UC San Diego Moores Cancer Center

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ucsdhealthsciences:

Enzyme Controlling Metastasis of Breast Cancer Identified
Researchers at the University of California, San Diego School of Medicine have identified an enzyme that controls the spread of breast cancer.  The findings, reported in the current issue of PNAS, offer hope for the leading cause of breast cancer mortality worldwide. An estimated 40,000 women in America will die of breast cancer in 2014, according to the American Cancer Society.
“The take-home message of the study is that we have found a way to target breast cancer metastasis through a pathway regulated by an enzyme,” said lead author Xuefeng Wu, PhD, a postdoctoral researcher at UC San Diego.
The enzyme, called UBC13, was found to be present in breast cancer cells at two to three times the levels of normal healthy cells. Although the enzyme’s role in regulating normal cell growth and healthy immune system function is well-documented, the study is among the first to show a link to the spread of breast cancer.
Specifically, Wu and colleagues with the UC San Diego Moores Cancer Center found that the enzyme regulates cancer cells’ ability to transmit signals that stimulate cell growth and survival by regulating the activity of a protein called p38 which when “knocked down” prevents metastasis. Of clinical note, the researchers said a compound that inhibits the activation of p38 is already being tested for treatment of rheumatoid arthritis.
In their experiments, scientists took human breast cancer cell lines and used a lentivirus to silence the expression of both the UBC13 and p38 proteins. These altered cancer cells were then injected into the mammary tissues of mice.  Although the primary tumors grew in these mice, their cancers did not spread.
“Primary tumors are not normally lethal,” Wu said. “The real danger is cancer cells that have successfully left the primary site, escaped through the blood vessels and invaded new organs. It may be only a few cells that escape, but they are aggressive. Our study shows we may be able to block these cells and save lives.”
Pictured: A tumor with reduced levels of enzyme UBC13 (top) and a control tumor (bottom) that has spread to the lungs.

ucsdhealthsciences:

Enzyme Controlling Metastasis of Breast Cancer Identified

Researchers at the University of California, San Diego School of Medicine have identified an enzyme that controls the spread of breast cancer.  The findings, reported in the current issue of PNAS, offer hope for the leading cause of breast cancer mortality worldwide. An estimated 40,000 women in America will die of breast cancer in 2014, according to the American Cancer Society.

“The take-home message of the study is that we have found a way to target breast cancer metastasis through a pathway regulated by an enzyme,” said lead author Xuefeng Wu, PhD, a postdoctoral researcher at UC San Diego.

The enzyme, called UBC13, was found to be present in breast cancer cells at two to three times the levels of normal healthy cells. Although the enzyme’s role in regulating normal cell growth and healthy immune system function is well-documented, the study is among the first to show a link to the spread of breast cancer.

Specifically, Wu and colleagues with the UC San Diego Moores Cancer Center found that the enzyme regulates cancer cells’ ability to transmit signals that stimulate cell growth and survival by regulating the activity of a protein called p38 which when “knocked down” prevents metastasis. Of clinical note, the researchers said a compound that inhibits the activation of p38 is already being tested for treatment of rheumatoid arthritis.

In their experiments, scientists took human breast cancer cell lines and used a lentivirus to silence the expression of both the UBC13 and p38 proteins. These altered cancer cells were then injected into the mammary tissues of mice.  Although the primary tumors grew in these mice, their cancers did not spread.

“Primary tumors are not normally lethal,” Wu said. “The real danger is cancer cells that have successfully left the primary site, escaped through the blood vessels and invaded new organs. It may be only a few cells that escape, but they are aggressive. Our study shows we may be able to block these cells and save lives.”

Pictured: A tumor with reduced levels of enzyme UBC13 (top) and a control tumor (bottom) that has spread to the lungs.

Exercise and Cancer
For years we’ve known that exercise is an important part of a healthy lifestyle by keeping us strong and reducing the risk of heart disease and diabetes. It releases endorphins that make us feel better, physically and mentally – even if when we’re huffing and puffing we’re feeling a little tired.
We also know that physical activity is associated with reduced risk of colon, breast, uterine, lung and prostate cancers. But having cancer doesn’t change the equation. Indeed, for patients diagnosed with and treated for cancer, a life of regular physical activity can become even more critical to having a life with quality.
Physical activity is a critical component of energy balance, a term researchers use to describe how weight, diet and physical activity influence health. Indeed, researchers at UC San Diego Moores Cancer Center are currently conducting a pair of studies to assess the effects of healthy diets and exercise programs on women at risk of breast cancer and breast cancer survivors. 
In a seminal series of papers published in 2012 in the journal Lancet, scientists from multiple institutions, including the UC San Diego, concluded that physical inactivity could explain more than 5 million deaths worldwide each year — a number comparable to mortality figures associated with smoking.
“A surprising finding was that inactivity explains 10 percent of deaths from both breast cancer and prostate cancer,” said Jim Sallis, PhD, Distinguished Professor of Family and Preventive Medicine and director of the Active Living Research program at UC San Diego. “Thus physical inactivity is a major contributor to common cancers of men and women.”
Regular exercise prevents obesity, which increases a person’s risk of a host of different cancers. It helps reduce inflammation, also linked to cancer, while boosting the body’s immune system function, which helps prevent cancer.
How much exercise do you need?The Centers for Disease Control and Prevention broadly recommends adults engage in “moderate-intensity physical activity for at least 150 minutes per week” (about 30 minutes per day) or “vigorous-intensity” exercise for at least 75 minutes per week. The former is defined as activities like walking briskly, dancing or riding a bike on flat terrain. The latter refers to stuff like race-walking, high-impact aerobics, robustly climbing stairs or participating in fast-moving sports like basketball or soccer.
The best time to begin a lifelong anti-cancer exercise program is today, right now. Once you’ve been diagnosed with cancer, the best time is still today, right now. Often, patients become sedentary after a cancer diagnosis and treatment. They’re going through or have been through a lot. It might seem too much to launch into an exercise regimen. People tend to slow down.
Don’t.
As contrary as it may seem, physical activity is the most effective long-term solution to fatigue, a common characteristic of cancer and its treatment. How and how much you exercise while undergoing cancer treatment depends upon you, your condition, treatment protocols and your doctor. You may need to take special care to monitor issues like blood counts, hydration or new or unexplained symptoms.
Exercise for some cancer patients can carry a slightly higher risk for heart problems. You’ll likely need to adjust your intensity — at least at first. You’ll have to adapt. For example, older cancer patients with impacted bones or problems like arthritis or peripheral neuropathy (numbness in hands or feet) should only do exercises with minimal risk of falling or injury. Patients undergoing radiation should not expose treated skin to excessive sunlight or chlorine in swimming pools.
Regular exercise boosts cancer survivorship. One study, for example, found that women diagnosed with breast cancer who exercised moderately (the equivalent of walking three to five hours per week at an average pace) had better survival rates than comparable sedentary patients. Physical activity has also been shown to help patients cope psychologically with the rigors of their disease and treatment.

 

Exercise and Cancer

For years we’ve known that exercise is an important part of a healthy lifestyle by keeping us strong and reducing the risk of heart disease and diabetes. It releases endorphins that make us feel better, physically and mentally – even if when we’re huffing and puffing we’re feeling a little tired.

We also know that physical activity is associated with reduced risk of colon, breast, uterine, lung and prostate cancers. But having cancer doesn’t change the equation. Indeed, for patients diagnosed with and treated for cancer, a life of regular physical activity can become even more critical to having a life with quality.

Physical activity is a critical component of energy balance, a term researchers use to describe how weight, diet and physical activity influence health. Indeed, researchers at UC San Diego Moores Cancer Center are currently conducting a pair of studies to assess the effects of healthy diets and exercise programs on women at risk of breast cancer and breast cancer survivors. 

In a seminal series of papers published in 2012 in the journal Lancet, scientists from multiple institutions, including the UC San Diego, concluded that physical inactivity could explain more than 5 million deaths worldwide each year — a number comparable to mortality figures associated with smoking.

“A surprising finding was that inactivity explains 10 percent of deaths from both breast cancer and prostate cancer,” said Jim Sallis, PhD, Distinguished Professor of Family and Preventive Medicine and director of the Active Living Research program at UC San Diego. “Thus physical inactivity is a major contributor to common cancers of men and women.”

Regular exercise prevents obesity, which increases a person’s risk of a host of different cancers. It helps reduce inflammation, also linked to cancer, while boosting the body’s immune system function, which helps prevent cancer.

How much exercise do you need?The Centers for Disease Control and Prevention broadly recommends adults engage in “moderate-intensity physical activity for at least 150 minutes per week” (about 30 minutes per day) or “vigorous-intensity” exercise for at least 75 minutes per week. The former is defined as activities like walking briskly, dancing or riding a bike on flat terrain. The latter refers to stuff like race-walking, high-impact aerobics, robustly climbing stairs or participating in fast-moving sports like basketball or soccer.

The best time to begin a lifelong anti-cancer exercise program is today, right now. Once you’ve been diagnosed with cancer, the best time is still today, right now. Often, patients become sedentary after a cancer diagnosis and treatment. They’re going through or have been through a lot. It might seem too much to launch into an exercise regimen. People tend to slow down.

Don’t.

As contrary as it may seem, physical activity is the most effective long-term solution to fatigue, a common characteristic of cancer and its treatment. How and how much you exercise while undergoing cancer treatment depends upon you, your condition, treatment protocols and your doctor. You may need to take special care to monitor issues like blood counts, hydration or new or unexplained symptoms.

Exercise for some cancer patients can carry a slightly higher risk for heart problems. You’ll likely need to adjust your intensity — at least at first. You’ll have to adapt. For example, older cancer patients with impacted bones or problems like arthritis or peripheral neuropathy (numbness in hands or feet) should only do exercises with minimal risk of falling or injury. Patients undergoing radiation should not expose treated skin to excessive sunlight or chlorine in swimming pools.

Regular exercise boosts cancer survivorship. One study, for example, found that women diagnosed with breast cancer who exercised moderately (the equivalent of walking three to five hours per week at an average pace) had better survival rates than comparable sedentary patients. Physical activity has also been shown to help patients cope psychologically with the rigors of their disease and treatment.

 

ucsdhealthsciences:

Finding Keys to Glioblastoma Therapeutic Resistance
Researchers at the University of California, San Diego School of Medicine have found one of the keys to why certain glioblastomas – the primary form of a deadly brain cancer – are resistant to drug therapy. The answer lies not in the DNA sequence of the tumor, but in its epigenetic signature. These findings have been published online as a priority report in the journal Oncotarget.
“There is a growing interest to guide cancer therapy by sequencing the DNA of the cancer cell,” said Clark Chen, MD, PhD, vice-chairman of Research and Academic Development, UC San Diego Division of Neurosurgery and the principal investigator of the study. “Our study demonstrates that the sensitivity of glioblastoma to a drug is influenced not only by the content of its DNA sequences, but also by how the DNA sequences are organized and interpreted by the cell.”
The team of scientists, led by Chen, used a method called comparative gene signature analysis to study the genetic profiles of tumor specimens collected from approximately 900 glioblastoma patients. The method allows investigators to discriminate whether specific cellular processes are “turned on” or “turned off” in glioblastomas. “Our study showed that not all glioblastomas are the same. We were able to classify glioblastomas based on the type of cellular processes that the cancer cells used to drive tumor growth,” said Jie Li, PhD, senior postdoctoral researcher in the Center for Theoretical and Applied Neuro-Oncology at UC San Diego and co-first author of the paper.
One of these cellular processes involves Epidermal Growth Factor Receptor (EGFR). The study revealed that EGFR signaling is suppressed in a subset of glioblastomas. Importantly, this suppression is not the result of altered DNA sequences or mutations. Instead, EGFR is turned off as a result of how the DNA encoding the EGFR gene is organized in the cancer cell. This form of regulation is termed “epigenetic.” Because EGFR is turned off in these glioblastomas, they become insensitive to drugs designed to inhibit EGFR signaling.
“Our research suggests that the selection of appropriate therapies for our brain tumor patients will require a meaningful synthesis of genetic and epigenetic information derived from the cancer cell,” said co-first author Zachary J. Taich.

ucsdhealthsciences:

Finding Keys to Glioblastoma Therapeutic Resistance

Researchers at the University of California, San Diego School of Medicine have found one of the keys to why certain glioblastomas – the primary form of a deadly brain cancer – are resistant to drug therapy. The answer lies not in the DNA sequence of the tumor, but in its epigenetic signature. These findings have been published online as a priority report in the journal Oncotarget.

“There is a growing interest to guide cancer therapy by sequencing the DNA of the cancer cell,” said Clark Chen, MD, PhD, vice-chairman of Research and Academic Development, UC San Diego Division of Neurosurgery and the principal investigator of the study. “Our study demonstrates that the sensitivity of glioblastoma to a drug is influenced not only by the content of its DNA sequences, but also by how the DNA sequences are organized and interpreted by the cell.”

The team of scientists, led by Chen, used a method called comparative gene signature analysis to study the genetic profiles of tumor specimens collected from approximately 900 glioblastoma patients. The method allows investigators to discriminate whether specific cellular processes are “turned on” or “turned off” in glioblastomas. “Our study showed that not all glioblastomas are the same. We were able to classify glioblastomas based on the type of cellular processes that the cancer cells used to drive tumor growth,” said Jie Li, PhD, senior postdoctoral researcher in the Center for Theoretical and Applied Neuro-Oncology at UC San Diego and co-first author of the paper.

One of these cellular processes involves Epidermal Growth Factor Receptor (EGFR). The study revealed that EGFR signaling is suppressed in a subset of glioblastomas. Importantly, this suppression is not the result of altered DNA sequences or mutations. Instead, EGFR is turned off as a result of how the DNA encoding the EGFR gene is organized in the cancer cell. This form of regulation is termed “epigenetic.” Because EGFR is turned off in these glioblastomas, they become insensitive to drugs designed to inhibit EGFR signaling.

“Our research suggests that the selection of appropriate therapies for our brain tumor patients will require a meaningful synthesis of genetic and epigenetic information derived from the cancer cell,” said co-first author Zachary J. Taich.

Prostate Cancer Diagnosis Improves with MRI Technology

An ultrasound machine provides an imperfect view of the prostate, resulting in an under-diagnosis of cancer, said J. Kellogg Parsons, MD, MHS, an UC San Diego Moores Cancer Center urologic oncologist. Patients who have rising prostate-specific antigen (PSA) levels, a protein that is often elevated in men with prostate cancer, but who have not been diagnosed with cancer could benefit from the new use of MRI images in combination with the traditional prostate biopsy. The technology offers physicians a new view and changes the patient experience by reducing the number of false-positive biopsies and resulting in earlier diagnosis when cancer is present, said Dr. Parsons. 

In this video, Dr. Parsons explains how the procedure works while one of his patients describes his experience with prostate cancer and diagnosis.

As science continues to reveal more about cancer, you may notice that research seems to contradict what we previously knew to be true about this disease. Read about the newest cancer research but discuss with your medical team what applies to you. Remember, no two cancers are the same. 
David A. Cheresh, PhD, Associate Director for Innovation and Industry Alliances at UC San Diego Moores Cancer Center, and colleagues have found a link between breast cancer and pregnancy. However, they caution that the findings should not be interpreted as a reason to avoid pregnancy as the cancer does not appear to be caused by the pregnancy itself. Read the full story from our sister blog.  

ucsdhealthsciences:

How Breast Cancer Usurps the Powers of Mammary Stem Cells
During pregnancy, certain hormones trigger specialized mammary stem cells to create milk-producing cells essential to lactation. Scientists at the University of California, San Diego School of Medicine and Moores Cancer Center have found that mammary stem cells associated with the pregnant mammary gland are related to stem cells found in breast cancer. 
Writing in the August 11, 2014 issue of Developmental Cell, David A. Cheresh, PhD, Distinguished Professor of Pathology and vice-chair for research and development, Jay Desgrosellier, PhD, assistant professor of pathology and colleagues specifically identified a key molecular pathway associated with aggressive breast cancers that is also required for mammary stem cells to promote lactation development during pregnancy. 
“By understanding a fundamental mechanism of mammary gland development during pregnancy, we have gained a rare insight into how aggressive breast cancer might be treated,” said Cheresh. “This pathway can be exploited. Certain drugs are known to disrupt this pathway and may interfere with the process of breast cancer progression.”
During pregnancy, a new mammary stem cell population arises, distinct from those involved in development and maintenance of the non-pregnant gland. These stem cells remodel the breasts and lactating glands in preparation for feeding the newborn child. Normally, these stem cells contribute only to early remodeling events and are switched off by the time milk production begins.
The researchers found, however, that signals regulating stem cell activation during pregnancy appear to be hijacked by cancer cells to produce faster-growing, more aggressive tumors. “This normal pathway ends up contributing to the progression of cancer,” said Desgrosellier, first author of the study.
A connection between pregnancy and breast cancer has long been known. But the association between pregnancy and breast cancer risk is complex. While having a child reduces a woman’s risk of developing breast cancer later in life, there is also an increased short-term risk for the development of a highly aggressive form of breast cancer following each pregnancy. The current study suggests that molecules important for stem cell behavior during pregnancy may contribute to these more aggressive pregnancy-associated breast cancers, a possibility the researchers plan to investigate further.
The authors are quick to point out that their findings should not be interpreted as a reason to avoid pregnancy. The signaling pathway usurped by cancer cells is not the cause of breast cancer. Rather, they said, it may worsen or accelerate a cancer caused by other factors, such as an underlying mutation or genetic predisposition.
“Our work doesn’t speak to the actual cause of cancer. Rather, it explains what can happen once cancer has been initiated,” said Cheresh. “Here’s an analogy: To get cancer, you first have to start with an oncogene, a gene that carries a mutation and has the potential to initiate cancer. Think of the oncogene as turning on a car’s ignition. The signaling pathway exploited by cancer cells is like applying gas. It gets the car moving, but it means nothing if the oncogene hasn’t first started the process.”
The researchers focused on a family of cell surface receptor proteins called integrins that act as key communications conduits, ultimately zeroing in on the role of one member of this family called beta-3 integrin. Also known as CD61, it was already linked to metastasis and resistance to cancer drugs.
Cheresh noted that CD61 represents a good marker for the incriminated signaling pathway involved in both mammary development during pregnancy and cancer. It’s easily detected and could be used to both diagnose and treat breast cancer cases. “Detecting CD61 might help doctors determine what kind of therapeutic approach to use, knowing that they might be dealing with a more aggressive yet treatable form of breast cancer. For example, there are existing drugs that block CD61 signaling, which might be another potential aspect of treatment.”

As science continues to reveal more about cancer, you may notice that research seems to contradict what we previously knew to be true about this disease. Read about the newest cancer research but discuss with your medical team what applies to you. Remember, no two cancers are the same. 

David A. Cheresh, PhDAssociate Director for Innovation and Industry Alliances at UC San Diego Moores Cancer Center, and colleagues have found a link between breast cancer and pregnancy. However, they caution that the findings should not be interpreted as a reason to avoid pregnancy as the cancer does not appear to be caused by the pregnancy itself. Read the full story from our sister blog.  

ucsdhealthsciences:

How Breast Cancer Usurps the Powers of Mammary Stem Cells

During pregnancy, certain hormones trigger specialized mammary stem cells to create milk-producing cells essential to lactation. Scientists at the University of California, San Diego School of Medicine and Moores Cancer Center have found that mammary stem cells associated with the pregnant mammary gland are related to stem cells found in breast cancer. 

Writing in the August 11, 2014 issue of Developmental Cell, David A. Cheresh, PhD, Distinguished Professor of Pathology and vice-chair for research and development, Jay Desgrosellier, PhD, assistant professor of pathology and colleagues specifically identified a key molecular pathway associated with aggressive breast cancers that is also required for mammary stem cells to promote lactation development during pregnancy. 

“By understanding a fundamental mechanism of mammary gland development during pregnancy, we have gained a rare insight into how aggressive breast cancer might be treated,” said Cheresh. “This pathway can be exploited. Certain drugs are known to disrupt this pathway and may interfere with the process of breast cancer progression.”

During pregnancy, a new mammary stem cell population arises, distinct from those involved in development and maintenance of the non-pregnant gland. These stem cells remodel the breasts and lactating glands in preparation for feeding the newborn child. Normally, these stem cells contribute only to early remodeling events and are switched off by the time milk production begins.

The researchers found, however, that signals regulating stem cell activation during pregnancy appear to be hijacked by cancer cells to produce faster-growing, more aggressive tumors. “This normal pathway ends up contributing to the progression of cancer,” said Desgrosellier, first author of the study.

A connection between pregnancy and breast cancer has long been known. But the association between pregnancy and breast cancer risk is complex. While having a child reduces a woman’s risk of developing breast cancer later in life, there is also an increased short-term risk for the development of a highly aggressive form of breast cancer following each pregnancy. The current study suggests that molecules important for stem cell behavior during pregnancy may contribute to these more aggressive pregnancy-associated breast cancers, a possibility the researchers plan to investigate further.

The authors are quick to point out that their findings should not be interpreted as a reason to avoid pregnancy. The signaling pathway usurped by cancer cells is not the cause of breast cancer. Rather, they said, it may worsen or accelerate a cancer caused by other factors, such as an underlying mutation or genetic predisposition.

“Our work doesn’t speak to the actual cause of cancer. Rather, it explains what can happen once cancer has been initiated,” said Cheresh. “Here’s an analogy: To get cancer, you first have to start with an oncogene, a gene that carries a mutation and has the potential to initiate cancer. Think of the oncogene as turning on a car’s ignition. The signaling pathway exploited by cancer cells is like applying gas. It gets the car moving, but it means nothing if the oncogene hasn’t first started the process.”

The researchers focused on a family of cell surface receptor proteins called integrins that act as key communications conduits, ultimately zeroing in on the role of one member of this family called beta-3 integrin. Also known as CD61, it was already linked to metastasis and resistance to cancer drugs.

Cheresh noted that CD61 represents a good marker for the incriminated signaling pathway involved in both mammary development during pregnancy and cancer. It’s easily detected and could be used to both diagnose and treat breast cancer cases. “Detecting CD61 might help doctors determine what kind of therapeutic approach to use, knowing that they might be dealing with a more aggressive yet treatable form of breast cancer. For example, there are existing drugs that block CD61 signaling, which might be another potential aspect of treatment.”

Photo credit: “Chili (633442211)” by Randi Hausken from Bærum, Norway - Chili Uploaded by russavia. Licensed under Creative Commons Attribution-Share Alike 2.0 via Wikimedia Commons 



Food for thought: Chili peppers are more than spice in your diet
Attend one of our free Healing Foods Kitchen cooking classes and you’ll hear Susan Faerber tell you that capsaicin, the active ingredient that makes chili peppers hot, has protective benefits against cancer. In a study published in the Aug. 1 issue of The Journal of Clinical Investigation, UC San Diego Moores Cancer Center researchers say capsaicin triggers a reaction that reduces the risk of colorectal tumors.
But before you add a Carolina Reaper, the world’s hottest pepper, to one of Susan’s cancer fighting recipes or your own healthy meal, read about the science behind the study at our sister blog ucsdhealthsciences.
We asked the researchers to break down this spicy news for our own consumption and tell us what does it mean for you and me? Do countries with a traditionally high use of chili peppers in their diet see lower incidence of colorectal cancer?
The answer is a bit complicated and we must be cautious to infer any cause-and-effect relationships from epidemiological data, said Petrus de Jong, MD, first author of the study. Still, a 2009 study on colorectal cancer incidence shows there are benefits.
“Countries with a high dietary intake of capsaicinoids (e.g. India, Bangladesh, Thailand, Mexico) show a five to 10-fold lower incidence of colorectal cancer compared to Western countries,” said Dr. de Jong.
“Various factors may be associated with the reduced incidence of colorectal cancer in these countries, including dietary factors such as low consumption of red meats and high consumption of non-starch polysaccharides, vegetables and phytochemicals (i.e. capsaicin). Indeed, a shift from a traditional Mexican to a predominantly Western diet has been associated with an increased risk of this cancer as shown by a 2003 study.”
So there is a benefit! But, how much do we need to eat?
“A significant anti-tumor effect would require more than just ‘a spicy diet’,” said Dr. de Jong.
The amount of capsaicin used in the experiments is at least five times higher than what the average people in countries who eat lots chili pepper consume. Dr. de Jong says a good starting point to determine how much capsaicin we need to ingest would be a feasibility study that would target the active substance mainly to the large intestine. So until then, eat your habanero, jalapeño, piri piri or the pepper of choice depending on your heat level tolerance and know that it has some health benefits in addition to adding flavor to your meals.
Bon appétit. 

Photo credit: “Chili (633442211)” by Randi Hausken from Bærum, Norway - Chili Uploaded by russavia. Licensed under Creative Commons Attribution-Share Alike 2.0 via Wikimedia Commons

Food for thought: Chili peppers are more than spice in your diet

Attend one of our free Healing Foods Kitchen cooking classes and you’ll hear Susan Faerber tell you that capsaicin, the active ingredient that makes chili peppers hot, has protective benefits against cancer. In a study published in the Aug. 1 issue of The Journal of Clinical Investigation, UC San Diego Moores Cancer Center researchers say capsaicin triggers a reaction that reduces the risk of colorectal tumors.

But before you add a Carolina Reaper, the world’s hottest pepper, to one of Susan’s cancer fighting recipes or your own healthy meal, read about the science behind the study at our sister blog ucsdhealthsciences.

We asked the researchers to break down this spicy news for our own consumption and tell us what does it mean for you and me? Do countries with a traditionally high use of chili peppers in their diet see lower incidence of colorectal cancer?

The answer is a bit complicated and we must be cautious to infer any cause-and-effect relationships from epidemiological data, said Petrus de Jong, MD, first author of the study. Still, a 2009 study on colorectal cancer incidence shows there are benefits.

“Countries with a high dietary intake of capsaicinoids (e.g. India, Bangladesh, Thailand, Mexico) show a five to 10-fold lower incidence of colorectal cancer compared to Western countries,” said Dr. de Jong.

“Various factors may be associated with the reduced incidence of colorectal cancer in these countries, including dietary factors such as low consumption of red meats and high consumption of non-starch polysaccharides, vegetables and phytochemicals (i.e. capsaicin). Indeed, a shift from a traditional Mexican to a predominantly Western diet has been associated with an increased risk of this cancer as shown by a 2003 study.”

So there is a benefit! But, how much do we need to eat?

“A significant anti-tumor effect would require more than just ‘a spicy diet’,” said Dr. de Jong.

The amount of capsaicin used in the experiments is at least five times higher than what the average people in countries who eat lots chili pepper consume. Dr. de Jong says a good starting point to determine how much capsaicin we need to ingest would be a feasibility study that would target the active substance mainly to the large intestine. So until then, eat your habanero, jalapeño, piri piri or the pepper of choice depending on your heat level tolerance and know that it has some health benefits in addition to adding flavor to your meals.

Bon appétit. 

From our sister blog, a new look at appendix cancer that may lead to new and improved therapies for this rare disease.

ucsdhealthsciences:

Study gives promise to new treatment for appendix cancer
Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.
The study was published in a recent issue of Genome Medicine.
Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.
The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.
“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  
The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.
The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.
“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”
To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu         Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

From our sister blog, a new look at appendix cancer that may lead to new and improved therapies for this rare disease.

ucsdhealthsciences:

Study gives promise to new treatment for appendix cancer

Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.

The study was published in a recent issue of Genome Medicine.

Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.

The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.

“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  

The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.

The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.

“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”

To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu        

Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

ucsdhealthsciences:

Finding the Achilles’ Heel of Ovarian Tumor Growth
A team of scientists, led by principal investigator David D. Schlaepfer, PhD, professor in the Department of Reproductive Medicine at the University of California, San Diego School of Medicine report that small molecule inhibitors to a protein called focal adhesion kinase (FAK) selectively prevent the growth of ovarian cancer cells as tumor spheroids.
The findings come in a pair of studies published online this week in the journals Gynecologic Oncology and Molecular Cancer Therapeutics.
Ovarian cancer is a leading cause of female cancer death in the United States. On average, more than 21,000 women are diagnosed with ovarian cancer each year and 14,270 die. Many women achieve remission, but cancer recurrence rates exceed 75 percent, prompting the need for new treatments.
“Ovarian cancer spreads within a women’s peritoneal space through a unique mechanism that involves the survival of small clusters of tumor cells termed spheroids,” said Schlaepfer. “Our studies show that FAK signaling functions at the center of a tumor cell survival signaling network.”
In the first study, published in Gynecologic Oncology, first author Nina Shah, MD, a gynecological oncology fellow in the Department of Reproductive Medicine, found that ovarian tumor cells with low levels of a tumor suppressor protein, called merlin, displayed heightened sensitivity to FAK inhibitor growth cessation.
“With FAK inhibitor clinical trials already testing a similar linkage in mesothelioma (a rare cancer that affects the protective lining of many internal organs), our results support the hypothesis that protein biomarkers such as merlin may identify those patients who may best respond to FAK inhibitor therapy,” said Schlaepfer.
In the second study in Molecular Cancer Therapeutics, first author Isabelle Tancioni PhD, an assistant project scientist at UC San Diego Moores Cancer Center discovered that a network of signals generated by osteopontin – a beta-5 integrin receptor used in cell-to-cell signaling – and FAK control ovarian cancer spheroid growth. High levels of beta-5 integrin and FAK expression are associated with a poor prognosis for some ovarian cancer patients. “Thus, high levels of beta-5 integrin may serve as a novel biomarker for ovarian carcinoma cells that possess active FAK signaling,” said Schlaepfer.
Schlaepfer noted that tumor recurrence and metastasis are responsible for the majority of ovarian cancer-related deaths and said the new findings support ongoing clinical trials of FAK inhibitors as new agents in the fight to prevent ovarian cancer progression.

ucsdhealthsciences:

Finding the Achilles’ Heel of Ovarian Tumor Growth

A team of scientists, led by principal investigator David D. Schlaepfer, PhD, professor in the Department of Reproductive Medicine at the University of California, San Diego School of Medicine report that small molecule inhibitors to a protein called focal adhesion kinase (FAK) selectively prevent the growth of ovarian cancer cells as tumor spheroids.

The findings come in a pair of studies published online this week in the journals Gynecologic Oncology and Molecular Cancer Therapeutics.

Ovarian cancer is a leading cause of female cancer death in the United States. On average, more than 21,000 women are diagnosed with ovarian cancer each year and 14,270 die. Many women achieve remission, but cancer recurrence rates exceed 75 percent, prompting the need for new treatments.

“Ovarian cancer spreads within a women’s peritoneal space through a unique mechanism that involves the survival of small clusters of tumor cells termed spheroids,” said Schlaepfer. “Our studies show that FAK signaling functions at the center of a tumor cell survival signaling network.”

In the first study, published in Gynecologic Oncology, first author Nina Shah, MD, a gynecological oncology fellow in the Department of Reproductive Medicine, found that ovarian tumor cells with low levels of a tumor suppressor protein, called merlin, displayed heightened sensitivity to FAK inhibitor growth cessation.

“With FAK inhibitor clinical trials already testing a similar linkage in mesothelioma (a rare cancer that affects the protective lining of many internal organs), our results support the hypothesis that protein biomarkers such as merlin may identify those patients who may best respond to FAK inhibitor therapy,” said Schlaepfer.

In the second study in Molecular Cancer Therapeutics, first author Isabelle Tancioni PhD, an assistant project scientist at UC San Diego Moores Cancer Center discovered that a network of signals generated by osteopontin – a beta-5 integrin receptor used in cell-to-cell signaling – and FAK control ovarian cancer spheroid growth. High levels of beta-5 integrin and FAK expression are associated with a poor prognosis for some ovarian cancer patients. “Thus, high levels of beta-5 integrin may serve as a novel biomarker for ovarian carcinoma cells that possess active FAK signaling,” said Schlaepfer.

Schlaepfer noted that tumor recurrence and metastasis are responsible for the majority of ovarian cancer-related deaths and said the new findings support ongoing clinical trials of FAK inhibitors as new agents in the fight to prevent ovarian cancer progression.

Six new guidelines published in the Journal of the American College of Nutrition describe ways to reduce a person’s risk of cancer. Gordon Saxe, MD, PhD, a ucsdhealthsciences researcher and physician, says cancer rates are substantially higher in the United States due in part to diet. The guidelines he helped draft advise people to avoid or limit exposure to red meat, grilled meats, alcohol and dairy while increasing consumption of fresh fruits and vegetables.

Look for nutrition classes that offer ways to blend more fruits and vegetables into your diet in way that even picky eaters will enjoy. At UC San Diego Moores Cancer Center we offer free, monthly cooking classes that include recipes, food demonstrations and tasting at the Healing Foods Kitchen.

ucsdhealthsciences:

Melanoma of the Eye Caused by Two Gene Mutations
Researchers at the University of California, San Diego School of Medicine have identified a therapeutic target for treating the most common form of eye cancer in adults. They have also, in experiments with mice, been able to slow eye tumor growth with an existing FDA-approved drug.
The findings are published online in the May 29 issue of the journal Cancer Cell.
“The beauty of our study is its simplicity,” said Kun-Liang Guan, PhD, professor of pharmacology at UC San Diego Moores Cancer Center and co-author of the study. “The genetics of this cancer are very simple and our results have clear implications for therapeutic treatments for the disease.”
The researchers looked specifically at uveal melanoma. Uveal collectively refers to parts of the eye, notably the iris, that contain pigment cells. As with melanoma skin cancer, uveal melanoma is a malignancy of these melanin-producing cells.
Approximately 2,000 people in the United States are diagnosed with uveal melanoma each year. If the cancer is restricted to just the eye, the standard treatment is radiation and surgical removal of the eye. But uveal melanoma often spreads to the liver, and determining the metastatic status of the disease can be difficult. In cases of uveal melanoma metastasis, patients typically succumb within two to eight months after diagnosis.
Scientists have long suspected a genetic association with uveal melanoma because one of two gene mutations is present in approximately 70 percent of all tumors. Until this study, however, they had not identified a mechanism that could explain why and how these mutations actually caused tumors.
The work by Guan and colleagues unravels the causal relationship between the genetic mutations and tumor formation, and identifies a molecular pathway along which drugs might counterattack.
The two genes implicated – GNAQ and GNA11 – code for proteins (known as G proteins) that normally function as molecular on-off switches, regulating the passage of information from the outside to the inside of a cell.
In their experiments, the scientists showed that mutations in these genes shift the G proteins to a permanent “on” or active status, which results in over-activation the Yes-associated protein (YAP). The activation of the YAP protein induces uncontrolled cell growth and inhibits cell death, causing malignancies.
Earlier research by other scientists has shown that the drug verteporfin, used to treat abnormal blood vessel formation in the eye, acts on the YAP pathway inhibiting the protein’s YAP function.
In experiments with mice, the UC San Diego-led team showed that verteporfin also suppresses the growth of uveal melanoma tumors derived from human tumors.
“We have a cancer that is caused by a very simple genetic mechanism,” Guan said. “And we have a drug that works on this mechanism. The clinical applications are very direct.”
Pictured: An untreated uveal melanoma tumor (left) covers entire eye of a mouse. A tumor treated with verteporfin (right) is smaller and much of the structure of the mouse’s eye is visible.

ucsdhealthsciences:

Melanoma of the Eye Caused by Two Gene Mutations

Researchers at the University of California, San Diego School of Medicine have identified a therapeutic target for treating the most common form of eye cancer in adults. They have also, in experiments with mice, been able to slow eye tumor growth with an existing FDA-approved drug.

The findings are published online in the May 29 issue of the journal Cancer Cell.

“The beauty of our study is its simplicity,” said Kun-Liang Guan, PhD, professor of pharmacology at UC San Diego Moores Cancer Center and co-author of the study. “The genetics of this cancer are very simple and our results have clear implications for therapeutic treatments for the disease.”

The researchers looked specifically at uveal melanoma. Uveal collectively refers to parts of the eye, notably the iris, that contain pigment cells. As with melanoma skin cancer, uveal melanoma is a malignancy of these melanin-producing cells.

Approximately 2,000 people in the United States are diagnosed with uveal melanoma each year. If the cancer is restricted to just the eye, the standard treatment is radiation and surgical removal of the eye. But uveal melanoma often spreads to the liver, and determining the metastatic status of the disease can be difficult. In cases of uveal melanoma metastasis, patients typically succumb within two to eight months after diagnosis.

Scientists have long suspected a genetic association with uveal melanoma because one of two gene mutations is present in approximately 70 percent of all tumors. Until this study, however, they had not identified a mechanism that could explain why and how these mutations actually caused tumors.

The work by Guan and colleagues unravels the causal relationship between the genetic mutations and tumor formation, and identifies a molecular pathway along which drugs might counterattack.

The two genes implicated – GNAQ and GNA11 – code for proteins (known as G proteins) that normally function as molecular on-off switches, regulating the passage of information from the outside to the inside of a cell.

In their experiments, the scientists showed that mutations in these genes shift the G proteins to a permanent “on” or active status, which results in over-activation the Yes-associated protein (YAP). The activation of the YAP protein induces uncontrolled cell growth and inhibits cell death, causing malignancies.

Earlier research by other scientists has shown that the drug verteporfin, used to treat abnormal blood vessel formation in the eye, acts on the YAP pathway inhibiting the protein’s YAP function.

In experiments with mice, the UC San Diego-led team showed that verteporfin also suppresses the growth of uveal melanoma tumors derived from human tumors.

“We have a cancer that is caused by a very simple genetic mechanism,” Guan said. “And we have a drug that works on this mechanism. The clinical applications are very direct.”

Pictured: An untreated uveal melanoma tumor (left) covers entire eye of a mouse. A tumor treated with verteporfin (right) is smaller and much of the structure of the mouse’s eye is visible.

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