UPDATE 1-Bayer profit misses estimates on generic rivalry

July 30, 2010 By Leave a Comment

FRANKFURT, July 29 (Reuters) – Bayer’s (BAYGn.DE) quarterly earnings fell short of market expectations because generic competition for its two best-selling drugs overshadowed a rebound at its plastics unit.

In the second quarter, group underlying profit — or earnings before interest, taxes, depreciation and amortisation (EBITDA) before special items — rose 8.6 percent to 1.92 billion euros, Germany’s largest drugmaker, said on Thursday.

Analysts had expected adjusted EBITDA, which serves as the group’s main gauge of success, to rise to 1.98 billion. [ID:nLDE66P093] Quarterly net income of 525 million euros at the maker of cancer drugs, weed killers and car coatings also missed the 768 million estimated by analysts.

Generic-drug industry leader Teva (TEVA.TA) has brought a copycat version of Bayer’s YAZ birth-control pill to U.S. markets earlier than expected, while a generic version by Novartis (NOVN.VX) is chipping away at sales of blockbuster multiple sclerosis drug Betaferon. [ID:nLDE6501SV] [ID:nN29138356]

Bayer, the inventor of Aspirin and synthetic rubber, is meanwhile pinning its hope on potential blockbuster Xarelto, an experimental blood thinner for stroke prevention for which crucial test results are expected this year.

The group reiterated it expected 2010 core adjusted operating profit above 7 billion euros ($9.1 billion) as a rosier outlook for its plastics and foams unit MaterialScience offset expected weakness in drugs and crop chemicals sales.

The group’s CropScience division, one of the world’s largest makers of conventional pesticides, was hit by an unusually cold winter, followed by a hot and dry summer in the Northern Hemisphere.

(Reporting by Ludwig Burger)

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Research and Markets: Overview of Indian Oncology Market Report – Expanding Ageing Population and Better Outreach of Modern Therapies Fuels Growth

July 23, 2010 By Leave a Comment

DUBLIN–(Business Wire)–
Research and Markets
(http://www.researchandmarkets.com/research/5d1b7e/overview_of_indian) has
announced the addition of Frost & Sullivan’s new report “Overview of Indian
Oncology Market” to their offering.

This Frost & Sullivan research service titled Overview of Indian Oncology Market
provides an understanding of various cancer indications and their market
structure. In this research, Frost & Sullivan’s expert analysts thoroughly
examine the following markets: breast cancer, lung cancer market, prostate
cancer market, head and neck cancer market, ovarian cancer market, cervical
cancer market, renal cell carcinoma market and pancreatic cancer market.

Market Overview

Expanding Ageing Population and Better Outreach of Modern Therapies Fuels Growth
in the Indian Oncology Market

The Indian oncology market is witnessing strong growth alongside fast-paced
development in the pharmaceutical sector. The market is expected to grow at a
compound annual growth rate (CAGR) of 21 percent from 2008 to 2014, driven by
the introduction of new treatments, increasing number of patients on
chemotherapy, and improved access to modern cancer therapies. Cancer is one of
the ten leading causes of death in India. Nearly half the cases are curable if
detected early. Due to the high prevalence of cancer, the oncology market is
witnessing fast-paced growth. High spending on therapeutic drugs for cancer in
the emerging economies including India is fuelling market growth. “With the
expanding base of patients undergoing chemotherapy in the major markets and
greater access to modern therapies, cancer drugs are poised for widespread
uptake,” notes the analyst of this research service. “Moreover, the increase in
the ageing population is another factor contributing positive momentum for the
market.” A 40 to 50 percent increase in incidences can be seen for some of the
major cancer indications such a prostate cancer, breast cancer, ovarian cancer,
head and neck cancer. Also the high prevalence of smoking is loading to the
proliferation in the number of patients afflicted with lung cancer.

Trends indicate that the incidence of cancer will is set to assume dangerous
proportions in the future, making the disease one of the major chronic diseases
that will continue to impact peoples lives. Going forward, greater progress in
cancer therapy is envisioned along with more light being thrown on the cause of
the disease. Yet, it remains to be seen how much the refinement in the present
detection, diagnostic, and therapeutic technologies will help in containing the
spread of the disease. Large quantities of generic drugs are available in the
market for cancer treatment. Chemotherapy is highly genericised. These products
are low-priced and hence place restrictions on potential revenues.

In this market with increasing competition and generic players, it is important
to strategically position products as early in their life cycle as possible to
generate the most revenue prior to patent expiration. For the competitive
chemotherapy market, showing superior efficacy and less toxicity in combination
with targeted therapy drugs is one of the best ways to distinguish the product
over others. “To be successful in the cancer market of the future, it is
imperative for product to be established as an integral part of the standard
combination therapy regimen,” says the analyst. “This will guarantee strong
revenue and the most value to patients.” Identifying optimal drug combinations,
which significantly increase median survival, tumor resolution and reduce
toxicity and adverse effects should be the prime task for companies in the
cancer therapeutic market.

Market Sectors

Expert Frost & Sullivan analysts thoroughly examine the following market sectors
in this research:

* Pharmaceuticals
* Biotechnology

Key Topics Covered:

1. Executive Summary

2. Indian Oncology Market

3. Breast Cancer Market

4. Lung Cancer Market

5. Ovarian Cancer Market

6. Prostate Cancer Market

7. Head and Neck Cancer Market

8. Cervical Cancer Market

9. Renal Cell Carcinoma Market

10. Pancreatic Cancer Market

For more information visit

http://www.researchandmarkets.com/research/5d1b7e/overview_of_indian

Research and Markets
Laura Wood, Senior Manager,
press@researchandmarkets.com
U.S. Fax: 646-607-1907
Fax (outside U.S.): +353-1-481-1716

Copyright Business Wire 2010

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Cellceutix CFO Discusses Autism Drug, Kevetrin(TM) and Company Progressions With CEOCFO Interviews and News

June 4, 2010 By Leave a Comment

BEVERLY, MA, Jun 03 (MARKET WIRE) —
Cellceutix Corporation (OTCBB: CTIX) is pleased to announce that its
Chief Financial Officer, Leo Ehrlich, has been featured in an interview
with leading online financial publication, CEOCFO Interviews and News.
The interview was conducted by CEOCFO Senior Editor Lynn Fosse and
highlighted the uniqueness of Cellceutix and the details that make it
stand out from all other biotechnology companies in the industry.

In the interview, Mr. Ehrlich discusses the progressions of KM-391,
Cellceutix’s compound for the treatment of autism, and Kevetrin, their
drug being developed as a treatment for drug-resistant cancers. Mr.
Ehrlich explained why their autism drug is revolutionary as there is no
drug available today for the treatment of autism. Additionally, Mr.
Ehrlich also discusses the company’s growth strategy as it relates to
future potential partnerships, shareholder value and the strength of the
Cellceutix management team.

“We are not dealing with just another cancer drug; we have indications
that it is effective against drug-resistant cancers, which is a
multibillion dollar market,” Mr. Ehrlich explained. “Most cancer drugs
currently out there are just another variation of existing cancer drugs,
whether they be another platinum based drug or another Taxol. We,
however, have a completely new and novel compound.”

“We are pleased to have been interviewed by CEOCFO. The interview
provides us another opportunity to showcase to our shareholders the many
milestones we are achieving and the progressions of our business
strategy,” commented Mr. Ehrlich.

The interview is available at:

http://www.cellceutix.com/CTIX-Cellceutix10-RLO-Changes-Color.pdf

http://ceocfointerviews.com

About CEOCFO Interviews & News

CEOCFO Interviews & News is a weekly print online publication, marketing
engine featuring publicly traded & venture capital companies on the U.S.
(NYSE, NASDAQ, AMEX, OTC: BB, Pink Sheets) and Canadian (TSX & TSX-V)
stock exchanges, Investment & Money Management Ideas.

About Cellceutix
Cellceutix Corporation is a preclinical cancer and
anti-inflammatory drug developer. Cellceutix owns the rights to eight
drug compounds, including Kevetrin(TM), which it is developing as a
treatment for certain cancers, and KM-391, which it is developing for the
treatment of autism. More information is available on the Cellceutix web
site at www.cellceutix.com.

This Press Release contains forward-looking statements that are based on
our current expectations, beliefs and assumptions about the industry and
markets in which Cellceutix Corporation operates. Such forward-looking
statements involve known and unknown risks, uncertainties, and other
factors that may cause Cellceutix’s actual results to be materially
different from any future results expressed or implied by these
statements. Actual results may differ materially from what is expressed
in these statements, and no assurance can be given that Cellceutix can
successfully implement its core business strategy and improve future
earnings.

The factors that may cause Cellceutix’s actual results to differ from its
forward-looking statements include: Cellceutix’s current critical need
for additional cash to sustain existing operations and meet ongoing
existing obligations and capital requirements; Cellceutix’s ability to
implement its new product development and commercialization, enter into
clinical trials, expand the intellectual property portfolio, and receive
regulatory approvals in a timely and cost-effective manner. All
forward-looking statements are also expressly qualified in their entirety
by the cautionary statements included in Cellceutix’s SEC filings,
including its quarterly reports on Form 10-Q and its annual report on
Form 10-K.

Kevetrin and KM-391 have not been studied in humans at this time. The
Company’s positive results in animal studies do not necessarily guarantee
success in humans, though they may form the basis for beginning Phase 1
trials.

Contact:
Cellceutix Corp.
Leo Ehrlich
CFO
(978) 633-3623
Leo@Cellceutix.com

Copyright 2010, Market Wire, All rights reserved.

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New drug type developed to kill lymphoma cells

May 11, 2010 By Leave a Comment

Washington, May 11 (ANI): Scientists have developed a new type of drug designed to kill non-Hodgkin lymphoma tumour cells.

The breakthrough could lead to potential non-toxic therapies for cancer patients.

The researchers, including Dr. Ari Melnick, of Weill Cornell Medical College, Dr. Alexander MacKerell, of the University of Maryland and Dr. Gilbert Prive, of the University of Toronto, have identified a drug that targets an oncogene known as BCL6.

BCL6 functions as a master regulatory protein.

“It”s a protein that controls the production of thousands of other genes. Because of that, it has a very profound impact on cells and is required for lymphoma cells to survive and multiply,” said Melnick.

BCL6 causes the majority of diffuse large B cell lymphomas, the most common form of non-Hodgkin lymphoma.

Currently, about 60 percent of diffuse large B cell lymphomas can be cured with chemo-immunotherapy, said Melnick.

“The hope is that we can improve that to a higher percent, and in the long term reduce the need for chemotherapy,” he added.

Traditional cancer drugs target enzymes, which have small pockets on their surfaces that can be blocked with molecules.

Until now, pharmaceutical companies have been reluctant to create drugs that target a protein like BCL6 because they function through a different mechanism involving interactions with cofactor proteins involving extensive protein surfaces.

“And because the real estate covered by these interactions is so large, the drug companies have viewed these as being not druggable targets,” said Melnick.

The researchers could identify a “hot spot” on BLC6 that they predicted would play a critical role in protein interactions.

They showed that their BCL6 inhibitor drug was specific to BCL6, and did not block other master regulatory proteins.

The drug had powerful lymphoma killing activity and yet was non-toxic to normal tissues.

“This is the first time a drug of this nature has been designed and it shows that it”s not actually impossible to target factors like BCL6,” he said.

Emerging data from other investigators suggests that BCL6 is important in many other tumor types, including forms of leukemia.

The study has been published in a recent issue of Cancer Cell. (ANI)

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Flower can boost efficiency of anti-cancer drugs by one million times

April 29, 2010 By Leave a Comment

London, Apr 29 (ANI): An extract from the white bloom can boost the efficiency of anti-cancer drugs by one million times, claim scientists.

According to experts working for Leukaemia Busters, molecules from Gypsophila Paniculata – commonly known as Baby”s Breath – appeared in trials to break down the membrane of deadly cancer cells.

This makes it far easier for antibody-based drugs to attack the cancer itself, reports The Sun.

The Southampton-based charity was set up by Dr David Flavell and his wife Bee.

Dr Flavell said yesterday: “This could truly revolutionise the way these antibody-based drugs work and it will save lives. And there is a really big possibility this can be used for many cancers.”

Scientists are now preparing for clinical trials. (ANI)

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Nearby bone cells may trigger some blood cancers

March 22, 2010 By Leave a Comment

Certain blood cancers may be triggered by signals sent from surrounding bone cells, not by individual cells going bad, and interrupting those signals may offer a new approach to treating leukemia, US researchers said.

“Cancer is generally thought to be a single cell going rogue. It does so by accumulating a series of genetic injuries,” said Dr. David Scadden of the Harvard Stem Cell Institute, whose study appears in the journal Nature.

But Scadden and colleagues instead found that genetic changes in bone cells — where blood stem cells reside — can cause mice to develop myelodysplasia, a condition that can lead to an acute form of the blood cancer leukemia.

Studies in mice showed that when the team altered a gene in the bone cells called Dicer1, it had a damaging effect on blood stem cells as well.

“The blood started to take on a picture which resembled a very poorly understood human disease called myelodysplasia,” Scadden, who directs the Center for Regenerative Medicine at Massachusetts General Hospital, said in a telephone interview.

“It has a complication of developing leukemia,” he said, which is exactly what some of the animals in the study did.

“The reason that this is important is it says the environment can actually become such an important part of the function of the tissue — the blood in this case — that it can lead to the emergence of new genetic abnormalities that can become fatal for the whole organism,” Scadden said.

He said the findings offer a new understanding of the source of some cancers, which can come from outside of cells.

Scadden said interrupting the communication between surrounding cells and cancer cells could offer another approach to making cancer drugs.
Agencies

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New drug kills cancer like a vampire slayer

September 19, 2009 By Leave a Comment

Washington, Sept 18 (ANI): Scientists at Tel Aviv University have developed a novel drug that delivers anti-cancer compounds straight to the tumour.

Lead researcher Dr. Ronit Satchi-Fainaro believes that the new invention may alleviate particularly malicious forms of cancers like osteosarcomas and bone metastases and combat resistance to anti-cancer drugs like Taxol, keeping other normal healthy cells around the tumor safe.

Most of us have small tumors in our body at all times. They start the size of a pinhead and usually remain at that size as dormant and asymptomatic tumors. Then, at some point, cancer cells proliferate and the tumor grows in mass.

At that point the tumor cells migrate to the bones and start recruiting blood vessels using a chemical attractant in order to draw blood for their continued growth in a process called angiogenesis.

The researchers looked into the chemical that causes the blood, or endothelial cells, to gravitate to the activated, newly malignant cancer cells.

According to Satchi-Fainaro, the innovative drug delivery system delivers compounds like Taxol known to stop blood vessel growth to cancerous tumors.

She bound existing cancer drugs to an inert polymer that doesn’t react with the immune system.

“Like a stealth airplane,” she says, the polymer passes through the body’s defense system unnoticed.

Then, programmed to find the tumour using the bisphosphonate drug Alendronate, a drug that binds to bones, the carrier delivers its cancer-killing payload.

The study conducted over animal models, found that the researchers were able to reverse the growth of bone cancer tumors.

In a second study, she found that loading her polymer with the anti-cancer drug Taxol could inhibit tumour growth by 50pct, compared to a Taxol dose that had no effect on tumour growth at all.

The study is published is published in prestigious journals Angewandte Chemie and PLoS One. (ANI)

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Natural compounds in vegetables may make chemotherapy more effective

September 1, 2009 By Leave a Comment

Washington, September 1 (ANI): Natural compounds present in plants and some vegetables may help treat cancer even more effectively, when used side-by-side with chemotherapy drugs, according to new research.

A study published in the International Journal of Cancer has found that chlorophyllin-a water-soluble derivative of chlorophyll that makes possible the process of photosynthesis and plant growth from the sun’s energy-is, on a dose-by-dose basis, 10 times more potent at causing death of colon cancer cells than the chemotherapeutic drug hydroxyurea.

Experts in the Linus Pauling Institute at Oregon State University say that the study has also shown that chlorophyllin kills cancer cells by blocking the same phase of cellular division that hydroxyurea does, but by a different mechanism.

Based on that finding, the researchers suggest that it may be possible to developed to have a synergistic effect with conventional cancer drugs, helping them to work better or require less toxic dosages.

“We conclude that chlorophyllin has the potential to be effective in the clinical setting, when used alone or in combination with currently available cancer therapeutic agents,” the researchers wrote in their study report.

They, however, stressed the need for both in laboratory and animal studies, with combinations of chlorophyllin and existing cancer drugs, before it would be appropriate for human trials.

Other studies published in the journals Carcinogenesis and Cancer Prevention Research have explored the role of organic selenium compounds in killing human prostate and colon cancer cells.

During the studies, a form of organic selenium found naturally in garlic and Brazil nuts was converted in cancer cells to metabolites that acted as “HDAC inhibitors” – a promising field of research in which silenced tumour suppressor genes are re-activated, triggering cancer cell death.

Rod Dashwood, professor and director of the Cancer Chemoprotection Program in the Linus Pauling Institute, says that the concept of combining conventional or new cancer drugs with natural compounds, which have been shown to have anti-cancer properties, is very promising.

“Most chemotherapeutic approaches to cancer try to target cancer cells specifically and do something that slows or stops their cell growth process. We’re now identifying such mechanisms of action for natural compounds, including dietary agents. With further research we may be able to make the two approaches work together to enhance the effectiveness of cancer therapies,” Dashwood said. (ANI)

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New method to block protein fusion behind rare cancer unveiled

July 6, 2009 By Leave a Comment

London, July 6 (ANI): Scientists at Georgetown University Medical Center (GUMC) have discovered a new method to block the activity of the fusion protein behind Ewing’s sarcoma-a rare cancer found in children and young adults.

In a new study, the researchers have discovered and successfully tested a small molecule that prevents the fusion protein from sticking to another protein that is critical for tumour formation.

The researchers claim that this unique interaction is especially surprising as the Ewing’s sarcoma fusion protein is extremely flexible, which allows it to change shape constantly.

“Most targeted small molecule cancer drugs inhibit the intrinsic activity of a single protein, but our agent stops two proteins from interacting. This has never been shown before with a cancer-causing fusion protein and represents a potentially novel medical therapy in the future,” Nature magazine quoted the study’s lead investigator, Dr. Jeffrey Toretsky, as saying.

According to the researchers, the study could provide a model on which it would be possible to design treatment for other disorders caused by the interaction between two proteins.

The model could also be useful in cancers caused by translocations of genes, such as sarcomas and leukaemias.

Currently, the agents that work against fusion proteins inhibit a single protein to stop intrinsic enzymatic activity, for example Gleevec, which is used for chronic myelogenous leukemia (CML).

The Ewing’s sarcoma fusion protein, known as EWS-FLI1, lacks enzymatic activity, “and this difference is why our work is significant,” said Toretsky.

The researchers are the first to make a recombinant EWS-FLI1 fusion protein, and use it to discover that the fusion protein stick to another protein, RNA helicase A (RHA)-a molecule that forms protein complexes in order to control gene transcription.ater, they searched for a small molecule that would bind on to EWS-FLI1 from a library of 3,000 small molecules.

The researchers zeroed in on one, called NSC635437, and further discovered that it could stop EWS-FLI1′s fusion protein from sticking to RHA.

The researchers believe that this is a wonderful discovery because scientists have long believed that it is not possible to block protein-protein interactions given that the surface of many of these proteins are slippery – much too flexible for a drug to bind to.

“We may be able to use this strategy to attack proteins we thought to be impervious to manipulation,” said the researchers.

The study has been published online in Nature Medicine. (ANI)

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New ‘minicell therapy’ to crash cancer resistance

June 29, 2009 By Leave a Comment

London, June 29 (ANI): Aussie scientists have developed a new therapy that uses minicells to deliver cancer drugs, in order to prevent resistance in cancer cells.

The researchers are confident that the breakthrough could pave way for cheaper cancer treatments with fewer side effects.

While experimenting on mice, the researchers used minicells to deliver cancer drugs to resistant tumours.

The minicells were made from bacteria and contained pieces of genetic material, known as short interference RNA (siRNA), which knockout or ‘silence’ the drug-resistant genes of tumours.

After a few days, the researchers injected another dose of minicells filled with chemotherapy drugs, which the tumour was previously resistant to.

Dr Himanshu Brahmbhatt, molecular biologist and joint director of the biotechnology company Engeneic, said that cancer cells have an inbuilt mechanism to develop drug resistance over time.

“(Drug resistance) is one of our biggest killers in terms of cancer therapy,” Nature magazine quoted him as saying.

He claimed that silencing the genes of the drug-resistant tumour cell makes the cancers sensitive to the chemotherapy again.

Earlier, it was believed that siRNA could pass through cells membranes due to their size, but Brahmbhatt says that the new study has shown that this isn’t necessarily the case.

“Bacterial membranes might be quite different because they have protein channels (in their membrane) through which siRNA’s can enter (the minicell),” he said.

The outer surface of the minicell membrane is not only packed with gene silencing siRNA, but is also coated with antibodies, which lock onto (antigen) receptors on the tumour cells.

“The cancer cell then swallows the entire minicell,” said Brahmbhatt.

He added that once the minicell is inside the cancer cell, its breaks down and the siRNA or the drug floods the interior of the tumour cell.

“That’s why we haven’t seen any toxic side effects because this is intra-cellular delivery,” he said.

The study has shown that the combined minicell therapy can inhibit the growth of drug-resistant tumour xenographs, artificially manufactured tumours, for up to four months.

The findings appear in the online edition of Nature Biotechnology. (ANI)

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Cancer-causing Ras protein may help fight its own malign effects

June 20, 2009 By Leave a Comment

Washington, June 19 (ANI): Scientists at Tel Aviv University (TAU) in Israel have found that a cancer-causing protein can also help fight tumours it causes. he researchers have shown that an oncogene called Ras-which can cause normal cells to be come cancerous when mutated or expressed in high concentrations-has the power to heal as well as harm.

Ph.D. student Oded Rechavi and his fellow researchers at the university’s Department of Neurobiology have found that Ras has the ability to transfer from cancer cells into immune cells – such as T-cells – a transfer that may be the key to creating new drugs to fight cancerous tumours.

Revealing their findings in the journal Public Library of Science One and a recent review about such cell-to-cell transferring of proteins in FEBS Letters, the researchers say that the idea that proteins can transfer between cells challenges the original theory of the cell.

“All the energy flow, metabolism, and biochemistry of life is supposed to happen within the boundaries of an individual cell. Here we show that when cells in the immune system interact with other cells, proteins are exchanged without being secreted from the cell, and act in both the immune and original cells alike,” Rechavi said.

“When Ras transfers from one cell to another, it strengthens the immune system. The immune cell that adopts the mutated Ras gets activated and reacts against the cancerous cell that donated the Ras. This does not happen for advanced tumors, but if we could control the movement of Ras, we would have a better understanding of how immune cells react against cancer,” he added.

This, according to the researcher, might provide the scientific basis for an entirely new class of cancer drugs.

The TAU researchers are trying to discover the mechanisms whereby the Ras protein is transferred, and their initial findings seem to be promising.

Rechavi is investigating a current theory that the membranes of the cells temporarily fuse together. What is certain, however, is that once T-cells acquire mutated Ras, they are able to generate clones with the ability to respond against this specific threat.

“When immune cells scan their targets they bind to their targets. When immune cells acquire normal Ras, nothing happens. But when they acquire mutated Ras from a potential tumor, it starts a cascade. This results in the production of cytokines that help the immune system and act against the cancer,” he said.

According to him, understanding the nature of this interaction between mutated Ras and immune T-cells can unlock mysteries about the nature of proteins and cells.

He has revealed that the next step will be to identify other proteins that, like Ras, are able to transfer outside of their cell of origin. (ANI)

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Even short-term exposure to pollutants can increase cancer risk

May 18, 2009 By Leave a Comment

Washington, May 18 (ANI): Exposure to environmental pollutants even for a short period can prompt genes to undergo reprogramming, and thereby increase an individual’s risk of developing cancer and other diseases, say Italian scientists.

University of Milan researchers have shown that inhaling certain environmental pollutants can damage DNA as early as three days.

“Recently, changes in gene programming due to a chemical transformation called methylation have been found in the blood and tissues of lung cancer patients,” said investigator Dr. Andrea Baccarelli, assistant professor of Applied Biotechnology at the University of Milan.

“We aimed at investigating whether exposure to particulate matter induced changes in DNA methylation in blood from healthy subjects who were exposed to high levels of particulate matter in a foundry facility,” Baccarelli added.

The researchers compared the blood samples of 63 healthy subjects who worked in a foundry near Milan, and found significant changes in four genes associated with tumour suppression.

“The changes were detectable after only three days of exposure to particulate matter, indicating that environmental factors need little time to cause gene reprogramming which is potentially associated with disease outcomes,” said Baccarelli.

“As several of the effects of particulate matter in foundries are similar to those found after exposure to ambient air pollution, our results open new hypotheses about how air pollutants modify human health.

“The changes in DNA methylation we observed are reversible and some of them are currently being used as targets of cancer drugs,” he added.

Baccarelli said that study results indicated that early interventions might be designed to reverse gene programming to normal levels, reducing the health risks of exposure.

The findings were presented at the 105th International Conference of the American Thoracic Society in San Diego. (ANI)

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New implantable device can help monitor cancer for months after biopsy

May 14, 2009 By Leave a Comment

Washington, May 14 (ANI): Scientists at the Massachusetts Institute of Technology (MIT) have developed the first implantable device that can help monitor a tumour for weeks or months after the biopsy, tracking its growth and how it responds to treatment.

Michael Cima, a professor of Materials Science and Engineering who led the creation of the device, has revealed that it was found to successfully track a tumour marker in mice for one month during a recent study.

He and his colleagues reckon that such implants may one day provide up-to-the-minute information about what a tumour is doing-whether it is growing or shrinking, how it’s responding to treatment, and whether it has metastasized or is about to do so.

“What this does is basically take the lab and put it in the patient,” said Cima, who is also an investigator at the David H. Koch Institute for Integrative Cancer Research at MIT.

The device can be implanted at the time of biopsy. It can also be tailored to monitor chemotherapy agents, so that doctors can determine whether cancer drugs are reaching the tumours.

Cima says that his device can also be designed to measure pH (acidity) or oxygen levels, which reveal tumour metabolism and how it is responding to therapy.

He points out that with current tools for detecting whether a tumour has spread, such as biopsy, by the time you have test results it’s too late to prevent metastasis, said Cima.

“This is one of the tools we’re going to need if we’re going to turn cancer from a death sentence to a manageable disease,” he said.

During an experiment, Cima and his colleagues transplanted human tumours into the mice, and then used the implants to track levels of human chorionic gonadotropin, a hormone produced by human tumor cells.

The cylindrical, 5-millimeter implant contains magnetic nanoparticles coated with antibodies specific to the target molecules that bind to the particles and cause them to clump together. That clumping can be detected by magnetic resonance imaging (MRI).

Cima believes that an implant to test for pH levels could be commercially available in a few years, followed by devices to test for complex chemicals like hormones and drugs.

A research paper describing the novel implantable device has been published online in the journal Biosensors and Bioelectronics. (ANI)

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Brit girl, 17, gets boob job to deal with stress

April 26, 2009 By Leave a Comment

London, April 26 (ANI): A 17-year-old girl, who could not take the pressure of having small breasts, has got a 4,000-pound boob job done on the NHS.

Amanda Ryan was jealous of her school pals’ bigger busts and she was just 16 when she decided to go under the knife, even though her body was not fully developed.

Girls under 18 are usually not allowed to have the operation, but after looking at how the stress of being flat-chested was making Amanda grumpy, a counsellor at her health centre suggested her to get boob job done.

However, now she wishes it had never been done as she has been plagued by problems ever since.

“It is worryingly easy to get a free boob job at an age when you might not be ready for it,” News of the World quoted her as saying.

“If I could advise anyone, I would tell them to wait until they are at least 18. You aren’t ready for it at such a young age,” she added.

Campaign group TaxPayers’ Alliance hit out at the decision.

Spokeswoman Susie Squire said: “The NHS is struggling to provide basic and life-saving surgery.

“Cancer drugs should always come above boob jobs. Some serious questions need to be asked about the spending priorities of this NHS trust.”(ANI)

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New insights into cancer progression

April 23, 2009 By Leave a Comment

Washington, Apr 22 (ANI): A University of Leicester researcher has made some significant advancements on the causes of cancer, which can lead to improved and effective therapies.

Professor Andrew Fry, of the Department of Biochemistry aims to understand the molecular control of cell division and as a result identify proteins, which can be targeted in specific tumours, leaving other cells unharmed.

Many current cancer treatments act by killing all dividing cells and are not necessarily specific for the cancer cells, hence the severe side effects.

While studying how cancer cells divide and spread in the body, Fry has got significant insights on the causes of many human diseases, including cancer, and has identified a number of new targets for cancer treatment.

“An adult human being contains millions of cells that all arise following the fertilization of an egg cell by a sperm cell,” said Fry.

“Human development therefore requires cells to divide again and again to create the tissues and organs of our body.

“Cell division is a complex mechanical process that not only leads to the production of new cells but ensures that each one maintains the right genetic content required to sustain life.

“Loss of control over cell proliferation and the development of genetic and chromosomal abnormalities are classic hallmarks of cancer,” Fry added.

He studied a family of proteins that play a role in cell division and cilia organization, which makes them attractive targets for the development of new anti-cancer drugs.

Fry looked at a particular structure that lies at the heart of each and every cell, called the centrosome (standing for “central body”), and how centrosome defects contribute to cancer progression. (ANI)

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Roche’s Humer said to have had Genentech buy doubts

April 15, 2009 By Leave a Comment

NEW YORK (Reuters) – Roche Chairman Franz Humer, the driving force behind the company’s acquisition of the 44 percent of Genentech it did not already own, apparently did not always think that was good idea.

David Mott, who was chief executive of MedImmune when it was acquired by AstraZeneca (AZN.L), said on Tuesday that he had sought Humer’s advice in 2007 as Mott pondered his future with AstraZeneca shortly after that $15.6 billion deal was announced.

“Our model is a lot like your model with Genentech. We’re going to have an independent operating entity and run it that way,” Mott recalled telling Humer of his integration plan.

“He laughed at me and he said, ‘it will never work because if we owned all of Genentech we would kill it’,” Mott said Humer told him at the time.

“‘We wouldn’t be able to resist tinkering and playing with it and AZ owns all of you, so they say it’s going to be independent but we’d never be able to have that discipline,’” Mott said, quoting Humer.

Mott, who left AstraZeneca a year later, was speaking on a panel at the Windhover Pharmaceutical Strategic Outlook conference at a New York hotel when he related his anecdote about the then CEO of Roche Holding AG (ROG.VX). Mott is currently general partner of venture capital firm New Enterprise Associates.

Roche now believes it can resist the kind of tinkering that might kill the golden goose.

Current Roche management, including Humer and new CEO Severin Schwan, have insisted they will preserve the informal California science-based culture at Genentech that has produced a remarkable number of innovative and lucrative medicines.

The nearly $47 billion deal made sense for Roche as it not only gives it full U.S. revenue from Genentech’s multibillion-dollar cancer drugs, such as Avastin and Herceptin, but fills out what had been a rather sparse developmental pipeline for the Swiss drugmaker.

Following the panel discussion on the ability of biotech companies to survive within big pharmaceutical companies, Mott was asked what he thought Humer might tell him today about Roche owning all of Genentech.

“That it’s going to work,” Mott said with a chuckle. “It’s pretty interesting with hindsight, isn’t it?”

(Reporting by Bill Berkrot; Editing by Tim Dobbyn)

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Novel human-in-mouse cancer model may lead to improved drugs

April 7, 2009 By Leave a Comment

Washington, Apr 7 (ANI): Scientists have successfully created a human-in-mouse cancer model mimicking human tumour behaviours and response – a finding that would pave way for improved cancer drugs.

Researchers at AVEO Pharmaceuticals, Inc., a biopharmaceutical company have engineered normal human breast tissue to express oncogenes, which when introduced in mice, formed human breast tissue in mouse mammary microenvironment.

The tumours, which then develop spontaneously, acquire common and distinct mutations during tumour progression.

This process results in tumours in mice that reflect their human counterparts – exhibiting natural genetic variation akin to that seen in patients.

“Historically, the xenograft models created to analyze how human cancers behave have not been accurate predictors of human responses to various therapeutic agents,” said Dr Robert A. Weinberg, member, Whitehead Institute and professor of biology, MIT.

The HIM tumours also displayed characteristic responses to a targeted therapy known to be effective in humans, specifically Herceptin.

“This represents a big step forward in developing xenograft models that will accurately predict patient responses to agents that are in preclinical development,” he said.

“The HIM model is an exciting, experimentally tractable human in vivo system that holds great potential for advancing our basic understanding of cancer biology and for the discovery and testing of targeted therapies,” he added.

The findings are published in Proceedings of the National Academy of Sciences. (ANI)

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DNA repair enzymes relocate when cells are under stress

March 29, 2009 By Leave a Comment

Washington, Mar 27 (ANI): In times of stress and genetic damage, some DNA repair enzymes can relocate to the part of the cell that needs their help, according to a collaborative team study led by scientists at Emory University School of Medicine.

The study found that the signal that prompts relocation is oxidative stress-an imbalance of cellular metabolism connected with several human diseases.

Dr. Paul Doetsch, professor of Biochemistry, Radiation Oncology, and Hematology and Oncology, says that the finding may lead to new targets for anti-cancer drugs that interfere with DNA repair.

“DNA damage and oxidative stress are very closely related. For example, the way radiation inflicts most of its damage on DNA is through oxidative stress. The more we know about how cells respond to oxidative stress, the more chances there could be to influence those responses for diagnostic or therapeutic purposes,” said Doetsch.

The DNA inside cells already remains under assault by heat, radiation, and oxygen.

And cells have an extensive set of repair enzymes that comb through DNA, continually excising and re-copying damaged segments. Also, mitochondria (cells’ miniature power plants) have their own DNA.

For the study, the researchers genetically modified strains of yeast so that two different DNA repair enzymes would be fluorescent.

They could track the enzymes around the cell when yeast was exposed to hydrogen peroxide, causing oxidative stress, or to other chemicals causing DNA damage.

It was found that one DNA repair enzyme they studied, Ntg1, moves to the nucleus or the mitochondria depending on where DNA damage is concentrated.

On the other hand, a related enzyme, Ntg2, remains in the nucleus under all conditions.

The authors found that the cells apparently direct Ntg1′s relocation by briefly attaching a small protein called SUMO to what needs to be moved around.

SUMO is found in fungi, plants and animals and is already being investigated by several research groups as a possible target for anti-cancer drugs.

The study has been published in the journal Molecular and Cellular Biology. (ANI)

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Herbal medicines can help treat gastrointestinal disease

March 25, 2009 By Leave a Comment

Washington, Mar 25 (ANI): A new study has suggested that herbal medicines could benefit patients suffering from gastrointestinal (GI) motility disorders that cannot be treated using conventional drug therapy.

For the study, researchers reviewed data on Japanese herbal medicines and found them to be effective in reducing the symptoms of GI disorders such as functional dyspepsia, constipation, and postoperative ileus.

“Japanese herbal medicines have been used in East Asia for thousands of years,” says lead researcher Hidekazu Suzuki, Associate Professor at the Keio University School of Medicine.

“Our review of the world medical literature reveals that herbal medicines serve a valuable role in the management of patients with functional gastrointestinal disorders,” Suzuki added.

The researchers reviewed data from studies looking at the effect of several different Japanese herbal medicines including the use of Rikkunshi-to, Dai-Kenchu-to, and other herbal medicines.

Rikkunshi-to, which is prepared from eight crude herbs, was effective in reducing discomfort caused by functional dyspepsia.

Dai-Kenchu-to, a mixture of ginseng, ginger, and zanthoxylum fruit, was beneficial for constipation in children and patients suffering from post-operative ileus – disruption of normal bowel movements following an operation.

Another herbal medicine, hangeshashin-to, reduced the severity and frequency of diarrhoea caused by anti-cancer drugs.

The study has been published in Neurogastroenterology and Motility. (ANI)

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How cancer cells become more ‘gloopy’ when they die

March 16, 2009 By Leave a Comment

London, Mar 16 (ANI): New images providing fundamental insights into how cancer cells die have revealed that there is a dramatic increase in the viscosity, or ‘gloopiness’, of different parts of cancer cells, when they are blasted with light-activated cancer drugs.

The images reveal the physical changes that occur inside cancer cells at the time when they are dying because of Photodynamic Therapy (PDT)-a cancer treatment that uses light to activate a drug that creates a short-lived toxic type of oxygen, called singlet oxygen, which kills cancerous cells.

The researchers behind this study say that revealing what happens to viscosity within a dying cancer cell is important because it may help better understand how cells function and which factors are important for controlling reactions inside cells.

And this could ultimately help scientists design more efficient drugs for Photodynamic Therapy and other treatments.

Also, the research holds significance because these are the first ever real-time maps showing viscosity changing over a period of time inside a cell during a biologically important process like cell death.

Lead author Dr Marina Kuimova, from Imperial College London’s Department of Chemistry, has revealed that previous studies have shown that the viscosity of human cells and organs also changes in patients with diseases, including diabetes and atherosclerosis.

“We’re still not quite sure exactly what the relationship is between increased stickiness inside cells and disease, but we expect that the two are related,” Nature magazine quoted her as saying.

She added: “Knowing more about these changes, and being able to map them when they occur in all kinds of different scenarios, from dying cancer cells, to diseased blood cells, could help us to better understand how some diseases and their treatments affect cell and organ function.”

During the study, the researchers could track viscosity as it changed inside live cancer cells because of a newly developed Photodynamic Therapy drug, with unusual fluorescent properties.

Made of a molecule with a spinning component like a rotor, the drug emits different wavelengths of light depending on the viscosity of its surroundings.

The changing wavelengths of light emitted during experiments, and captured over a period of 10 minutes, showed that once the PDT drug was activated, the level of viscosity inside the cell increased dramatically.

According to the researchers, the toxic oxygen molecules released into the cell causes the increasing ‘gloopiness’.

In their opinion, increased levels of viscosity might even contribute directly to the cancer cell’s further deterioration by slowing down vital communication and transport processes inside the cell.

However, the researchers noted that as viscosity in the cancerous cell increases, the toxic oxygen molecule’s mission to kill the cell is slowed down too.

The study has been published in the journal Nature Chemistry.(ANI)

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