Cancer Is My Herpes: Living With Recurrent Disease

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About a year ago, I learned about some "worrisome" spots that had shown up on my quarterly CT scan. This was about six months after my last of 24 chemotherapy infusions, and to say I was bummed upon hearing the news would be an understatement. But I slowly wrapped my brain around the notion of a "third option" relating to cancer, the third option being something between permanent remission from cancer... and death.

Now the thought of just "learning to live with" cancer was unappealing then and is unappealing now. Of course, I (and anyone else without a death wish) would prefer to live a long life, free of illness and disease, without the scepter of cancer hanging over my head. But as a couple of wise blokes named Mick Jagger and Keith Richards once wrote, you can't always get what you want.

Over the course of the past year, I and my oncology team have watched and monitored those worrisome nodules, hoping they'd either go away or at least remain unchanged. The nodes were too small and scattered to biopsy; but since cancer rarely remains completely stagnant, the thought was that if they didn't grow, they likely weren't cancer. Unfortunately, they grew. Not at an alarming rate, but slowly and steadily they grew. And just as slowly and steadily, my CA125 (cancer marker) levels crept upward.

My family and I watched and waited, hoping for the best but fearing the worst, until a couple of weeks ago, my oncologist called me in for the hard conversation.

"Given the growth of these nodules over the past several months, and the increase in your CA125 levels, we do believe your cancer has returned."

As difficult as this was to hear, I have to say I wasn't surprised. I had never rested easily with the knowledge of those mysterious nodules inside me, not even for a day. In my heart of hearts, I think I always knew they were dangerous. I'd hoped with every fiber of my being I was wrong, but my gut told me my fears were well placed.

I did, however, question the use of the terminology about my cancer having "returned." Because even though I was told at the end of treatment more than 18 months ago that my scans and blood work showed "no evidence of disease", we've essentially been watching these spots for more than a year. So my cancer hasn't actually returned. The truth is, my cancer likely never left. When I pressed my oncologist about this, she acknowledged that I was correct. The nodes on my CT scan were now simply large enough to see. However, they'd likely been there all along.

Cancer.org published a helpful informational paper about recurrent cancer, describing how sometimes small clusters of cancer cells that could not be seen or found on scans or other tests, grow large enough over time to be detected or cause symptoms. While I'm not yet experiencing symptoms as a result of the nodules in my pelvic region -- they're still too small -- they are definitely now detectible and need to be addressed.

Right now the plan is for me to resume chemotherapy after the first of the year. And this time I'll likely be on some form of chemo drug for the rest of my life or until there's a cure. The thought of this both exhausts and terrifies me. I don't want to die. My daughter just turned two. I want to be around to see her grow up. I want to grow old with my husband. I'm not ready to go anytime soon... not by a long shot. So I'm scared and even a little angry.

Aside from processing these feelings, exploring treatment options and second opinions, and learning to cope with the stress and anxiety that came with this news, I'm also learning to reframe my thinking about cancer as a recurrent disease. I can no longer look myself in the eye and tell myself with 100 percent certainty that "this time" I'm going to beat cancer for good. In actuality, the cancer will likely continue to crop up, just hopefully with longer periods of time with no detectible activity between "episodes."

While I strongly dislike the thought of this, I also have to acknowledge that many people live long lives with recurrent, incurable disease. Those with rheumatoid arthritis, diabetes, COPD, severe asthma and even HIV, all learn to manage their symptoms with medication, diet, exercise and other lifestyle changes and therapies, and deal with flare-ups as necessary when they occur.

I remember when an HIV/AIDS diagnosis was considered a death sentence. And it was. I lost several friends to the disease in the late 1980s and early 1990s, before the advent of the "AIDS cocktail" of antiretroviral therapy. Today HIV/AIDS is manageable, and considered a chronic illness rather than a fatal one. Turns out, many cancers fall into the same category.

I have to wrap my mind around the fact that, unless a cure is discovered in my lifetime, cancer is going to be part of my life for the rest of my life. Cancer is my herpes. Or my diabetes or RA or COPD. It's in me and I am going to have to accept it and learn to manage and dominate it. I want to live a long life, so in my mind, I have no other choice.

Image via Brooke Kelly Photography

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Researchers on the trail of a treatment for cancer of the immune system

ScienceDaily (Aug. 22, 2011) — Danish researchers from the University of Copenhagen have become the first in the world to regulate a special receptor or bio-antenna that plays a vital part when the Epstein Barr herpes virus infects us and when this infection appears to be mutating into cancer of the immune system. Using a biochemical blueprint and a tiny bio-molecule the Danish researchers have succeeded in blocking the receptor concerned. This will make it possible to adjust and regulate the memory cells of the immune system.

Infection with Epstein Barr means that the B cells, which are the primary memory cells of the immune system, are hi-jacked.

When the virus has penetrated, researchers observe an excess of a special bio-antenna, a receptor known as EB12, suddenly sprouting from the surface of the B cells. But why they do so remains a mystery.

The receptors are a vital component of the way cells communicate with their surroundings via hormones and other bio-molecules, for example, but in a body consisting of millions of cells and transmitters it can be hard to determine the part each molecule plays.

"It is possible that the large numbers of EB12 receptors could actually be the B cells response to the virus and an attempt to combat the infection. Another possibility is that the EB virus reprogrammes the cell for this explosive growth in the number of EB12 receptors. What we know for certain is that more EB12 receptors assist the B cell infected by the EB virus to multiply more rapidly thus spreading the infection faster," says postdoc Tau Benned-Jensen from the Faculty of Health Sciences, University of Copenhagen.

The Epstein Barr virus can cause cancer

No fewer than 95 per cent of us carry the Epstein Barr Herpes virus.

We often encounter it as kids and it is normally harmless. Are we infected later in life EB virus may cause mononucleosis, and it seems to play a part in some forms of cancer, just as HPV affects the risk of cervical cancer. But we have no drugs to combat the Epstein Barr virus, and no vaccines for it.

"Under normal circumstances our immune systems can keep the EB virus infection in a latent state and a truce or stand-off may arise between the immune system and the virus," explains Mette Rosenkilde, professor of pharmacology at the Department of Neuroscience and Pharmacology, University of Copenhagen.

"We cannot dispense with the infection and we carry it all life long, but to most of us it is harmless. For people whose immune systems do not function due to disease or because they are suppressed by drugs in conjunction with organ transplants it is a very different matter. Now the Epstein Barr virus is suddenly free to reproduce so uninhibitedly and dramatically that it may lead to cancer," says Mette Rosenkilde.

The first step on the road to solving the EB12-puzzle

While researchers know that the B cell EB12 receptors play a part when the cell visits the lymph glands, the immune system's Central Station, we have not yet explained the exact role of the receptor.

So the Danish researchers started by mapping the bio-antenna molecule by molecule and then, as the first in the world, they made a blueprint of a tiny molecule they thought could bind to the B cell EB12 receptor.

"When we know what receptors react to, it tells us more about the part they play," Mette Rosenkilde explains, "and our tiny molecule, a ligand, blocks the EB12 receptor, preventing it from doing its job."

"In time this block may be able to help transplant patients. If we can restrain EB virus reproduction when the immune system is being medically suppressed, we may well be able to avoid cancer," Tau Benned-Jensen says.

"On the other hand the EP virus also appears to play a part in other immune diseases such as autoimmune disease, where the ability to adjust the immune system would be beneficial," says Mette Rosenkilde.

And shortly after the Danish researchers published their article on their ligand, the first articles appeared about natural substances in the body, which activate the EB12 receptor and direct the B cell to specific areas in the lymph glands.

"Our molecule can inhibit the activation of the new substances, and the next step in our research will be experiments to identify even more biochemical dials to twiddle and to help us develop new drugs," Tau-Benned says.

The discovery has just been published in the Journal of Biological Chemistry.

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Story Source:

The above story is reprinted from materials provided by University of Copenhagen.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

T. Benned-Jensen, C. Smethurst, P. J. Holst, K. R. Page, H. Sauls, B. Sivertsen, T. W. Schwartz, A. Blanchard, R. Jepras, M. M. Rosenkilde. Ligand Modulation of the Epstein-Barr Virus-induced Seven-transmembrane Receptor EBI2: IDENTIFICATION OF A POTENT AND EFFICACIOUS INVERSE AGONIST. Journal of Biological Chemistry, 2011; 286 (33): 29292 DOI: 10.1074/jbc.M110.196345

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Researchers on the trail of a treatment for cancer of the immune system

ScienceDaily (Aug. 19, 2011) — Danish researchers from the University of Copenhagen have become the first in the world to regulate a special receptor or bio-antenna that plays a vital part when the Epstein Barr herpes virus infects us and when this infection appears to be mutating into cancer of the immune system. Using a biochemical blueprint and a tiny bio-molecule the Danish researchers have succeeded in blocking the receptor concerned. This will make it possible to adjust and regulate the memory cells of the immune system.

Infection with Epstein Barr means that the B cells, which are the primary memory cells of the immune system, are hi-jacked.

When the virus has penetrated, researchers observe an excess of a special bio-antenna, a receptor known as EB12, suddenly sprouting from the surface of the B cells. But why they do so remains a mystery.

The receptors are a vital component of the way cells communicate with their surroundings via hormones and other bio-molecules, for example, but in a body consisting of millions of cells and transmitters it can be hard to determine the part each molecule plays.

"It is possible that the large numbers of EB12 receptors could actually be the B cells response to the virus and an attempt to combat the infection. Another possibility is that the EB virus reprogrammes the cell for this explosive growth in the number of EB12 receptors. What we know for certain is that more EB12 receptors assist the B cell infected by the EB virus to multiply more rapidly thus spreading the infection faster," says postdoc Tau Benned-Jensen from the Faculty of Health Sciences, University of Copenhagen.

The Epstein Barr virus can cause cancer

No fewer than 95 per cent of us carry the Epstein Barr Herpes virus.

We often encounter it as kids and it is normally harmless. Are we infected later in life EB virus may cause mononucleosis, and it seems to play a part in some forms of cancer, just as HPV affects the risk of cervical cancer. But we have no drugs to combat the Epstein Barr virus, and no vaccines for it.

"Under normal circumstances our immune systems can keep the EB virus infection in a latent state and a truce or stand-off may arise between the immune system and the virus," explains Mette Rosenkilde, professor of pharmacology at the Department of Neuroscience and Pharmacology, University of Copenhagen.

"We cannot dispense with the infection and we carry it all life long, but to most of us it is harmless. For people whose immune systems do not function due to disease or because they are suppressed by drugs in conjunction with organ transplants it is a very different matter. Now the Epstein Barr virus is suddenly free to reproduce so uninhibitedly and dramatically that it may lead to cancer," says Mette Rosenkilde.

The first step on the road to solving the EB12-puzzle

While researchers know that the B cell EB12 receptors play a part when the cell visits the lymph glands, the immune system's Central Station, we have not yet explained the exact role of the receptor.

So the Danish researchers started by mapping the bio-antenna molecule by molecule and then, as the first in the world, they made a blueprint of a tiny molecule they thought could bind to the B cell EB12 receptor.

"When we know what receptors react to, it tells us more about the part they play," Mette Rosenkilde explains, "and our tiny molecule, a ligand, blocks the EB12 receptor, preventing it from doing its job."

"In time this block may be able to help transplant patients. If we can restrain EB virus reproduction when the immune system is being medically suppressed, we may well be able to avoid cancer," Tau Benned-Jensen says.

"On the other hand the EP virus also appears to play a part in other immune diseases such as autoimmune disease, where the ability to adjust the immune system would be beneficial," says Mette Rosenkilde.

And shortly after the Danish researchers published their article on their ligand, the first articles appeared about natural substances in the body, which activate the EB12 receptor and direct the B cell to specific areas in the lymph glands.

"Our molecule can inhibit the activation of the new substances, and the next step in our research will be experiments to identify even more biochemical dials to twiddle and to help us develop new drugs," Tau-Benned says.

The discovery has just been published in the Journal of Biological Chemistry.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Copenhagen.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

T. Benned-Jensen, C. Smethurst, P. J. Holst, K. R. Page, H. Sauls, B. Sivertsen, T. W. Schwartz, A. Blanchard, R. Jepras, M. M. Rosenkilde. Ligand Modulation of the Epstein-Barr Virus-induced Seven-transmembrane Receptor EBI2: IDENTIFICATION OF A POTENT AND EFFICACIOUS INVERSE AGONIST. Journal of Biological Chemistry, 2011; 286 (33): 29292 DOI: 10.1074/jbc.M110.196345

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Herpes Virus Effective in Treating Triple Negative Breast Cancer - Med India

Moreover, Dr. Gholami explained that TNBC cells have high levels of p-MAPK, a protein that promotes cancer cells to grow and has been reported as a potential cause for resistance to current conventional therapies. Knowing that the herpes virus specifically targets cells that over express this protein is the reason she chose to test this treatment protocol. "When we infect TNBC cells with the herpes virus and measure p-MAPK levels, the protein level decreases with time after treatment with the virus," Dr. Gholami said.

The hope is that advances in oncolytic viral therapy, which uses viruses tailored to target and destroy cancer cells while sparing healthy cells, will allow researchers to develop more effective strategies for hard-to-treat cancers. A similar herpes virus has been tested in clinical trials against head and neck cancers. But this is the first laboratory study to show promise in using the therapy to treat TNBC.

The next steps, Dr. Gholami said, are to map out the pathways in which the virus kills the tumor cells to determine how to improve upon this mechanism. In the future, the Fong laboratory, which is on the forefront in oncolytic viral therapy research, will continue this avenue of investigation in animal studies. The team will also work to identify leads to understand what existing chemotherapy drugs can be used synergistically with this viral therapy. Finding complementary treatments that kill fast-growing cancer cells and combat resistance is the key to possibly making a cure a reality.

If additional animal studies are also positive, human clinical trials could be on the horizon. "Our goal is to improve this version of the virus and get it into a clinical trial," Dr. Gholami said. "Ultimately, I believe the treatment for TNBC will be a multimodality targeted treatment approach: potentially using a viral-based therapy plus some other targeted chemotherapy or radiation."

The study was supported by grants from the National Institutes of Health and the Flight Attendant Medical Research Institution.

Source-Newswise

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Herpes Virus Shows Early Promise In Treating Triple-Negative Breast Cancer

Oncolytic viral therapy shows great potential
for treating an aggressive form of breast cancer

Newswise — SAN FRANCISCO: Researchers from Memorial Sloan-Kettering Cancer Center in New York City report they have successfully treated triple-negative breast cancer (TNBC) in petri dishes and in mouse models with a method based upon a herpes simplex virus. The study on the viral-based therapy was reported today at the 2011 Annual Clinical Congress of the American College of Surgeons.

Triple-negative breast cancer is an aggressive type of breast cancer that can account for up to 20 percent of all cases and is responsible for a disproportionate number of breast cancer deaths, according to the researchers. Moreover, the disease is most likely to surface in younger women (< 35 years old), especially if they are African American or Hispanic.

Because these types of cancerous tumors do not express the estrogen receptor, progesterone receptor, or HER-2 receptor, found in other more common types, newer targeted therapies such as tamoxifen and Herceptin are ineffective against the disease.

“Triple-negative breast cancer patients are in dire need of targeted therapies,” according to Sepideh Gholami, MD, a research fellow in the laboratory of Yuman Fong, MD, FACS, at Memorial Sloan-Kettering Cancer Center. “Although these tumors respond to a variety of chemotherapies, they have a high recurrence and metastatic rate.”

In the study, Dr. Gholami and her colleagues examined TNBC cell lines and infected them with a herpes simplex virus called NV1066. After treatment with the virus, more than 90 percent cell kill was achieved in all cell lines within a week. Furthermore, the researchers injected TNBC cells into laboratory mice. After treating the mouse models with the virus, and measuring the change in the tumors over 20 days, they found that the tumors had largely disappeared.

It was very surprising to see such an intense response. “The difference was dramatic, because sometimes we can stop tumor growth and achieve tumor regression,” Dr. Gholami said. “Our results are very exciting because we may be coming up with an approach that could potentially exploit the unique vulnerabilities of these specific cancer cells.”

Moreover, Dr. Gholami explained that TNBC cells have high levels of p-MAPK, a protein that promotes cancer cells to grow and has been reported as a potential cause for resistance to current conventional therapies. Knowing that the herpes virus specifically targets cells that over express this protein is the reason she chose to test this treatment protocol. “When we infect TNBC cells with the herpes virus and measure p-MAPK levels, the protein level decreases with time after treatment with the virus,” Dr. Gholami said.

The hope is that advances in oncolytic viral therapy, which uses viruses tailored to target and destroy cancer cells while sparing healthy cells, will allow researchers to develop more effective strategies for hard-to-treat cancers. A similar herpes virus has been tested in clinical trials against head and neck cancers. But this is the first laboratory study to show promise in using the therapy to treat TNBC.

The next steps, Dr. Gholami said, are to map out the pathways in which the virus kills the tumor cells to determine how to improve upon this mechanism. In the future, the Fong laboratory, which is on the forefront in oncolytic viral therapy research, will continue this avenue of investigation in animal studies. The team will also work to identify leads to understand what existing chemotherapy drugs can be used synergistically with this viral therapy. Finding complementary treatments that kill fast-growing cancer cells and combat resistance is the key to possibly making a cure a reality.

If additional animal studies are also positive, human clinical trials could be on the horizon. “Our goal is to improve this version of the virus and get it into a clinical trial,” Dr. Gholami said. “Ultimately, I believe the treatment for TNBC will be a multimodality targeted treatment approach: potentially using a viral-based therapy plus some other targeted chemotherapy or radiation.”

The study was supported by grants from the National Institutes of Health and the Flight Attendant Medical Research Institution.

Other participants in the study include Chun-Hao Chen, MD; Sizhi Paul Gao, MD, PhD; Joshua Carson, MD, PhD; Taejin Song, MD, PhD, FACS; Jackie Bromberg, MD, PhD; and Yuman Fong, MD, FACS.

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Herpes Virus Could Kill Aggressive Breast Cancer

A genetically engineered version of the virus that causes herpes shows promise as a treatment for a particularly aggressive type of breast cancer, according to a new study in animals.

The virus targeted and killed triple-negative breast cancer cells in mice. Triple-negative breast cancer is a form of breast cancer that cannot be treated with hormone therapies, such as tamoxifen and Herceptin.

The results are preliminary, and it's not clear whether the therapy will have the same effect on tumors growing in people. Much more research is needed to determine this. If a treatment is developed, it will likely be used in conjunction with other cancer therapies, including chemotherapy and radiation, the researchers said.

The study will be presented today (Oct. 24) at the meeting of the American College of Surgeons in San Francisco.

Herpes therapy

Triple-negative breast cancer accounts for about 20 percent of all breast cancer cases. It disproportionally effects young, African-American women and is usually treated with chemotherapy. (Triple-negative breast cancers are not fueled by the hormone estrogen, so they do no respond to treatments designed to block the hormone.)

Study researcher Dr. Sepideh Gholami, a research fellow in the at Memorial Sloan-Kettering Cancer Center in New York City. and colleagues infected breast cancer cells in a dish with a herpes virus called NV1066. Within a week, the virus killed up to 90 percent of the tumor cells.

The researchers then injected breast cancer cells into mice. After treating the mice with the virus for 20 days, they saw the tumors had largely disappeared, Gholami said.

The dramatic response may be due to the fact that triple-negative breast cancer cells have high levels of a protein called p-MAPK. The herpes virus specifically targets cells with high levels of this protein, the researchers said.

The therapy is just one of many in recent years to explore the use of viruses as a means to target and destroy cancer cells. The herpes virus has been tested in people as a treatment for head and neck cancer, but not for breast cancer, the researchers said.

More research

The study is an "extremely exciting step" in the pursuit of a cancer therapy that uses the herpes virus, said Dr. Stefan Gluck, a medical oncologist at the University of Miami's Sylvester Comprehensive Cancer Center.

However, the researchers still need to show that this herpes virus is safe to use in patients. After all, the herpes virus is known to cause infection in humans, including infections in the brain. Proving the therapy's safety will likely be a lengthy process, and will involve testing it on other animals first, such as dogs and primates, Gluck said.

The researchers plan to figure out exactly how the virus works to kill the breast cancer cells, and try to bolster its effect.

Pass it on: The herpes virus can infect and kill breast cancer cells in a dish and in mice.

This story was provided by MyHealthNewsDaily, a sister site to LiveScience. Follow MyHealthNewsDaily staff writer Rachael Rettner on Twitter @RachaelRettner. Find us on Facebook.

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