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Showing posts with label Promising. Show all posts
Showing posts with label Promising. Show all posts

Wednesday, July 17, 2013

Promising Advances in Early Cancer Detection

Early detection is key in the fight against cancer. Since most therapy is focused around treating cells at the site of origin, it is important to detect cancerous cells as early as possible, before it has had the chance to metastasize. Therefore, having testing procedures to detect cancer at initial onset is vital to successfully eliminate the disease.

The most effective screening test would possess attributes such as being non-invasive, safe, reliable and inexpensive. The Pap smear developed in the 1930s was one of the first screening tests available for cervical cancer, and has since become routine for women during yearly pelvic exams. This procedure is inexpensive and relatively non-invasive although it may be uncomfortable for some. However, the reliability is scrutinized due to the incident of false positives where cells are wrongly diagnosed as cancerous. This screening procedure requires subjective analysis by a cytologist reading hundreds of samples a day, at this point, human error becomes inevitable. Despite the shortcomings, most would agree that they would elect to take the test.

Other diagnostic procedures include imaging techniques, endoscopy, and biopsy. Imaging techniques, such as x-ray and MRI, are not invasive like endoscopy and biopsies, but most of these techniques are only effective at later stages in cancer development for obvious reasons. Many of these procedures are used as a final definitive screen in diagnosis because they do carry some patient risk.

The field of biomarker screening in biological fluids such as blood and urine has really become the focal point of cancer research for early detection. The routinely used prostate-specific antigen (PSA) and Cancer Antigen CA-125 screens measure individual biomarkers. Although these are good screening tools, the new wave of biomarker screening is focused on forms of testing that can cover a broad spectrum of cancer types in one analysis.

Exosome Diagnostics is researching & developing a newly discovered cancer cell fragment called exosomes. Tumors shed exosomes into the blood supply and these exosomes carry genetic material and proteins that can reveal the type and progression of the cancer.

ONCOblotR Labs has a Laboratory Developed Test that is a blood test for cancer. The test uses a protein screening method and focuses on ENOX2 protein expressed only by cancer cells. These proteins are shed into the circulation and can be detected in the blood. Different cancers produce a different type of ENOX2 protein that is identified by the ONCOblotR Test. Therefore, the origin of the cancer can be detected. Both of these revolutionary tests can detect cancer very early, even before clinical symptoms are presented.

The future of screening and diagnostic testing looks promising and provides another valuable tool to fight cancer. These early detection capabilities are especially promising for those types that can only be detected at later stages when clinical symptoms arise and survival rates are low. Tests such ONCOblotR and Exosome Diagnostics' RNA tests are limitless. These procedures are high- throughput and all-encompassing so new cancer types will be added as additional markers are found. As research continues in the area of high-throughput biomarker screening, early detection will certainly save millions of lives.

Cheri M. Turman, PhD. - Cheri completed her bachelor's degree in chemistry with a minor in biology and a master's degree in chemistry specializing in biotechnology from Stephen F. Austin State University. She received her doctorate at The University of Texas Health Science Center at Houston and MD Anderson Cancer Center specializing in biochemistry and molecular biology. Cheri consults with ONCOblotR Labs, which offers the ONCOblotR Test. To read more about ONCOblotR Labs, and their latest test for cancer visit their website at http://www.oncoblotlabs.com/ .

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Thursday, June 27, 2013

Why Does Promising Anti-Cancer Therapy Suddenly Stop Working?

Editor's Choice
Academic Journal
Main Category: Cancer / Oncology
Article Date: 24 Jun 2013 - 9:00 PDT Current ratings for:
Why Does Promising Anti-Cancer Therapy Suddenly Stop Working?
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Why does anti-cancer therapy stop working at a specific stage? Scientists in Israel and the USA believe they have made a breakthrough in understanding why a hopeful anti-cancer therapy fails to destroy tumor cells successfully.

The researchers, whose study is published in PNAS (Proceedings of the National Academy of Sciences), believe their findings may lead to new approaches in overcoming this cul-de-sac.

Suppressing the mTOR (mammalian target Of Rapamycin) protein has been extremely challenging for oncologists.

mTOR plays a key role in regulating vital cell growth processes - it is a bit like a communications command center, receiving external signals from hormones, growth factors and proteins. It then sends out "on" or "off" signals for the cell to grow and divide, seek nutrition, or use that nutrition. mTOR is strongly activated in several solid cancers.

While drugs have been shown to suppress mTOR and have been successful in causing the death of cancer cells in the outer layers of malignant tumors, in clinical trials they have failed in destroying the core of those tumors.

Hypoxia (lack of oxygen) is an almost-universal characteristic of solid tumors that can affect how tumors respond to therapies. Scientists know that the condition of hypoxia affects the behavior of mTOR signaling, but nobody knew what the mechanism was.

Prof. Emeritus Raphael D. Levine, from the Institute of Chemistry at the Hebrew University of Jerusalem, Israel, and scientists from the David Geffen School of Medicine at UCLA and the California Institute of Technology set out to determine what role hypoxia plays on mTOR signaling in model brain cancer systems and whether this could explain why promising mTOR drugs fail.

They used a new microchip technology to measure the mTOR protein-signaling network in cancer cells. They also used a new set of theoretical tools derived from the physical sciences to interpret the results. This dual approach simplified an otherwise extremely complex biological system.

MTOR-pathway-v1.7
The mTOR biochemical pathway is a complex one

The investigators found that at a specific level of hypoxia, which is typical in solid tumors, the mTOR signaling network switches between two sets of properties. At exactly the moment when the switching over takes places, the theoretical models predicted that mTOR would not respond to mTOR-inhibiting medications.

According to the combined experiment finding, the researchers believe that the switching over might be a kind of phase transition, something not observed before in biological systems.

This phase transition happened very suddenly, and cells being studied stopped responding like they had done before. The authors wrote "In the case of the tumor, the 'drugging' of the mTOR ceased, meaning that the tumor was no longer inhibited."

These results: explain why promising mTOR-inhibiting drugs stop working at a specific stage"indicate that certain complex biological behaviors, which often confound scientists who are seeking to find effective therapies for human diseases, may be understood by the effective application of experimental and theoretical tools derived from the physical sciences."Levine wrote in the PNAS Abstract:

"We find a hypoxia-induced switch within a mammalian target of rapamycin (mTOR) signaling network. At the switching point, mTOR is predicted, and then shown by experiment, to be unresponsive to inhibition. These results may help explain the undistinguished performance of mTOR inhibitors in certain clinical trials."

In an animal study, scientists from the University of California San Diego, La Jolla, found that mTOR-inhibitors may have adverse effects on heart function in patients with ongoing heart problems.

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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posted by Greg Pawelski on 24 Jun 2013 at 12:17 pm

One of the themes at the 103rd Annual American Association of Cancer Research was the growing recognition that human tumors exist as microenvironments and not isolated single cells. The tumor microenvironment is characterized by regions of fluctuating hypoxia, low pH, and nutrient deprivation. Each of these microenvironment factors has been shown to cause severe disturbance in cell metabolism and physiology.

By examining drug-induced cell death events in native-state 3D (three dimensional) microclusters, the functional profiling platform has the unique capacity to capture stromal, cytokines (chemokines), macrophages, lymphocytes, vascular and inflammatory cell interactions with tumor cells, known to be crucial for clinical response prediction.

The microclusters recapitulate the human tumor environment, while the "3D" advancement recreates the extracellular matrix (metalloproteinases). The platform studies cancer response to drugs within this microenvironment, enabling it to provide clinically relevant predictions to cancer patients. It is this capacity to study human tumor microenvironments that distinguishes it from other platforms in the field.

Tumors are very complex organisms. Ignoring this complexity, most studies of human cancer in culture have focused upon individual tumor cells that have been removed from their complex microenvironment.

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Friday, May 24, 2013

T-DM1 Produces Promising Results Against Advanced HER2-Positive Breast Cancer

Among women with metastatic, HER2-positive breast cancer, trastuzumab emtansine (T-DM1)—an investigational drug that combines HerceptinR (trastuzumab) and a chemotherapy drug—resulted in better progression-free survival than standard chemotherapy and Herceptin. The results of this Phase II clinical trial were presented at the 2011 European Multidisciplinary Cancer Congress.??

Approximately 20-25% of breast cancers overexpress (make too much of) the HER2 protein. HER2-targeted therapies such as Herceptin have dramatically improved outcomes for women with HER2-positive breast cancer, but researchers continue to explore new approaches to treatment.???

T-DM1 links Herceptin with a chemotherapy drug (DM1). T-DM1 delivers Herceptin and DM1 directly to HER2-positive cells, and limits exposure of the rest of the body to the chemotherapy.??

To evaluate T-DM1 for the initial treatment of metastatic, HER2-positive breast cancer, researchers conducted a Phase II clinical trial among 137 women. Study participants were treated with either T-DM1 or Herceptin plus TaxotereR (docetaxel).??

Survival without cancer progression was 14.2 months among women in the T-DM1 group and 9.2 months among women in the Herceptin plus Taxotere group.?In addition to delaying cancer progression, T-DM1 was also better tolerated by patients. Discontinuation of treatment due to side effects occurred in 7.2% of women in the T-DM1 group and 28.8% of women in the Herceptin plus Taxotere group.?

These results suggest that T-DM1 may be safe and effective for the treatment of advanced, HER2-positive breast cancer. Results from ongoing Phase III trials will provide additional information about this drug.?

Reference: Hurvitz S, Dirix L, Kocsis J et al. Trastuzumab emtansine (T-DM1) vs trastuzumab plus docetaxel (H+T) in previously untreated HER2-positive metastatic breast cancer (MBC): primary results of a randomized, multicenter, open-label phase II study (TDM4450g/BO21976). Presented at the 2011 European Multidisciplinary Cancer Conference. Stockholm, Sweden. September 23-27, 2011. Abstract 5001.?

Posted October 5, 2011?


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