deciphering the Eph system in cancer, there is much more to learn.

“Gaining a deeper understanding of how the Eph system functions in cancer is challenging but will be essential for the development of targeted therapies and personalized treatment approaches for patients.”

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Three Sanford Burnham Prebys faculty receive promotions

AuthorMiles Martin
Date

June 30, 2022

Ani Deshpande, Brooke Emerling and Charles Spruck

Sanford Burnham Prebys is proud to announce the promotion of three of our faculty from assistant to associate professor. 

The promoted faculty, all from the Institute’s NCI-designated Cancer Center, include Ani Deshpande, PhD, Brooke Emerling, PhD and Charles Spruck, PhD

Ani Deshpande, PhD

Deshpande studies developmental processes in stem cells that get hijacked by cancer, focusing specifically on acute myeloid leukemia, one of the most common types of blood cancer. Earlier last year, Deshpande published a study with researchers at the National Institutes of Health (NIH) revealing that CRISPR gene editing can sometimes favor cells with cancer mutations, encouraging a cautious approach when using CRISPR therapies for certain cancers

Deshpande joined the Institute in 2015. Prior to that, he held positions at Memorial Sloan Kettering Cancer Center and Harvard Medical School.

Brooke Emerling, PhD

Emerling studies the metabolism of cancer cells, specifically how certain signaling proteins can contribute to the uninhibited growth typical of tumors. Emerling recently received a $2.3 million grant from the NIH to continue her work over the next four years.

Emerling joined the faculty at Sanford Burnham Prebys in 2016. Prior to that, she held positions at Weill Cornell Medicine and Harvard Medical School.

Charles Spruck, PhD 

Spruck develops new, effective, nontoxic treatments for patients with advanced cancers. Specifically, his recent studies have focused on the potential to treat cancer with viral mimicry, which tricks the body into thinking it has a viral infection, stimulating immune responses that can help the body fight cancer and improve the effects of other treatments. 

Spruck joined the Institute in 2010. Prior to that, he held positions at the Sidney Kimmel Cancer Center and Scripps Research.

Institute News

Prestigious Forbeck Scholar Award granted to Sanford Burnham Prebys cancer researcher

AuthorMonica May
Date

December 23, 2019

Brooke Emerling, PhD, headshot

Breast cancer expert Brooke Emerling, PhD, an assistant professor at Sanford Burnham Prebys, has been named a Forbeck Scholar by the William Guy Forbeck Research Foundation. This prestigious award recognizes early-career cancer researchers for their achievements, research and dedication to the field. As an award winner, Emerling receives rare access to several three-day “think tank” events featuring the world’s top cancer clinicians and scientists.

“My goal is to create therapies that help more breast cancer patients survive cancer,” says Emerling. “The opportunity to discuss my ideas and research with the absolute leaders in my field is incredible and only accelerates my work toward that end.”

Emerling is working to find treatments for triple-negative breast cancer, which is treatable only with standard surgery, chemotherapy and radiation. The lack of specific treatments means that it has a mortality rate three times higher than the other types of breast cancer. Emerling is working to find a personalized medicine that blocks several proteins she identified that allow the triple-negative breast cancer to grow, called PI5P4Ks.

The William Guy Forbeck Research Foundation was established in 1985 by George and Jennifer Forbeck in honor of their son, who succumbed to a rare childhood cancer at age 11. Today the foundation promotes advances in cancer research through collaboration. The foundation began the Forbeck Scholar award as a way to recognize early-career cancer researchers with great future promise. Past Forbeck Scholar award winners hail from Dana-Farber Cancer Institute, the Broad Institute, Cold Spring Harbor Laboratory and other top-tier institutes.