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Autor Thema: Might Smallpox Virus Help Fight a Lethal Breast Cancer?  (Gelesen 1818 mal)


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Might Smallpox Virus Help Fight a Lethal Breast Cancer?
« am: 03. Oktober 2012, 19:19:17 »

Might Smallpox Virus Help Fight a Lethal Breast Cancer?

Promising results for triple-negative form of disease seen in tests with mice
October 1, 2012 RSS Feed Print

By Alan Mozes
HealthDay Reporter

MONDAY, Oct. 1 (HealthDay News) -- New animal research suggests it may be possible to use a form of smallpox virus to infect and kill the tumor cells of a particularly virulent form of breast cancer.

To date, this novel approach to attacking what's known as triple-negative breast cancer has centered exclusively around work with mice.

More information
The U.S. National Cancer Institute explains triple-negative breast cancer.


Here is another article about the same incident:

At the end of my entry I add the background about TNBC found at

Now to the important part, something NOT mentioned in the above articles: Just one year ago, the very same researcher went into public with a new treatment against TNBC (triple-negative breast cancer), and it was ... a HERPES VIRUS

As a piece of proof I copy the complete press release of the congress, October 2011:

News from the Clinical Congress
2011 Clinical Congress
October 23–27, 2011    CONTACT: Sally Garneski
or Cory Petty

Monday, October 24, 1:00 p.m. (PDT)

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

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, but not necessarily 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.

# # #

So, the facit is: Stay calm and wait. A press release does not a therapy make.

Triple-Negative Breast Cancer

Current Clinical Trials

Triple-negative breast cancer (TNBC) is defined as the absence of staining for estrogen receptor, progesterone receptor, and HER2/neu. TNBC is insensitive to some of the most effective therapies available for breast cancer treatment including HER2-directed therapy such as trastuzumab and endocrine therapies such as tamoxifen or the aromatase inhibitors. Combination cytotoxic chemotherapy administered in a dose-dense or metronomic schedule remains the standard therapy for early-stage TNBC.[1] A prospective analysis of 1,118 patients who received neoadjuvant chemotherapy at a single institution, of whom 255 (23%) had TNBC, found that patients with TNBC had higher pathologic complete response (pCR) rates compared with non-TNBC patients (22% vs. 11%; P = 0.034).[2][Level of evidence: 3iiDiv] Improved pCR rates may be important since in some studies, pCR is associated with improved long-term outcomes.

Platinum agents have recently emerged as drugs of interest for the treatment of TNBC. One trial that treated 28 women with stage II or stage III TNBC with four cycles of neoadjuvant cisplatin resulted in a 22% pCR rate.[3][Level of evidence: 3iiiDiv] An ongoing randomized clinical trial, CALGB-40603 (NCT00861705), is evaluating the benefit of carboplatin added to paclitaxel and adriamycin plus cyclophosphamide chemotherapy in the neoadjuvant setting. Another trial, entitled the Triple Negative Trial (NCT00532727), is evaluating carboplatin against docetaxel in the metastatic setting. These trials will help to define the role of platinum agents for the treatment of TNBC. Currently, there is no established role for adding platinum agents to the treatment of early-stage TNBC outside of a clinical trial.

The poly (ADP-ribose) polymerase (PARP) inhibitors are emerging as promising therapeutics for the treatment of TNBC.[4] PARPs are a family of enzymes involved in multiple cellular processes, including DNA repair. Because TNBC shares multiple clinicopathologic features with BRCA-mutated breast cancers, which harbor dysfunctional DNA repair mechanisms, it is possible that PARP inhibition, in conjunction with the loss of DNA repair via BRCA-dependent mechanisms, would result in synthetic lethality and augmented cell death. PARP inhibitors are currently being evaluated in clinical trials for patients with BRCA mutations and in TNBC.
Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with triple-negative breast cancer. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.


    Mehta RS: Dose-dense and/or metronomic schedules of specific chemotherapies consolidate the chemosensitivity of triple-negative breast cancer: a step toward reversing triple-negative paradox. J Clin Oncol 26 (19): 3286-8; author reply 3288, 2008.  [PUBMED Abstract]

    Liedtke C, Mazouni C, Hess KR, et al.: Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer. J Clin Oncol 26 (8): 1275-81, 2008.  [PUBMED Abstract]

    Silver DP, Richardson AL, Eklund AC, et al.: Efficacy of neoadjuvant Cisplatin in triple-negative breast cancer. J Clin Oncol 28 (7): 1145-53, 2010.  [PUBMED Abstract]

    Anders CK, Winer EP, Ford JM, et al.: Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer. Clin Cancer Res 16 (19): 4702-10, 2010.  [PUBMED Abstract]
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