cancer Archives - Page 6 of 11 - Sanford Burnham Prebys

Tag: cancer

Institute News

Starving the “world’s toughest cancer”

AuthorMonica May
Date

November 18, 2019

Moderator Andrea Decker of the Fleet Science Center; Darren Sigal, a clinician at Scripps Health; Russell Gold, a pancreatic cancer survivor; and Cosimo Commisso, a researcher at Sanford Burnham Prebys

Russell Gold is lucky to be alive. Only 9% of people with pancreatic cancer survive longer than five years—making it one of the deadliest cancers. This January, he will be a six-year survivor. 

To help the public better understand what makes pancreatic cancer so lethal—and how we can develop medicines so there are “more of me,” as Gold said—our Institute teamed up with the Fleet Science Center to host a panel discussion on Sunday, November 17. Gold was joined by a clinician and a scientist who both work on pancreatic cancer: Darren Sigal, MD, of Scripps Health; and Cosimo Commisso, Ph.D., an assistant professor at Sanford Burnham Prebys’ National Cancer Institute (NCI)-designated Cancer Center, respectively. 

As the speakers explained, pancreatic cancer is often difficult to diagnose because symptoms—such as pain in the abdomen, yellow skin and eyes, and weight loss—do not typically occur until the disease is advanced. As a result, pancreatic cancer is the 11th most common cancer but the second-leading cause of cancer death. More than 56,000 Americans are expected to receive a pancreatic cancer diagnosis in 2019, according to the American Cancer Society. 

Commisso, who was recently named a NextGen Star by the American Association for Cancer Research, is hopeful that his research will lead to effective treatments for pancreatic cancer. Commisso’s research focuses on how rapidly growing pancreatic tumors scavenge nutrients using an alternative supply route, called macropinocytosis. His lab has found that blocking this process, often described as “cellular drinking,” causes pancreatic tumors to shrink—indicating that the approach could lead to tumor-starving drugs. 

This event was the fourth of our five-part “Cornering Cancer” series. Register today to join us for a discussion on pediatric brain cancer in December.

Institute News

Sanford Burnham Prebys joins the fight to end cancer at Padres Pedal the Cause fundraiser

AuthorMonica May
Date

November 18, 2019

SBP pedal the cause team

Nearly everyone knows someone who has been affected by cancer: One in three Americans will be diagnosed in their lifetime. In San Diego, it’s the number one cause of death.

With the goal of improving these statistics, on November 16, 2019, more than 50 scientists, staff and supporters of Sanford Burnham Prebys joined thousands of fellow cancer fighters—including former Padre Tony Gwynn Jr. and San Diego Mayor Kevin Faulconer—at the seventh annual Padres Pedal the Cause (PPTC) fundraiser. Together, team Sanford Burnham Prebys raised more than $30,000 to accelerate collaborative cancer research taking place in San Diego.

Launched in 2013, the annual fundraiser has since expanded from a cycling-only event to include a 5K run or walk and stationary spin classes. To date, the event has raised more than $10 million to accelerate cancer cures, with 100% of the proceeds funding collaborative research taking place at four San Diego research institutes, including Sanford Burnham Prebys. Past PPTC grants have advanced our Institute’s research into cancers of the breast, skin, brain, colon, pancreas and more.

This year’s event had an ambitious goal of raising $3.3 million. Fundraising will continue until December 7, 2019; the final amount raised will be revealed on January 30, 2020, at a special check-presentation ceremony.

Want to help Padres Pedal the Cause meet its fundraising goal? Donate today.

Institute News

On the path to personalized breast cancer treatments

AuthorMonica May
Date

October 24, 2019

Fleet Cancer series-breast cancer

Ruth Claire Black wasn’t entirely surprised when she was diagnosed with breast cancer six and a half years ago. Her mother had died at age 52 of breast cancer, only two years after she was first diagnosed, Black explained at our recent Fleet Science Center event. New treatments have allowed Black’s story to differ from her mother’s—but as breast cancer experts from Sanford Burnham Prebys and UC San Diego Health explained, there is still a long way to go. 

“There is a great misconception that breast cancer is extremely easy to treat and is always cured. But the truth is that one in three women with early-stage breast cancer will relapse and eventually die from the disease,” said speaker Rebecca Shatsky, MD, a breast cancer oncologist at UC San Diego Health. “We are learning there aren’t one or two kinds of breast cancer—there are up to 30 different subtypes. To cure breast cancer, we need to look at treatments through a personalized lens.” 

Breast cancer is the second most common cancer in American women. One in eight women will be diagnosed with breast cancer in her lifetime, and more than 40,000 women die each year from the cancer. Targeted treatments—such as those that block the HER2 receptor—and hormone-based therapies have extended survival. However, 30% of people with estrogen-positive breast cancer, the most common form, eventually stop responding to standard-of-care treatments, for reasons that are largely unknown.

Speaker Svasti Haricharan, PhD, assistant professor at Sanford Burnham Prebys, is working to change these realities. Her work centers on a breast cancer subtype caused by defects in DNA repair machinery—a genomic “spell check” that normally corrects DNA copy errors during cell division. Nearly 20% of people who do not respond to breast cancer treatment have mutations in this machinery. Working with Shatsky, Haricharan’s team identifies breast cancer samples that have DNA damage repair defects. Then she tests these samples against thousands of FDA-approved treatments—with the goal of finding an effective treatment. 

For people like Black, these advances can’t come soon enough. 

“We have so much information about breast cancer. We have great diagnostics. Because of these tests, I know I’m a carrier of the BRCA2 mutation. I also know that it’s only a matter of time until my cancer returns,” said Black, who is a member of Sanford Burnham Prebys’ Community Advisory Board. “But doctors don’t know what to do with all of this information. That’s why I’m so supportive of the work taking place at Sanford Burnham Prebys. They are taking this information and doing something with it.” 

This event was the third of our five-part “Cornering Cancer” series. Register today to join us for discussions on pancreatic cancer in November and pediatric brain cancer in December. 
 

Institute News

Scientists discover new survival strategy for oxygen-starved pancreatic cancer cells

AuthorMonica May
Date

October 23, 2019

Cancer tumor

Oxygen is essential to life. When fast-growing tumor cells run out of oxygen, they quickly sprout new blood vessels to keep growing, a process called angiogenesis. 

By blocking pancreatic cancer’s oxygen-sensing machinery—the same field of research studied by the winners of the 2019 Nobel Prize in Medicine—Sanford Burnham Prebys scientists have uncovered a new way that tumors turn on angiogenesis in an animal model. The discovery, published in Cancer Research, could lead to a treatment that is given with an anti-angiogenetic medicine, thereby overcoming drug resistance. 

“Treatment resistance is a major challenge for cancer treatments that block blood vessel growth,” says Garth Powis, D.Phil., professor and director of Sanford Burnham Prebys’ National Cancer Institute (NCI)-designated Cancer Center and senior author of the study. “Our research identifies a new way angiogenesis is activated, opening new opportunities to find medicines that might make existing cancer treatments more effective.” 

Many cancer treatments work by blocking angiogenesis, which rarely occurs in healthy tissues. However, these medicines eventually stop working, and the cancer returns, sometimes in as little as two months. Scientists have been researching why this treatment resistance occurs so it can be stopped.

In this study, the scientists focused on pancreatic cancer, which is notoriously desperate for oxygen and also difficult to treat. Fewer than 10% of people diagnosed with pancreatic cancer are alive five years later. 

To see how a pancreatic tumor responds to a disruption in its oxygen supply, the Sanford Burnham Prebys researchers used a mouse model to block an oxygen-sensing protein called HIF1A—which should cripple the tumor’s growth. Instead of dying, however, after about a month the cells multiplied—indicating they had developed a new way to obtain oxygen. 

Further work revealed that the cancer cells were clear and swollen with the nutrient glycogen (a characteristic also seen in some ovarian and kidney cancers). In response to the excess glycogen, special immune system cells were summoned to the tumor, resulting in blood vessel formation and tumor survival. Each of these responses represents a new way scientists could stop pancreatic tumors from evolving resistance to treatment.

“Our team’s next step is to test tumor samples from people with pancreatic cancer to confirm this escape mechanism occurs in a clinical setting,” says Powis. “One day, perhaps we can create a second medicine that keeps anti-angiogenic drugs working and helps more people survive pancreatic cancer.”

Research reported in this press release was supported by the U.S. National Institutes of Health (NIH) (5F31CA203286, CA216424 and P30CA030199). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. The study’s DOI is 10.1158/0008-5472.CAN-18-2994. 

Institute News

Sanford Burnham Prebys scientists win two American Cancer Society awards

AuthorMonica May
Date

October 1, 2019

Robert Wechsler-Reya, PhD, Jorge Moscat, PhD, and Maria Diaz-Meco, PhD

Innovation and Collaboration of the Year Awards

The San Diego cancer community—including oncologists, oncology nurses, radiologists, cancer researchers and their friends and family—gathered on September 22 to celebrate progress made in reducing cancer deaths and recognize exceptional individuals and institutions at the inaugural American Cancer Society’s Celebration of Cancer Care Champions in San Diego.

More than 40 finalists were selected, including Sanford Burnham Prebys professors Robert Wechsler-Reya, PhD, who received the Innovation of the Year award for his team’s creation of a new model for studying a brain tumor that commonly arises in infants; and Jorge Moscat, PhD, and Maria Diaz-Meco, PhD, who received the Collaboration of the Year award for their partnership with clinicians at Scripps Clinic who uncovered a novel way to potentially identify a deadly form of colorectal cancer.

Nominations were reviewed by an independent review committee composed of representatives from 10 leading healthcare and research institutions, including Celgene, Kaiser Permanente, Rady Children’s Hospital, Scripps MD Anderson Cancer Center, Moores Cancer Center at UC San Diego Health and more. (Note: Members of the review committee did not score nominations for their own institutions.)

Read on to learn more about our award-winning research:

Innovation of the Year: A new model for studying brain tumors that strike infants
Robert Wechsler-Reya, PhD, a professor at Sanford Burnham Prebys and program director of the Joseph Clayes III Research Center for Neuro-Oncology and Genomics at the Rady Children’s Institute for Genomic Medicine, was honored for his development of a novel mouse model of a pediatric brain tumor called choroid plexus carcinoma. This tumor most commonly arises in infants under the age of one who are too young to undergo radiation treatment. Until now, drug development has been hindered by the lack of models that could help researchers better understand the cancer. Wechsler-Reya and his team have already used the model to identify potential drug compounds that may be therapeutically useful.

Collaboration of the Year (tie): Novel biomarkers to help detect a deadly colorectal cancer 
Sanford Burnham Prebys professors Jorge Moscat, PhD, and Maria Diaz-Meco, PhD; and Scripps Clinic clinicians Darren Sigal, MD, and Fei Baio, MD, were recognized for their successful collaboration. Together, the researchers revealed that loss of two genes drives the formation of the deadly serrated form of colorectal cancer—yielding promising biomarkers that could identify the tumor type. This insight could lead to the development of a diagnostic test to identify serrated colorectal cancer, a hurdle that previously limited our understanding of this deadly cancer type and the development of effective treatments. The research also identified a combination treatment that has treated the cancer in mice.

Institute News

5 things to know about immunotherapy and breast cancer

AuthorSusan Gammon
Date

September 30, 2019

Svasti Haricharan, PhD, Sanford Burnham Prebys

If you follow news about medical breakthroughs, you have undoubtedly heard about immunotherapy to treat cancer.

This form of therapy is designed to prime the body’s own immune system to fight the disease head-on. For some cancers, such as melanoma and lung cancer, immunotherapy has helped patients who once had only a life expectancy of months now live for years. But does it work for other cancers?

We sat down with Svasti Haricharan, PhD, assistant professor at Sanford Burnham Prebys and recipient of a Susan G. Komen Career Catalyst Award to discuss where we are with immunotherapy and breast cancer. Here are five things she wants us to know.

  1. As scientists, our job is to understand the biology of why immunotherapy works for some cancers but not others. Our goal is to develop approaches to expand the benefits of immunotherapy to as many patients as possible. With breast cancer, we are still in the early days, but there has been some success. Earlier this year a type of immunotherapy called an “immune checkpoint inhibitor” was approved to treat certain types of metastatic breast cancer. But immunotherapy doesn’t work—yet—for all breast cancers.
  2. No two breast cancers are alike. Even though two women with breast cancer may have the same size tumor, the individual characteristics of the tumor—the receptors, the genetics, even the way the tumor cells gather fuel to grow, can differ. Just as importantly, the way each woman’s body reacts to the growing cancer is predicated by her immune history: her exposure to immunological challenges, the strength of the immune response her body is capable of mounting, and how long she can sustain an immune response. These factors strongly influence the likelihood that a patient will respond to a specific therapy. The more we drill down on breast tumors, and the tricks they use to evade the immune system, the closer we get to outsmarting them.
  3. Today, immunotherapy seems to work best for triple negative breast cancer. Triple negative means three types of receptors—estrogen receptor, progesterone receptor and HER2—are not expressed on the cancer cells. Cancers that express these receptors are easier to treat because these receptors can be targeted directly. We believe part of the reason why immunotherapy is effective for triple negative breast cancer is because these cells can grow rapidly and produce more neoantigens—altered tumor proteins that have not previously been recognized by the immune system. So, these tumors may already have immune cells infiltrating the tumor, and when unleashed via immunotherapy, they can readily attack the cancer. 
  4. Immunotherapy—at least the immune checkpoint agents that are used today—target a protein called PD-1 found on T cells, which are the immune cells that roam the body looking for disease. PD-L1 is another protein found on some normal and some cancer cells. When PD-1 attaches to PD-L1, T cells are queued to leave the cell alone and not attack it. We believe cancer cells use PD-L1 to protect themselves from the immune system, and that cancers with large amounts of PD-L1 are the most likely to respond to checkpoint inhibitors. It’s possible that testing breast tumors for PD-L1 levels will help identify more women likely to benefit from these drugs. 
  5. Collaboration is key. Although we like to think of scientists as having “Eureka” moments, the reality is that much of the progress we make is incremental. We painstakingly plan, control and execute experiments—gathering and analyzing data to open new avenues that can be tested in the clinic. Working alongside professionals who are responsible for patient outcomes is an important part of the research spectrum. Their input provides direction for our goal of achieving cures—and a means to evaluate if what started in the lab will work in the clinic. There are nearly 300 clinical trials currently ongoing that are testing immunotherapeutic approaches for breast cancer. The information we gather from these trials helps guide the future of what we do next in the laboratory. Advances will be made, and progress is on the horizon.
     
Institute News

“We are desperate for new therapies”

AuthorMonica May
Date

September 23, 2019

Fleet Science Center: Cornering Cancer

Experts discuss AML during the Sanford Burnham Prebys community lecture series 

Bill Veljovich had never been sick in his life. “Not even joint pain,” shared the 80-year-old retired engineer at our recent Fleet Science Center discussion about acute myeloid leukemia (AML), a life-threatening type of blood cancer. He was joined by experts from Sanford Burnham Prebys and UC San Diego Health.
 
However, his doctor noticed that his white blood cells counts were off during a routine blood test. He was diagnosed with a blood cancer called myelodysplastic syndrome (MDS), which progressed to AML (this occurs in one out of three people with MDS). Fortunately, Veljovich responded well to a then off-label treatment that only recently was approved for older patients with AML. 

“The truth is, we are desperate for new therapies,” said speaker Rafael Bejar, MD, PhD, a clinician at UC San Diego who specializes in blood cancers. “AML typically occurs in people over the age of 60, who often aren’t able to tolerate intensive chemotherapies.” 

Until two years ago, the treatments for AML remained the same as those used in the 1970s: a chemotherapy combination and perhaps a bone marrow transplant. Only 24% of adults with AML remained alive five years after treatment. 

Now, thanks to foundational research that revealed the underlying genetic drivers of AML, eight new drugs have been approved in the past two years. Several more targeted therapies are nearing potential FDA approval. 

However, AML, which usually arises in cells that turn into white blood cells, is an incredibly complex and fragmented disease. Genome sequencing has revealed that more than 30 genes drive the cancer. Many different treatment types will be needed to truly conquer AML.

Peter Adams, PhD, a professor in Sanford Burnham Prebys’ National Cancer Institute (NCI)-designated Cancer Center, hopes to find a treatment that works for a broader AML population. He focuses on a protein called p53, often called the “guardian of our genome.” This protein senses DNA damage and kills the faulty cell—protecting us from developing cancer. However, to scientists’ surprise, 90% of people with AML have a normal p53 gene. 

“Emerging research suggests that AML inactivates p53 through other means,” said Adams. “My team is working to develop a drug combination that could reactivate the protective powers of p53—and thus fight AML.”

New research advances can’t come soon enough for people living with the cancer. 

“I’ve always taken the approach of learning as much as possible—and then fixing the problem,” said Veljovich, who designed and tested rocket engines before he retired. “I have learned that blood cancers are extremely complex. I wish there was a simple solution, but there isn’t. I’m grateful that we have smart folks like Dr. Bejar and Professor Adams who are working on these tough problems to find better medicines for AML.”

This event was the second of our five-part “Cornering Cancer” series. Join us for discussions on breast cancer (October 20), pancreatic cancer (November 17) and pediatric brain cancer (December 8). Register today.

Institute News

Sanford Burnham Prebys awarded Padres Pedal the Cause grants to advance cancer research

AuthorMonica May
Date

September 13, 2019

Sanford Burnham Prebys - Padres Pedal the Cause; team riders at SBP

Sanford Burnham Prebys scientists have been awarded two collaborative grants with Rady Children’s Hospital and UC San Diego Health from Padres Pedal the Cause (PPTC), an annual fundraiser that aims to accelerate cancer cures. The projects unite the complementary strengths of clinicians and scientists with the hope of uncovering new treatments for colorectal, lung, breast and prostate cancers. 

The grants stem from the record-breaking $2.94 million raised by thousands of participants in the November 2018 event. Launched in 2013, all of the proceeds raised by PPTC stay in San Diego to fund collaborative research that brings us closer to a world without cancer. Past PPTC grants have supported our Institute’s research into cancers of the breast, skin, brain, colon, pancreas and more.

The funded projects are described below:

  • Protecting the gut and halting colon cancer growth (Svasti Haricharan, PhD, and Scott Peterson, PhD, of Sanford Burnham Prebys; Soumita Das, PhD, and Pradipta Ghosh, MD, of UC San Diego Health; Debashis Sahoo, PhD, of UC San Diego Health and Rady Children’s Hospital; and Sherry C. Huang, MD, of Rady Children’s Hospital)

This project will discover and characterize a pathway in the gut that normally protects the gut barrier from microbes—and is lost during the initiation of colon cancers. The researchers aim to uncover a therapeutic target that protects the gut from cancer-causing microbes and halts the formation and progression of colon polyps. The team will also validate biomarkers for detecting polyps in the colon at high risk for progressing to colon cancer.

  • A new pathway to fractioning cancer (Michael Jackson, PhD, of Sanford Burnham Prebys; and Seth Field, MD, PhD, of UC San Diego Health)

To effectively combat cancer, therapies directed at new targets must be developed. A protein called GOLPH3 has been shown to drive the growth of several cancers, including lung, breast, prostate and colorectal cancers. This project aims to find a compound that blocks GOLPH3, which would add a unique approach to the arsenal of cancer treatments.

The seventh annual Padres Pedal the Cause event takes place on November 16, 2019. Participants will cycle, run, walk, spin or volunteer in support of a world without cancer. Join our team or volunteer at our aid station in Mountain Hawk Park in Chula Vista.

Institute News

Cancer’s final frontier: the tumor microenvironment

AuthorMonica May
Date

September 3, 2019

tumor microenvironment

Cancer researchers are setting their sights on a new kind of cancer treatment that targets the tumor’s surrounding environment, called the tumor microenvironment, in contrast to targeting the tumor directly. 

To learn more about this approach, we spoke with cancer experts Jorge Moscat, PhD, director and professor in the Cancer Metabolism and Signaling Networks Program at Sanford Burnham Prebys; and Maria Diaz-Meco, PhD, professor in the Cancer Metabolism and Signaling Networks Program at Sanford Burnham Prebys. Both scientists recently authored a review article centered on a family of cancer-linked proteins that regulate the tumor’s microenvironment. The paper was published in Cancer Cell. 

What is the tumor microenvironment exactly? 
Moscat: Just like every person is surrounded by a supportive community—their friends, family or teachers—every tumor is surrounded by a microenvironment. This ecosystem includes blood vessels that supply the tumor with nutrients; immune cells that the tumor has inactivated to evade detection; and stroma, glue-like connective tissue that holds the cells together and provides the tumor with nutrients.

Diaz-Meco: These elements are similar to the three legs of a stool. If we remove all three legs, we can deliver a deadly blow to the tumor. FDA-approved drugs exist that target blood vessel growth and reactivate the immune system to destroy the tumor. The final frontier is targeting the stroma.

When did scientists realize it’s important to focus on the tumor’s surroundings—not the tumor itself? 
Diaz-Meco: Scientists have known for more than a century that the tumor’s surroundings are different from normal cells. The tissue surrounding a tumor is inflamed—tumors are often called “wounds that never heal”—and their metabolism is radically different from healthy cells. 

Moscat: The discovery of oncogenes—genes that can lead to cancer—in the 1970s shifted the field’s focus to treatments that target the tumor directly. These targeted treatments work incredibly well, but only for a short time. Cancer researchers are realizing that tumors quickly adapt to this roadblock and become treatment resistant. In addition, many oncogenes are difficult to target, earning the title “undruggable.” As a result, cancer researchers are returning their focus to the tumor microenvironment—especially the stroma. Only a handful of stroma-targeting drugs are in development. None are FDA approved.

Which cancers could benefit most from a stroma-targeting drug? 
Moscat: Pancreatic, colorectal and liver cancers stand to benefit most from a stroma-targeting drug. For example, 90% of a pancreatic tumor consists of stroma—not cancer cells. Combined, these cancers are responsible for more than 20% of all cancer deaths in the U.S. each year. 

What is the focus of your lab’s research? 
Diaz-Meco: Our lab studies the cross talk between tumors and their environment. This conversation is very complex. In addition to “talking” with the tumor, the stroma also “speaks” with the immune system. We are working to map these interactions so we can create drugs that silence this conversation—or change it. For example, we recently showed—in a mouse model that faithfully recapitulates the most aggressive form of human colorectal cancer—that by altering the stroma’s interactions with the immune system, we might make tumors vulnerable to immunotherapy. 

What do new insights into the tumor microenvironment mean for cancer drug development? 
Moscat: It’s likely that the ultimate cancer “cure” won’t be just one drug that kills the tumor cells, but a combination of therapies. I expect this will be a three-part combination treatment that stops blood vessel growth, activates the immune system to attack the tumor and targets the stroma. 

Additionally, this research shows that experimental models of cancer drug development need to take the tumor microenvironment into account. Many current models use mice that lack an immune system—in order to get the tumor to grow—or focus on the tumor in isolation. Based on our knowledge of the tumor microenvironment, this isn’t an accurate representation of human disease. 

Diaz-Meco: In our lab, we have created several animal models of cancers that preserve the immune system and mirror tumor progression. In addition to better modeling human disease, this also allows us to study cancer from its earliest beginnings. This work could lead to early interventions—before the cancer has become large and hard to treat.

Anything else you’d like to add? 
Moscat: We are truly in the golden age of cancer biology. We understand more than we ever have before. New technologies are allowing us to obtain an unprecedented amount of information—we can even map every gene that is “turned on” in a single cancer cell. I am incredibly hopeful for the future. 

Learn more about the future of cancer treatment by attending our next “Conquering Cancer” event at the Fleet Science Center. Details. 

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.