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Immune Therapy to Fight Cancer

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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: May 11 2016 at 9:19pm
Antibody appears to attack cancer cells, leaving other cells unscathed
An antibody has been developed from the body's own immune system that preferentially attacks cancer cells. The antibody works by targeting a natural defense mechanism that cancer tumors exploit. Cells in the body essentially use a home security system that relies on certain proteins to protect the cell surface and keep it safe. These proteins help the cell avoid injury and even death from unwanted activation of the immune system.

A research team from Duke Health has developed an antibody from the body's own immune system that preferentially attacks cancer cells.

The antibody works by targeting a natural defense mechanism that cancer tumors exploit.

Cells in the body essentially use a home security system that relies on certain proteins to protect the cell surface and keep it safe. These proteins help the cell avoid injury and even death from unwanted activation of the immune system.

In a paper published online May 5, 2016 in Cell Reports, the Duke team describes the workings of a cancer-fighting antibody they discovered, developed and tested in cell lines and animal models. The antibody dismantles a specific part of a cancer cell's defense system and then employs several mechanisms of attack.

"This is the first completely human-derived antibody developed as an anti-cancer therapy, which is very different from other immunotherapy approaches," said senior author Edward F. Patz, Jr., M.D., the James and Alice Chen Professor of Radiology and professor in the Department of Pharmacology and Cancer Biology at Duke.

Patz and colleagues -- including principals from the Duke Human Vaccine Institute who have been advancing the development of antibodies for an HIV vaccine -- started with the observation that some lung cancer patients have early-stage tumors that never progress to advanced disease.

One of the features that separated these patients from those who had more lethal tumors was the presence of antibodies against a protein called complement factor H, or CFH, which protects cells from an immune system attack.

CFH works by preventing activation of an important immune response. It inhibits the deposit of a complement C3b protein on the cell surface. Complement C3b initiates the degradation of the cell membrane, which eventually leads to cell death.

Once the antibody for CFH was identified, Patz and colleagues sought to explore how this immune response could be optimized as a cancer therapy. Critical to that effort was finding a way to produce antibodies that recognized the exact same part of CFH as the autoantibodies made by the early-stage cancer patients, thus assuring that the antibodies would have a particular affinity for cancer cells.

Patz and colleagues pooled the white blood cells from CFH antibody-producing cancer patients and then isolated and cloned the antibody genes from single immune cells that make the specific antibodies.

This was an efficient process that enabled the researchers to produce mature antibodies that recognized the same region of CFH targeted by the original patient's immune systems -- therefore leading to the attack of cancer cells, not healthy cells.

The researchers then tested the antibodies in multiple cancer cell lines, including lung, gastric and breast cancers in lab dishes, and in tumors in living mice. They found that the antibodies caused tumor cell death without any obvious side effects. The antibodies also appeared to trigger an additional adaptive immune response when the damaged cells sent signals to recruit an army of lymphocytes, creating a potentially more lethal systemic attack.

"We believe it might be this additional cellular response that could potentially have the most profound impact on cancer outcomes long-term," Patz said, noting that further tests would be required to understand the full potential of the approach.

"This could represent a whole new approach to treating cancer, and it's exciting because the antibody selectively kills tumor cells, so we don't have significant side effects to achieve tumor control," Patz said. "We believe we can modulate the immune response and let the body's own immune system take over to either kill the tumor or keep it from growing."


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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Jan 09 2017 at 8:51pm
A class of drugs already approved for the treatment of estrogen receptor-positive breast cancer may also have the potential to halt the spread of hard-to-treat, triple-negative breast cancer, a new study finds. . . .

. . . .Now, study co-author Dr. Matthew Goetz, leader of the Women's Cancer Program at Mayo Clinic in Rochester, MN, and colleagues suggest that CDK 4/6 inhibitors may also be effective for the treatment of triple-negative breast cancer.

CDK 4/6 inhibitors reduced triple-negative breast cancer metastasis

Triple-negative breast cancer accounts for around 10-20 percent of breast cancers.

In triple-negative breast cancer, cancer cells are absent of estrogen, progesterone, and HER2 receptors. As such, the cancer does not respond to therapies that target these receptors, making it more difficult to treat.

According to Dr. Goetz and colleagues, previous research has shown that CDK 4/6 inhibitors are ineffective in reducing the growth of cancer cells in triple-negative breast cancer.

While the new study confirmed these findings, the team found that CDK 4/6 inhibitors may be effective for halting the spread of cancer cells to other areas of the body - otherwise known as cancer metastasis - in triple-negative breast cancer.

The researchers came to their findings by testing CDK 4/6 inhibitors in a number of triple-negative breast cancer models, including "patient-derived xenografts," which are immunodeficient mouse models implanted with human tumor tissue.

The team found that while CDK 4/6 inhibitors did not halt the growth of triple-negative breast cancer cells, the drugs significantly reduced the spread of cancer cells to distant organs by targeting a protein called SNAIL, which is known to promote cancer metastasis.

According to the researchers, their study results indicate that CDK 4/6 inhibitors may be beneficial for patients with triple-negative breast cancer.

"These findings may provide a new treatment for the prevention of cancer metastasis. Mayo Clinic is now developing new studies that will focus on the role of CDK 4/6 inhibitors and their potential to inhibit cancer metastasis in women with triple-negative breast cancer who are at highest risk for cancer metastasis."

Dr. Matthew Goetz


http://www.medicalnewstoday.com/articles/315110.php

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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Jun 03 2017 at 5:26pm
Tested on animals, but not on humans yet.
 

Combined use of two existing drugs appears to slow cancer's tendency to spread, study shows

A team led by Johns Hopkins researchers has discovered a biochemical signaling process that causes densely packed cancer cells to break away from a tumor and spread the disease elsewhere in the body. In their study, published online May 26 in Nature Communications, the team also reported that the combined use of two existing drugs disrupts this process and appears to significantly slow cancer's tendency to travel, a behavior called metastasis.

The new findings are important, the researchers said, because 90 percent of cancer deaths are caused by metastasis, and anything that derails this activity could improve the prognosis for patients. The crucial new signaling process turned up when the team took a closer look at cellular events that promote metastasis.

"We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor," said lead author Hasini Jayatilaka, a postdoctoral fellow at Johns Hopkins' Physical Sciences-Oncology Center. "At a fundamental level, we found that cell density is very important in triggering metastasis. It's like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere."

Jayatilaka and her colleagues found a medication mix that kept this microscopic message from being delivered. The team members cautioned that this treatment was tested in animal models, but not yet on human cancer patients. Nevertheless, they said the discovery contributes to a promising new focus for cancer research: disrupting the biochemical activity that prods cancer cells to spread through the body.

One of the study's senior authors, Denis Wirtz, who is Johns Hopkins University's vice provost for research and director of its Physical Sciences-Oncology Center, said no commercial drugs are now being produced specifically to inhibit metastasis because drug companies believe the best way to stop cancer from spreading is to destroy the primary tumor from which it originates.

"The pharmaceutical companies view metastasis as a by-product of tumor growth," said Wirtz, who also holds Johns Hopkins faculty appointments in chemical and biomolecular engineering, in pathology and at the Johns Hopkins Kimmel Cancer Center. "Our study looked more closely at the steps that actually initiate metastasis. By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor. This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes."

The two key drivers of metastasis, Wirtz said, are cancer cells' tendency to reproduce at a rapid rate and their ability to move through surrounding tissue until they reach the bloodstream, where they can then hitch a ride to spread the disease to other parts of the body.

By studying tumor cells in a three-dimensional environment that resembles human tissue, the researchers were able to determine how these activities begin. The team discovered that as two types of cancer cells reproduced and created more crowded conditions in the test site, these cells secreted certain proteins that encouraged migration. The researchers identified these proteins as Interleukin 6 (IL-6) and Interleukin 8 (IL-8).

"IL-6 and IL-8 seem to deliver a message to cancer cells, telling them to move away from the densely populated primary tumor," said lead author Jayatilaka, who recently earned her doctorate in chemical and biomolecular engineering as a member of Wirtz's lab team and earlier received her undergraduate degree from Johns Hopkins' Whiting School of Engineering.

In the team's animal studies, the researchers found that applying two existing drugs--Tocilizumab and Reparaxin--blocked the receptors that enable cancer cells to get their relocation orders. Tocilizumab is an approved medication for rheumatoid arthritis and is in trials for use in ovarian cancer cases. Reparaxin is being evaluated as a possible treatment for breast cancer.

"In our eight-week experiment, when we used these two drugs together, the growth of the primary tumor itself was not stopped, but the spread of the cancer cells was significantly decreased," Jayatilaka said. "We discovered a new signaling pathway that, when blocked, could potentially curb cancer's ability to metastasize."

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Post Options Post Options   Thanks (1) Thanks(1)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Jun 05 2017 at 9:47pm

Keytruda Shows Meaningful Clinical Benefit When Combined with Standard Therapy 


Two independent studies have added new evidence to the benefits of combined therapies with Merck‘s PD-1 inhibitor Keytruda (pembrolizumab) for the treatment of aggressive triple-negative breast cancer (TNBC).

Adding Keytruda to standard therapies for breast cancer improved the number of patients achieving a complete response to therapy.

The findings will be featured in a poster, “Efficacy/safety of epacadostat plus pembrolizumab in triple-negative breast cancer and ovarian cancer: Phase I/II ECHO-202 study,” to be presented at the American Society of Clinical Oncology (ASCO) 2017 Annual Meeting, set for June 2-6 in Chicago.

Designed to target the PD-1 receptor, Keytruda is meant to improve the activity of immune T-cells capable of fighting cancer cells. Originally approved by the U.S. Food and Drug Administration (FDA) to treat melanoma, Keytruda has since won FDA approval for several other cancers, such as non-small cell lung cancer, head and neck squamous cell carcinoma, classical Hodgkin lymphoma (cHL), and bladder cancer.

Researchers at the University of Pennsylvania’s Abramson Cancer Center are currently studying the benefits of Keytruda for other cancer types, including TNBC. Their Phase 1/2 ECHO-202 trial (NCT02178722) involved 39 patients with TNBC who received a combination of Keytruda and an investigational checkpoint inhibitor known as epacadostat, developed by Incyte.

Undergoing dose escalating evaluations, the combined therapy was found to be generally well-tolerated with no major adverse events being reported.

“In each patient group, the combination did not add any significant increase in side effects compared to what patients experience with the PD-1 inhibitor alone,” Dr. Tara Gangadhar, who led five of the new analyses from the ECHO-202 trial, said in a press release. Gangadhar is an assistant professor of hematology oncology at the university’s Perelman School of Medicine.


A second study, “Pembrolizumab plus standard neoadjuvant therapy for high-risk breast cancer (BC): Results from I-SPY 2,” evaluated the clinical benefits of Keytruda plus standard of care, given before surgery, to HER2-negative metastatic breast cancer.

The multicenter Phase 2 I-SPY 2 trial (NCT01042379) included 69 women who received Keytruda plus Taxol (paclitaxel) or standard therapy with Taxol alone. The Keytruda-Taxol combo more than tripled TNBC patients’ complete response rate compared to Taxol alone.

Patients with hormone receptor positive breast cancer had a 28 percent complete response rate, compared to the 14.8 percent response rate among the control group.

“This is incredibly exciting news for patients with aggressive cancers and the beginning of generating new and better curative options at diagnosis,” said Angela DeMichele, chair of trial operations for the study. “These findings reflect a growing body of knowledge about how these drugs interact with the immune system that will lead to safer use of PD-1 inhibitors in future studies.”

http://breastcancer-news.com/2017/06/01/keytruda-improves-aggressive-breast-cancer-response-to-standard-therapy



Edited by 123Donna - Jun 05 2017 at 9:47pm
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Post Options Post Options   Thanks (1) Thanks(1)   Quote mainsailset Quote  Post ReplyReply Direct Link To This Post Posted: Jun 06 2017 at 11:20am
'more than tripled the response' is a huge breakthrough and because Keytruda already has a track record I'm hopeful that it will join the lineup of drug therapies already approved soon.

All the more reason to keep up on these breakthroughs for everyone looking at treatment because it's good to go over these options with your oncology team as they just might be the treatment that saves your life!

Here's another article, check out the clinical trials

https://seekingalpha.com/article/4079115-lynparza-gets-parp-edge-breast-cancer

Edited by mainsailset - Jun 06 2017 at 11:26am
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Post Options Post Options   Thanks (1) Thanks(1)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Jun 09 2017 at 11:26am
This study is game changing - instead of trying to treat one type of cancer, they looked at the uniqueness of the responders to see what they had in common.

Cancer Drug Proves to Be Effective Against Multiple Tumors

The new study was based on a different idea. The immune system can recognize cancer cells as foreign and destroy them. But tumors deflect the attack by shielding proteins on their surface, making them invisible to the immune system.

Pembroluzimab is a new type of immunotherapy drug known as a PD-1 blocker, which unmasks the cancer cells so that the immune system can find and destroy them.

The drug is the happy result of a failed trial. A nearly identical drug, nivolumab, was given to 33 colon cancer patients, and just one showed any response — but his cancer vanished altogether.

What was special about that one patient? Dr. Diaz, a geneticist at Johns Hopkins until now, and lead author of the new study, found the answer: a genetic mutation that prevented the tumor from repairing DNA damage.

As a result, the man’s cancer cells contained a plethora of mutated genes, which produced thousands of strange-looking proteins on the surfaces of the cells. Once the tumor’s cloaking mechanism was short-circuited by the drug, the man’s immune system had no trouble targeting the foreign proteins on the cancer cells.

That led to the idea for the Dr. Diaz’s new study. He and his colleagues sought patients whose tumors had the same genetic defect, which can arise in any of four genes in a pathway that repairs damaged DNA. They gave these patients a PD-1 blocker and were surprised by the results.

The drug’s effects have been so durable that the investigators do not know how long the results should be expected to persist or how long these patients might expect to survive. That kind of result, Dr. Baselga said, “is insane.”

One patient in the study, Adrienne Skinner, 60, of Larchmont, N.Y., had an extraordinarily rare and deadly cancer, ampullary cancer, that arises at the end of the bile duct. There is no standard treatment, and the prognosis is dire.

Her doctors scheduled her for a drastic surgery that removes part of the pancreas, part of the small intestine, and the gall bladder. But her surgeon canceled the operation when he discovered her cancer had invaded her liver.

She tried chemotherapy instead — six months of one kind, then six months of another. Neither worked.

Then she qualified for Dr. Diaz’s clinical trial at Johns Hopkins. On April 15, 2014, Ms. Skinner had her first dose of the drug.

In July, her doctor inserted an endoscope for another biopsy. He turned to Ms. Skinner and said, “If someone hadn’t told me you have ampullary cancer, I would not have known.” The tumor was gone.

The trial involved giving patients the drug for two years, so Ms. Skinner continued to take the drug as a sort of insurance. Last year, she stopped, and her cancer has not returned.

“In effect, I was cured within months,” she said. “I have a great life.”

But even this promising trial has left a thread dangling: Why didn’t all of the patients respond?

There is now a fervid search for the answer. “Multiple labs are looking like crazy,” Dr. Balsega said.
http://www.nytimes.com/2017/06/08/health/cancer-drug-keytruda-tumors.html

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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Jun 16 2017 at 9:58am
Results from I-SPY 2 clinical trial has found that adding the drug pembrolizumab (Keytruda) in combination with standard therapy before surgery shows potential for meaningful outcomes in patients with locally advanced triple negative (TNBC) or hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) breast cancers.

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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Aug 16 2017 at 8:07pm

Triple Negative Breast Cancer Patients Who Responded to Immunotherapy Had Long-term Survival Benefit

Among patients with metastatic triple-negative breast cancer (TNBC) who were treated with the anti-PD-L1 cancer immunotherapy Tecentriq (atezolizumab), those who responded to the medicine lived significantly longer compared with those who did not respond, according to data from a small clinical study presented at the American Association of Cancer Research annual meeting.

About Triple Negative Breast Cancer

Approximately 12% of breast cancers are triple-negative breast cancers, meaning that they are estrogen-receptor negative (ER-), progesterone-receptor negative (PR-), and human epidermal growth factor receptor 2-negative (HER2-). This means that TNBC is not stimulated to grow from exposure to the female hormones estrogen or progesterone, nor through an overactive HER2 pathway.

Unfortunately, many available and effective treatment options for the majority of breast cancers block the growth stimulating effects of ER, PR and/or HER2; therefore, TNBC has limited therapeutic options.

In addition, TNBC tends to be an aggressive type of cancer, tends to be diagnosed at a more advanced stage, and proportionately affects younger women more often than other breast cancers. Novel treatment options for TNBC have lagged behind that of other types of breast cancers.

About Tecentriq

Tecentriq is an agent that helps to restore the body’s immune system in fighting cancer. It creates its anti-cancer effects by blocking a specific protein that is used by cancer cells to escape an attack by the immune system, called PD-L1. Once PD-L1 is blocked, cells of the immune system are able to identify cancer cells as a threat, and initiate an attack to destroy the cancer. Tecentriq and other “checkpoint inhibitors” have been approved for the treatment of several cancers recently.

In the current clinical study evaluating Tecentriq in patients with TNBC, the most significant findings were the difference in the overall survival between patients who responded to Tecentriq and patients who did not respond, and the prolonged average duration of response; 21 months, which is substantially longer than what has been seen with other treatments. All responders were alive after one year and the one-year survival rate for nonresponders was only 38 percent.

Immune therapy with checkpoint inhibitors appears to be a promising treatment approach for individuals with TNBC whether used alone or in combination with other therapies.2,3

References:

  1. #AACR17
  2. http://news.cancerconnect.com/keytrudahalaven-combo-may-effective-advanced-triple-negative-breast-cancer/
  3. http://news.cancerconnect.com/tecentriq-plus-abraxane-effective-combo-difficult-treat-breast-cancer/

    http://news.cancerconnect.com/triple-negative-breast-cancer-patients-responded-immunotherapy-long-term-survival-benefit/
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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Aug 17 2017 at 6:41pm
Cancer Drugs That Halt Tumors Can Also Shrink Them

A class of drugs known as CDK4/6 inhibitors, which have been approved for treating some types of breast cancer, may have much more to offer than previously thought. Not only can they stop tumors from growing by halting cell division, but they can also "spur the immune system to attack and shrink" them.

This was the main finding of a new study from the Dana-Farber Cancer Institute and Brigham and Women's Hospital, both in Boston, MA, the results of which have been published in the journal Nature.

CDK4/6 inhibitors are a class of drugs that work by blocking certain proteins called cyclin-dependent kinases (CDKs) 4 and 6, which promote the growth of cancer cells.

At present, these drugs have only been approved for treating some patients with metastatic breast cancer, "but they've also shown promise against others types of tumors in clinical trials," says co-first author Shom Goel, Ph.D., of the Dana-Farber Cancer Institute.

Shrink as well as halt tumors

Dr. Goel says that in early clinical trials of CDK4/6 inhibitors in breast cancer patients, they noticed that not only did the tumors stop growing - as you might expect with drugs that arrest cell division - but they also shrank, "sometimes quite dramatically."

He and his colleagues believe that scientists are only just beginning to discover the full potential of what CDK4/6 inhibitors may have to offer.

In their study, the researchers found that not only did the drugs stop cancer cells dividing, but they also promoted anti-cancer immunity in two ways.

One way was by getting cancer cells to increase their display of abnormal proteins on their surfaces, which made it easier for the immune system to find and destroy them.

Another way that the CDK4/6 inhibitors helped the immune system to attack tumors was by reducing immune cells called T regulatory cells (Tregs). Tregs usually dampen immune response, so the fewer there are, the fiercer the attack.

The team discovered the tumor-halting and tumor-shrinking effects when they treated mice with breast cancer and other solid tumors with the CDK4/6 inhibitor abemaciclib. The experimental drug recently received priority status from the U.S. Food and Drug Administration (FDA).

Confirmed in human samples

When they analyzed biopsy samples from women taking part in a clinical trial testing a CDK4/6 inhibitor for breast cancer, the researchers observed the same effects that they saw in the mice; not only did the drug halt the tumor cell cycle, but it also spurred the immune system to attack the tumors.

The authors explain that clinical trials show that around 20 percent of breast cancer patients treated just with abemaciclib show a "significant response," while another 20 to 30 percent experience "stabilizations of tumor growth." These effects emerge within 4 months of starting on the drug.

Dr. Goel and colleagues also found that the anti-cancer effect was even stronger when they coupled the CDK4/6 inhibitors with other immunotherapy drugs known as checkpoint inhibitors, which can stop cancer cells evading the immune system.

"It appears that the CDK4/6 inhibitors might be able to sensitize some patients' cancers to the anti-tumor effects of immune checkpoint inhibitors. The result might be especially encouraging for breast cancer patients, who have derived little benefit from immunotherapy in trials conducted to date."

The team says that more work should be done to discover why CDK4/6 inhibitors appear to benefit some patients more than others. They also hope that their findings will encourage others to look at how to combine CDK4/6 inhibitors with different immunotherapies.

http://www.medicalnewstoday.com/articles/319013.php



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Post Options Post Options   Thanks (0) Thanks(0)   Quote Sarahlou Quote  Post ReplyReply Direct Link To This Post Posted: Aug 18 2017 at 10:00pm
A friend is in a clinical trial using Keytruda and has had success with it shrinking her tumor. She has TNBC.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote 123Donna Quote  Post ReplyReply Direct Link To This Post Posted: Aug 31 2017 at 8:47am

Study sheds light on why some breast cancers have limited response to immunotherapy

UNC Lineberger Comprehensive Cancer Center researchers have identified a possible reason why some aggressive breast cancers are unresponsive to certain immunotherapy treatments, as well as a potential solution.

In the Journal of Clinical Investigation, researchers report on their study that explored a perplexing question: Why were drugs designed to unleash the immune system against cancer ineffective in a type of triple negative breast cancer with a heavy presence of immune cells? Their findings could lead to a strategy to improve immunotherapy responses in the "claudin-low" subtype of breast cancer.

"We were trying to figure out why a tumor made up, in some instances, of half immune cells doesn't respond to a treatment that should ramp up immune cells present in the tumor," said the study's senior author Jonathan Serody, MD, UNC Lineberger member and the Elizabeth Thomas Professor in the UNC School of Medicine. "I think it's important for us to try to start segregating out the types of tumors that don't respond to these treatments at a much granular genomic level, and try to figure out new mechanisms to enhance the response rate to immunotherapy."

The American Cancer Society estimates that approximately 12 percent of breast cancers are "triple negative," meaning they lack three cell surface receptors that are known to help drive the cancer. Triple negative breast cancer tumors typically grow faster and come back sooner than other breast cancer types. There are no targeted treatments for these cancers.

In a subset of triple negative breast cancers known as "claudin low," researchers found an elevated level of immune cells in and around the tumors. They believed this would help the body fight the cancer. However, the researchers found the opposite: "Checkpoint inhibitors," a type of immunotherapy that works by unlocking the immune system's brakes against cancer, were ineffective in this subtype.

They determined with gene expression analysis that, instead of being flooded with immune cells that attack cancer tumors, claudin-low tumors had a high concentration of regulatory T-cells - a type of immune cell that suppresses the body's defenses. Claudin-low tumors were releasing a chemical signal to attract these regulatory T-cells.

"This regulatory T-cell population is preventing the immune system from rejecting the cancer," said UNC Lineberger's Benjamin Vincent, MD, an assistant professor in the UNC School of Medicine. "We thought if we could get rid of those cells, we could help the immune system better fight the breast cancer cells."

In an effort to allow the immune-stimulating cancer treatments to work, the researchers tested an investigational approach to deplete the regulatory T-cells, and they combined the treatment with a checkpoint inhibitor in order to try to improve outcomes. This combination slowed tumor growth. They believe they have identified a key aspect of what is preventing immunotherapy treatments from working.

"This finding may shed some light on why response rates to immunotherapy treatments remain low in triple negative breast cancer," Vincent said. "We are looking to understand why patients who don't respond don't respond, and what we can do to render their tumors immunotherapy responsive."

Vincent is helping to lead a clinical trial testing this strategy to improve responses to checkpoint inhibitors. Researchers also believe these findings may also underscore the need to study other cancer types at a genomic level to understand differences in response rates to immunotherapy treatments.

"This speaks to the mission of UNC Lineberger, which is to conduct groundbreaking basic science research, but always with the mission of extending and improving the lives of patients as our end goal," Vincent said.


https://medicalxpress.com/news/2017-08-immune-cells-contribute-treatment-resistance.html



Edited by 123Donna - Aug 31 2017 at 8:48am
DX IDC TNBC 6/09 age 49, Stage 1,Grade 3, 1.5cm,0/5Nodes,KI-67 48%,BRCA-,6/09bi-mx, recon, T/C X4(9/09)
11/10 Recur IM node, Gem,Carb,Iniparib 12/10,MRI NED 2/11,IMRT Radsx40,CT NED11/13,MRI NED3/15

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Post Options Post Options   Thanks (0) Thanks(0)   Quote mainsailset Quote  Post ReplyReply Direct Link To This Post Posted: Aug 31 2017 at 10:56am
Donna, I saw that report this morning and it's so interesting and a good reminder how now more than ever it's important for our medical teams to id all the characteristics of our particular tumor to determine what choices in treatment can be made. Amazing to me to see the researchers perplexed by the finding that the Claudin low tumors reacted the opposite of what they expected.
dx 7/08 TN 14x6.5x5.5 cm tumor

3 Lymph nodes involved, Taxol/Sunitab+AC, 5/09 dbl masectomy, path 2mm tumor removed, lymphs all clear, RAD 32 finished 9/11/09. 9/28 CT clear 10/18/10 CT clear
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Post Options Post Options   Thanks (0) Thanks(0)   Quote 1maJ Quote  Post ReplyReply Direct Link To This Post Posted: Sep 04 2017 at 10:22pm
Hi Donna, thanks for posting all this info on new research.  I came back to the forum to look for the latest on TNBC treatments, and this gives me hope and calms me down.  I am 2 years out from diagnosis, the time when most women have their recurrence, so I am finding myself to have a bit more anxiety than I would like.  Every little headache is a reminder that something could be brewing :(  But I am doing fine though, and enjoying life more than ever :)

Thanks!

Ima
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