Cancer Center Archives - Page 9 of 12 - Sanford Burnham Prebys

Tag: Cancer Center

Institute News

Fleet Science Center cancer series kicks off with lung cancer discussion

AuthorMonica May
Date

August 22, 2019

Fleet Science Center-Garth Powis, Steven Snyder, Hatim Husain

New lung cancer treatments are making a difference for patients. Pill-based, personalized medicines and immunotherapies are allowing some individuals to survive for years instead of months. Still, lung cancer remains the deadliest cancer—killing more people each year than breast, prostate and colorectal cancer combined. 

To help the public better understand the newly available medicines—and the research advances on the horizon—our Institute teamed up with the Fleet Science Center to host a panel discussion on Sunday, August 18. 

“Many people who live in San Diego aren’t aware of the incredible research advances taking place in their backyard, especially in cancer,” said speaker Garth Powis, D. Phil., professor and director of Sanford Burnham Prebys’ National Cancer Institute (NCI)-designated Cancer Center (on left). “We hope this discussion and future events will help more people understand cancer research and the breakthroughs that might come from their own community.”

Powis was joined by Hatim Husain, MD, a clinician at UC San Diego (on right); and Steven Snyder, PhD, president and CEO of the Fleet Science Center (center), who moderated the discussion. The speakers described how targeted treatments, which are only prescribed if a patient’s tumor has a specific mutation; and immunotherapies, which harness a patient’s immune system to melt the tumor, are extending survival for lung cancer patients. Husain expressed excitement surrounding new blood tests to detect lung cancer—which he hopes will be more commonplace in five to ten years. The speakers also noted that advances made in lung cancer have the potential to extend to other tumor types. 

“Many of the mutations that drive lung cancers are found in other tumors,” said Husain. “Targeted treatments that shrink lung tumors are being studied broadly in patients with a variety of cancers.” 

Powis and Husain also touched on their own collaboration to learn how lung cancer becomes resistant to treatment. Fluid buildup in the pleural space, the area between the lungs and chest wall, is often removed during routine checkups to help patients breathe. Working with Husain, Powis’ team is tracking the cellular and molecular makeup of this pleural fluid over the course of the disease. By regularly analyzing this fluid, they hope to gain insights into how lung cancer becomes treatment resistant and how it can be stopped.

“Scientists are getting close to mapping all of the mutations that drive lung cancer growth,” said Powis. “One day, patients may take one pill that contains all the anti-cancer compounds they need to fight the tumor.”

Upcoming topics in the series include breast, brain, and pancreatic cancer and more. The events will take place from 7:00 p.m. to 8:30 p.m. on select Sundays in the Heikoff Giant Dome Theater at the Fleet Science Center in San Diego. Space is limited. Reserve your ticket today. 

Institute News

Solar power gone awry

AuthorZe’ev Ronai, PhD
Date

July 29, 2019

towel on beach - sun exposure - melenoma

Are you enjoying the summer? Out grilling, swimming and hiking? Beware: those sunny days may come with a cost. 

When the sun’s rays touch your skin, they don’t stop there. Ultraviolet (UV) light enters your cells, and photons—tiny particles of light—landing on the proteins and DNA in your cells. With just the right amount of activation energy, proteins change their shape and function, and your DNA becomes damaged, or as we say—mutated. Under normal circumstances, cells use special proteins to repair mutated DNA, but when the repair proteins are damaged, DNA mutations become permanent.

Certain DNA segments called genes are more vulnerable to mutations than others. The BRAF gene, which normally makes a protein that controls cell growth, is mutated in more than 50% of melanomas—the most dangerous type of skin cancer. Melanoma appears when BRAF mutations crop up with other mutations in the same skin cell. For patients with these tumors, drugs that target BRAF and related proteins are often successful at slowing or stopping melanoma growth—but only for a while.

Unfortunately, patients who initially respond to such targeted therapy often relapse. Some patients relapse because their tumors generate a new mutation, making it resistant to the drug.  Overall, it may be only a small fraction of cells within the original tumor that develop resistance. So although 99.5% of the cancer cells in a tumor may have a mutated BRAF gene, the other 0.5% can harbor different mutations that either evolved during therapy or were present in the first place, but didn’t drive the initial tumor. For these patients, the bulk of BRAF mutant cancer cells are killed with targeted therapy, but another melanoma can evolve from the remaining 0.5%. This is why combination therapy, where drugs aim for multiple targets, are important.

But targeting every single mutation in a tumor may not be feasible. There will always be a fraction of cells with a different mutation that evolves, making patients vulnerable to a relapse. This is where attacking the tumor from another angle comes into play.  

Checkpoint immunotherapies—which have revolutionized the treatment of melanoma—attack tumors independent of their mutational makeup. They work by loosening the brakes of the immune system—brakes that normally prevent immune cells from attacking our own self. Tumors are very good at hiding from the immune system, but with the brakes released, tumors become exposed and are successfully attacked by the immune system, irrespective of their mutational makeup. 

But not everyone responds to immunotherapy—and we don’t yet know why. Is it the tumor? Is it the patient’s immune system? There is even evidence that the gut microbiome plays a role. Once we understand why some patients respond and or stop responding to immunotherapy, we can improve selection of patients for therapy, the effectiveness of these treatments and the possible combinations that work best. 

So where is skin cancer therapy headed? A combination of checkpoint immunotherapy with targeted therapies, as well as some new tricks we are learning, such as coaching tumor cells to be better recognized by the immune system, are moving the needle.

In my lab at Sanford Burnham Prebys we are dissecting the cell signals that drive cancer. Our studies are guided by data derived from patients’ tumors, coupled with advanced bioinformatics. We seek to understand how physiological processes are modified as cancer develops and how they can be exploited for cancer therapy. For example, we recently demonstrated a connection between the composition of the gut microbiome and the response to immunotherapy, establishing new paradigms, but raising important new questions. Can we better predict who will respond to immunotherapy? Can we enhance the response to immunotherapy by manipulating the gut microbiome? Can we make tumors that don’t initially respond start responding to immunotherapy? The bar is always raised, as one discovery opens so many new avenues to explore and advance our understanding, aspects that members of my lab are working hard on to answer.  

Yes—we are making progress. But preventing the initial sun exposure by using protective gear and sunscreens is needed now as much as ever.

Ze’ev Ronai, PhD, professor in Sanford Burnham Prebys’ Tumor Initiation and Maintenance Program, is a world-renowned cancer research expert and recipient of the Lifetime Achievement Award from the Society of Melanoma Research. The award recognizes his major and impactful contributions to melanoma research over the course of his career.

Institute News

Capturing circulating cancer cell clusters using a new microfluidic device

AuthorMonica May
Date

July 16, 2019

cancer cell clusters

Nearly 90 percent of cancer deaths are a result of metastases, when tumors spread to other vital organs. Researchers are learning that cancer metastases are not due to individual cells but rather distinct clusters of cancer cells that circulate and metastasize to other organs. However, obtaining these clusters to learn more about the metastatic process has proved difficult. 

Now, in a study published in AIP Advances, researchers from Sanford Burnham Prebys, San Diego State University and TumorGen MDx™ have described a new microfluidic device that captures circulating cancer cell clusters. 

“The reason for such little research activity on cancer clusters is the overwhelming difficulty of capturing these extremely rare samples from a patient’s blood sample,” says Peter Teriete, PhD, a study author and a research assistant professor at Sanford Burnham Prebys. “But we realized that if we’re ever going to understand the complex process of cancer metastasis, we’d need to develop a tool to easily find these clusters.”

To do so, the researchers first identified the basic requirements essential to collecting useful information from isolated cancer cell clusters. It involves a sample size large enough to likely contain appreciable numbers of cancer cell clusters (about 10 milliliters of whole blood), as well as using whole blood to preserve rare circulating clusters. Whole blood, however, requires special channel-coating procedures that reduce nonspecific binding properties to prevent biofouling. And the device channel dimensions must be of a suitable size to accommodate single cells and cancer cell clusters of varying diameters.

“Our device’s channel design had to generate microfluidic flow characteristics suitable to facilitate cell capture via antibodies within the coated channels,” Teriete explains. “So we introduced microfeatures—herringbone recesses—to produce the desired functionality. We also developed a unique alginate hydrogel coating that can be readily decorated with antibodies or other biomolecules. By connecting bioengineering with materials science and basic cancer biology, we were able to develop a device and prove that it performs as desired.”

The group’s microfluidic device brings a new therapeutic strategy to the fight against cancer metastasis. Capturing viable circulating cancer stem cell clusters directly from cancer patients is a novel approach for the development of new anti-metastatic drug therapies.

“Drug development that specifically targets distant metastases has been greatly restricted due to the lack of adequate tools that can readily access the metastatic cells responsible for cancer’s dissemination,” says Teriete. “Our microfluidic device will provide cancer researchers with actual human cancer cell clusters so they can begin to understand the critical mechanisms involved with metastasis and develop highly effective drugs that ultimately can save more cancer patients’ lives.”

Story materials courtesy of the American Institute of Physics. Content has been edited for style and length. 

Institute News

Stepping into a scientist’s shoes at the Cancer Center Open House

AuthorMonica May
Date

June 20, 2019

Sanford Burnham Prebys Cancer Center Open House poster presentation

Cancer research has led to new insights and novel medicines that have transformed the lives of parents, grandparents and children around the world. Yet cancer remains the number-one cause of death in San Diego (nationally, it is the second-leading cause of death). The quest for new and better treatments—and a world free of the disease—remains urgent. 

On June 13, 2019, the San Diego community—including many cancer survivors and their loved ones—had a unique opportunity to step into the shoes of a cancer researcher and see how cancer drugs are discovered at the open house of our NCI-designated Cancer Center. The facility is one of only seven National Cancer Institute (NCI)–designated basic research cancer centers in the nation. 

Following an introduction by Garth Powis, D. Phil., professor and director of the NCI-designated Cancer Center, guests embarked on guided lab tours. Attendees discovered how we’re working to find better ways to combat cancer, viewed highly specialized equipment—such as machines that model the low-oxygen environment surrounding a tumor—and donned lab coats to catch a glimpse of our ultra-high-throughput drug screening robot in action at our Prebys Center for Drug Discovery. The state-of-the-art technology at the Prebys Center can screen hundreds of thousands of potential drug candidates in one run, accelerating the time it takes to find new, promising compounds that may become tomorrow’s cancer treatments.

Guests also learned how San Diego, with a multitude of world-class research institutes, universities and biotech companies, is shaping the future of cancer diagnosis and treatment. And our Community Advisory Board, comprised of cancer research advocates and cancer survivors, were on hand to share the importance of factoring in patients’ perspectives as breakthrough science moves from “bed to bedside.”

See the science in action in these event photos.

Missed the event? We hope you can join us at our next open house in November. The event is free and open to the public. Check for more details at sbpdiscovery.org/calendar.

Many thanks to our Community Advisory Board (CAB), the host of the open house. Comprised of nine cancer research advocates, including many cancer survivors, this committee strives to create a dialogue between our scientists and the community. We are grateful for CAB’s efforts surrounding the event, which included helping our scientists prepare lay-friendly presentations and posters that were critical to the event’s success.

Interested in keeping up with our latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries.

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AACR selects Sanford Burnham Prebys scientist as NextGen Star

AuthorMonica May
Date

April 4, 2019

Cosimo Commisso, PhD, Sanford Burnham Prebys

The American Association for Cancer Research (AACR) has named Cosimo Commisso, PhD, assistant professor in Sanford Burnham Prebys’ NCI-designated Cancer Center, as a NextGen Star. 

The program strives to increase the visibility of early career scientists at the organization’s annual meeting—one of the year’s largest gatherings of cancer researchers—and to support their professional development and advancement. The 2019 AACR Annual Meeting was held from March 29 to April 3 in Atlanta and attracted more than  21,000 scientists and clinicians. 

As a NextGen star, Commisso was featured on AACR’s website and was invited to give a presentation during a special “NextGen Star” session. He also presented in a session titled, “Features and Functions of the Pancreatic Tumor Microenvironment.” Both talks were well attended.

Commisso’s presentations focused on pancreatic cancer, a deadly and difficult-to-detect tumor. Less than 10 percent of people who are diagnosed with pancreatic cancer are alive five years later. More than 56,000 Americans are expected to be diagnosed with pancreatic cancer in 2019 and its incidence is on the rise. Pancreatic cancer is on track to become the second leading cause of cancer-related death in the U.S. next year, according to the Pancreatic Cancer Action Network. New studies have linked military service to an increased risk of pancreatic cancer, perhaps due to exposure to herbicides such as Agent Orange.

Commisso is working to halt pancreatic cancer growth by studying the way cells internalize nutrients, called macropinocytosis. In this process, cells extend their membranes to capture nutrients in their surrounding environment—similar to how humans swallow a pill by encasing it in water. 

“We’ve discovered that pancreatic tumors that have a mutation in the RAS gene—which occurs in almost all cases—fuel their growth by kicking macropinocytosis into overdrive,” says Commisso. “By halting macropinocytosis, essentially cutting off the cancer cells’ fuel supply, we hope we can develop effective, much-needed treatments for pancreatic cancer.”

In his NextGen Star presentation, Commisso detailed how macropinocytosis is dialed up or down depending on nutrient availability. Studies performed by Szu-Wei Lee, PhD, a postdoctoral fellow in the Commisso laboratory, indicate that RAS-mutated pancreatic tumors use two forms of macropinocytosis—one that is “always on” (constitutive) and another that is nutrient dependent.

“Uncovering the molecular differences between these two pathways could yield personalized targets that selectively target pancreatic cancer cells,” says Commisso. “In addition to pancreatic tumors, new evidence shows that lung, prostate and bladder cancers highjack macropinocytosis to keep growing. This means our work in pancreatic cancer may also lead to new treatments for these other tumor types.”

Watch Dr. Commisso explain his lab’s focus

View the full list of the NextGen stars 

Interested in keeping up with SBP’s latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries below.

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Padres Pedal the Cause presents record-breaking check for nearly $3 million to fund local cancer research

AuthorMonica May
Date

January 29, 2019

Padres Pedal the Cause-Check presentation-SBP

Local cancer research just got a big boost. 

On Thursday, January 24, SBP president Kristiina Vuori, MD, PhD, joined leaders from Moores Cancer Center at UC San Diego Health, Salk Institute for Biological Studies and Rady Children’s Hospital–San Diego to help Padres Pedal the Cause (PPTC) reveal that this year’s event raised a record-breaking $2.9 million for local cancer research. The leaders joined executive director Anne Marbarger onstage to receive the official check. 

This year’s event—which invited participates to cycle, spin, run or walk—had more than 2,500 participants, an increase of 35 percent. Total fundraising grew by 22 percent. SBP has participated in the event since its inception; and this year our team of more than 60 scientists, staff and SBP supporters raised more than $30,000 for the cause. Since the inaugural ride six years ago, PPTC has raised more than $10 million.

Nearly 300 of the event’s participants, including Tony Gwynn Jr., Pedal founders Bill and Amy Koman, San Diego business leaders, and top donors and fundraisers, gathered at the Del Mar racetrack to witness the funding reveal and check presentation in person. 

Gwynn shared a moving story about his father’s battle with salivary cancer, a journey he still finds difficult to recount. “If he saw this progress, he would be smiling today,” he said. 

A full 100 percent of the proceeds fund collaborative research taking place at the four San Diego research institutes. Past PPTC grants have accelerated SBP’s research into cancers of the breast, skin, brain, colon, pancreas and more. This year’s grant announcement will be revealed in the spring. 

In the meantime, make sure to mark your calendars for the 2019 event, which will take place on Saturday, November 16. Registration will open in mid-April.

Interested in keeping up with SBP’s latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries. 

Institute News

SBP scientist awarded Susan G. Komen® and NIH grants to advance breast cancer research

AuthorMonica May
Date

October 25, 2018

Svasti Haricharan, PhD

Breast cancer remains the second most common cancer for American women. While treatment advances are being made, more research is needed. Current treatments don’t work for every woman.
 
Now, breast cancer researcher Svasti Haricharan, PhD, assistant professor at Sanford Burnham Prebys Medical Discovery Institute (SBP), has been awarded more than half a million dollars in combined grants from Susan G. Komen® and the National Institutes of Health (NIH). 

This funding will advance Haricharan’s breast cancer research—including developing a diagnostic test that could guide therapeutic options—and allow her to apply lessons from breast cancer to additional cancers. 

Susan G. Komen grant

The majority of women diagnosed with breast cancer have the estrogen-positive (ER-positive) form, meaning the tumor grows in response to estrogen. Hormone therapies (anti-estrogen drugs) that block estrogen—and thus stop the tumor from growing—are available. However, this treatment doesn’t work for 40 percent of women with ER-positive breast cancer. 

“Currently, doctors are unable to predict which ER-positive patients will respond to treatment—so an estrogen-blocking medicine is given, and a ‘wait and see’ approach is taken to see if the treatment will work,” says Haricharan. “However, if a woman doesn’t respond to treatment, during this time the tumor is instead still growing and may metastasize—when it becomes deadlier and even harder to treat. Knowing upfront if an individual will respond to treatment allows doctors to skip a treatment that won’t work and move immediately to prescribing a medicine that may be effective.” 

Haricharan’s previous work found that about one-third of women with ER-positive breast cancer who were treatment resistant had a mutation in DNA damage-repair genes—providing a potential biomarker that could predict who would respond to treatment. 

Luckily, an FDA-approved test that detects defects in DNA damage repair is currently available for colorectal cancer patients. The grant from Susan G. Komen enables Haricharan to evaluate whether this same test can be used to predict response to anti-estrogen drugs in ER-positive breast cancer patients. 

Additionally, research from Haricharan’s previous lab identified a medicine that is FDA approved for advanced or metastatic breast cancer patients and holds potential as a frontline breast cancer treatment (the first treatment prescribed by a doctor). The grant will allow her to bring these pieces of the puzzle together—developing a predictive test and evaluating a potential alternative treatment. 

“Because an FDA-approved test is already on the market, development of a breast cancer test to predict response to hormone therapy may be accelerated. I’d estimate my work could enable a commercially available test in less than five years—though of course a real-world assessment will be needed to obtain doctor and insurance-company approval,” says Haricharan. “Pairing a new test that can guide therapeutic options with a potential treatment would be an important advance for ER- positive breast cancer. I want to express my greatest thanks to Susan G. Komen for funding this important work.” 

NIH grant

Haricharan was also awarded a K22 grant from the NIH, which helps early-career scientists transition to independent research careers. This grant will allow her to apply insights from her breast cancer research to additional cancers. 

Studies have indicated there are links between the growth of colorectal and bladder tumors and estrogen response. While women are less frequently diagnosed with bladder cancer, they tend to have a greater risk of dying from the disease. In contrast, estrogen may have a protective effect on the development of colorectal cancers. 

The NIH grant will enable Haricharan to work to better understand the role DNA damage-repair mutations may play in response to standard-of-care treatment for ER-positive breast, colorectal and bladder cancers. Once this role has been established, the grant will help fund a search for effective targeted treatments.

“Both bladder and colorectal cancers are often caught at a late stage, when the cancer is harder to treat,” says Haricharan. “I hope that this research will ultimately yield tests that can predict response to treatment and guide treatment options for these deadly cancers.” 

Link to the NIH grant: A pan-cancer role for MUTL loss in inducing treatment resistance 

More information about the Susan G. Komen grant: Susan G. Komen Announces $26 Million Investment in New Research to Find Solutions for Aggressive and Metastatic Breast Cancers, and to Help Communities Most at Risk
 

Interested in keeping up with SBP’s latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries.

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5 things to know about acute myeloid leukemia (AML)

AuthorMonica May
Date

September 26, 2018

Ani Deshpande, PhD

It’s no surprise that our blood is important. The cargo it transports—nutrients, infection-fighting cells, clotting factors, waste and more—keeps our body healthy and running smoothly. So when blood cells don’t form properly, serious cancers can occur. 

Scientists divide blood cancers into three broad categories—leukemia, lymphoma and myeloma—based on the cell type affected. Leukemias disrupt white blood cell production; lymphomas affect the lymphatic system, which removes extra fluid from the body; and myelomas affect plasma cells, which produce intruder-fighting antibodies. There are many subsets within each category.

In honor of Blood Cancer Awareness Month, we spoke with Sanford Burnham Prebys Medical Discovery Institute scientist Ani Deshpande, PhD, to learn more about the blood cancer he studies: acute myeloid leukemia (AML). Of the 60,000 American children and adults diagnosed with leukemias each year, nearly 30 percent will have AML. 

  • Most patients receive the same treatment used nearly five decades ago. Drug developers have created medicines for AML patients who have certain changes in their DNA, called mutations. But the majority of AML patients receive the treatments used in the ’70s: chemotherapy, radiation and possibly a bone marrow transplant. This isn’t last-decade science; it’s last-century science.
  • It’s deadly. The five-year survival rate for adults with AML—the number of people who are alive five years after diagnosis—is only 24 percent, according to the American Cancer Society. New medicines and treatment approaches are urgently needed. 
  • Sequencing is making strides. Now, scientists can sequence patients’ genomes to learn the underlying mutation driving their cancer. This technology has advanced our understanding to the point that about 60 to 70 percent of the time, their doctor knows the mutation involved. Our new problem is that we don’t have effective medicines that target most of these mutations. 
  • Speaking of sequencing. Because of DNA sequencing, we also know that a large fraction of the mutations in AML are epigenetic changes—alterations that affect which genes turn on but don’t change the DNA itself.

To better understand how epigenetic changes work, imagine a cookbook. If recipes are DNA,               then epigenetic changes are bookmarks. These bookmarks signal whether the recipe should be made or not, without altering the underlying text of the recipe.

Our laboratory is studying the epigenetic changes that drive AML. Our hope is that once we identify these changes, we can create drugs that restore the epigenome to its normal state. 

  • There is hope. After nearly 50 years of little progress, four new drugs have been approved for AML over the last 18 months. And there are currently more than 330 clinical trials enrolling patients in the U.S., so more treatments may soon follow. 

Resources:

Interested in keeping up with Sanford Burnham Prebys’ latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries.
 

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V Foundation grant to Ani Deshpande, PhD, supports pioneering research toward better leukemia treatments

AuthorJessica Moore
Date

December 2, 2016

ani deshpanda, ph.d.

Patients with a rare type of leukemia called acute promyelocytic leukemia (APL) have better outcomes than most leukemias because they can be treated with a very effective drug that converts their cancer cells back to normal. This success has convinced many cancer researchers that there’s a way to do the same for other leukemias. And with his recently awarded funding from the V Foundation, Ani Deshpande, PhD, assistant professor at Sanford Burnham Prebys Medical Discovery Institute, can now find targets for future drugs to do just that.

“We’re aiming to rehabilitate the cancer cells, in a sense, instead of destroying them,” said Deshpande. “The advantage to this approach is that, unlike conventional chemotherapy, it doesn’t harm normal cells, so it should have far fewer toxic side effects.”

Deshpande aims to make a big impact with this work—he’s first focusing on a group of acute myeloid leukemia (AML) with very poor survival outcomes. Worse, these leukemias, characterized by fusions of chromosome 11 with another partner chromosome, are especially common among children and infants.

This subgroup of AML is trickier than APL, where the product of the gene created by the chromosomal rearrangement directly blocks the cancer cells from becoming their normal type. In contrast, in the leukemias that Deshpande’s lab studies, the change in the cells’ programming is more complex. The mutation they carry alters the regulation of other genes, but which of these prevent AML cells from becoming normal blood-forming cells is largely unknown.

Fortunately, Deshpande is an expert in studying leukemic gene regulation. His lab specializes in epigenetics—analyzing the chemical tags on genes that influence their activity. The V Foundation funds will allow Deshpande’s team to apply an advanced sequencing-based approach to identify and validate potential targets for drugs that restore cancer cells’ epigenome to normal.

“This grant not only lets me expand my lab by hiring a new postdoc, but it also means I can take risks that wouldn’t be possible if I were proposing research to the NIH,” commented Deshpande. “I’m confident that we’ll get exciting results. The tools we’re using have gotten exponentially better over the last few decades, so we’re poised for a breakthrough.”

About the V Foundation

The V Foundation for Cancer Research was founded by ESPN and legendary basketball coach Jim Valvano with one goal in mind: to achieve victory over cancer. Since its start in 1993, the V Foundation has awarded over $170 million in cancer research grants nationwide.

Watch Dr. Deshpande talk about why foundation funding is important:

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Hearst Foundation’s new fellowship funds innovative research to fight breast cancer

AuthorJessica Moore
Date

October 20, 2016

Charles Spruck, PhD, and Mark Goldberg, PhD

Mark Goldberg, PhD, is working on a potential way to turn cancer stem cells into harmless cells. He and his advisor, Charles Spruck, PhD, assistant professor in the NCI-designated Cancer Center, are optimistic that they could turn this approach into new drugs that prevent breast cancer from returning.

Goldberg is supported by the first-ever research fellowship given by the David Whitmire Hearst Jr. Foundation. The funds were awarded specifically for this groundbreaking project.

“Breast cancer can spread to other organs very early, sometimes even before it’s detected,” said Spruck. “Those micrometastases—just one or a few cells—lie dormant for years, and are insensitive to anticancer drugs. Our goal is to switch those cells to a normal cell type that can’t generate a tumor.”

In as-yet unpublished research, Spruck’s lab recently discovered a protein that’s crucial for pre-cancerous cells to begin growing aggressively and out of control. Goldberg will use animal models of breast cancer to show that genetically inactivating this protein prevents secondary tumors from forming. The next step is to search for candidate drugs that inhibit the protein.

“If we find blockers of this protein that controls progression to malignancy, they could be given to breast cancer patients, after standard treatment has eradicated their primary tumor, to eliminate any remaining cancer stem cells,” added Spruck.

Goldberg’s background in bioengineering gives him a fresh perspective on cancer research. As a PhD student at Caltech, he designed implantable glucose and ion sensors using microfluidics and nanophotonics. That experience gives him a flexible, solutions-oriented approach to designing experiments.

“During Mark’s interview—the first time I met him—we came up with a really exciting way to apply what he was working on at Caltech to cancer research,” Spruck commented. “That kind of creative thinking and insight is invaluable—it’s why I hired him for this fellowship-supported spot.

“Because this research is so early-stage, it’s hard to get funded through traditional avenues. The Hearst Foundation fellowship allows us to get the evidence that this strategy works. That data will be key to getting the support we need for the drug discovery phase.”