Crizotnib or Xalkori: Helps 5 in 100 Lung Cancer Patients

Pfizer's Crizotinib, also trading as Xalkori, has been announced as being beneficial to 5 in 100 lung cancer patients.

Crizotinib caused tumours to shrink or stabilise in 90% of 82 patients carrying the ALK fusion gene. Tumours shrank at least 30% in 57% of people treated.

Most had adenocarcinoma, and had never smoked or were former smokers. They had undergone treatment with an average of three other drugs prior to receiving crizotinib, and only 10% were expected to respond to standard therapy.

They were given 250 mg Crizotinib twice daily for a median duration of six months. Approximately 50% of these patients suffered at least one side effect, such as nausea, vomiting, or diarrhea.

Some responses to crizotinib have lasted up to 15 month.

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No Relaxing for Cancer Cells

No relaxing for cancer cells

Many tumour cells would not be viable due to aberrant chromosome distribution if they had not developed a special trick. Scientists from the German Cancer Research Centre have investigated which genes are responsible for this survival strategy of cancer cells.

The revealed that cancer cells rely on the tension of specific protein fibers to be able to multiply. Thus, proteins which maintain this tension are promising targets for new, target-specific anticancer drugs: If they are switched off, cancer cells die.

The two centrosomes of a cell are responsible for cell division to proceed correctly. From these polar bodies in the cytoplasm protein fibers form which correctly distribute the duplicated chromosome set to the newly forming daughter cells. Seen under the microscope, these fibers have the shape of a spindle.

Cancer cells, however, often have more than two centrosomes. As a result, their spindle fibers do not necessarily assume the normal shape of a spindle with two poles; instead, they can have a dysfunctional, multipolar shape. Such malformed spindles distribute the chromosomes unevenly among the daughter cells, which are then no longer viable.

Hence, tumor cells only survive if they manage to partition their chromosomes correctly in spite of extra centrosomes. To do so, many cancer cells have developed a special trick: They form clusters of centrosomes.

Two clusters are formed per cell and a functioning bipolar spindle can develop between these two. Professor Dr. Alwin Krämer, head of a Clinical Cooperation Unit of DKFZ and Heidelberg University Hospitals has recognized this trick as a previously underrated Achilles’ heel of cancer cells, which might be used for destroying them.

Jointly with colleagues from DKFZ, Heidelberg University Hospitals, Mannheim Medical Faculty and Mayo Clinic in the U.S., he systematically investigated the question of which genes enable cancer cells to form centrosome clusters and, thus, to escape cell death.

Tumours hide out from the immune system by mimicking lymph nodes

Tumours hide out from the immune system by mimicking lymph nodes

A new mechanism explaining how tumours escape the body's natural immune surveillance has recently been discovered at EPFL (Ecole Polytechnique Fédérale de Lausanne) in Switzerland. The study shows how tumours can create a tolerant microenviroment and avoid attack by the immune system by mimicking key features of lymph nodes.

The discovery, published in Science and in Science Express, underscores the role of the lymphatic system in cancer and may open up new possibilities for cancer treatment.

"The tumour tricks the body into thinking it is healthy tissue," says lead author Melody Swartz, head of the Laboratory of Lymphatic and Cancer Bioengineering (LLCB) and EPFL professor. Swartz and her team set out to understand how immune tolerance is induced by tumours, allowing them to progress and spread.

The researchers from EPFL concentrated their efforts on a certain protein that is normally present in healthy lymph nodes to attract T cells and program them to perform vital immune functions. They found that some tumours can secrete this protein to transform the outer layer of the tumour into lymphoid-like tissue.

This outer layer then attracts and effectively re-programs the T cells to recognise the tumour as friend not foe, resulting in a tumour that goes undetected by the immune system.

Since most tumours progress only if they have escaped the immune system, this new understanding of one mechanism by which the tumour can bypasses or hides from immune defenses is an important step towards future cancer therapies.

Personalised Blood Test for Cancer DNA

A personalised blood test that can identify tumour DNA could be the first step towards a long-promised revolution in the way cancer is treated.

In the short term, the test - reported by Victor Velculescu of Johns Hopkins Kimmel Cancer Center in Baltimore, Maryland, and his colleagues in Science Translational Medicine - could be used to spot cancer recurrence before tumour growth shows up on scans, meaning that treatment could be started earlier.

The test detects genetic rearrangements that distinguish cancer cells from normal cells. Eventually it might also pave the way for more personalised cancer treatments tailored to the genetic signature of individuals' tumours.

Doctors already classify cancers by some of the genes that get switched on by the disease, and use this to guide treatment in some cases. For example, breast cancers are often divided into those that express oestrogen receptors on their surface and are therefore likely to respond to the drug tamoxifen, and those that don't.

Genes have also been identified that predict whether a variety of cancers are resistant to radiotherapy and certain drugs, and might therefore need a different sort of treatment. It is also possible to stratify cancers into aggressive and non-aggressive subtypes according to their genetic make-up.

But that's just the beginning. In the future, pretty much all cancers are likely to be defined by the genetic pathways that drive their growth, rather than where in the body they manifest themselves. And because cancers mutate as they grow, it should be possible to track these changes and tailor patients' therapies accordingly.

Velculescu's test is a step towards this. The real breakthrough will come when such blood tests become sophisticated enough to reveal how tumours are changing over time, rather than simply spotting that they have come back. That should truly revolutionise cancer treatment, enabling the most effective combinations of drugs to be tailored to individual patients - and without the need for painful tissue biopsies.

Tasmanian Devil Facial Cancer breakthrough

Scientists have discovered the true identity of a contagious form of cancer that is killing Tasmanian devils.

The cancer, called devil facial tumor disease, stems from cells that normally insulate nerve fibres, a new study shows.

Save the Tasmanian Devil Program

Genetic analysis of tumors taken from infected devils in different parts of Tasmania reveals that these insulating cells, known as Schwann cells, became cancerous in a single Tasmanian devil and have since passed to other devils, an international group of researchers reports in the Jan. 1 Science.

Previously, scientists had suspected that a virus might be the source of the infection, but the new study confirms that cancer cells themselves are transmitted from devil to devil.

Knowing the origin of the contagious tumors could help conservationists diagnose the disease more accurately and may eventually lead to a vaccine that would target tumor proteins, says Katherine Belov, a geneticist at the University of Sydney who was not involved with the project.

A vaccine against the facial tumor disease, “while now pie in the sky, in 10 years might not be,” says Gregory Hannon, a Howard Hughes Medical Institute investigator at Cold Spring Harbor Laboratory on Long Island, N.Y. “Ten years might be enough time” to save the devils from extinction, he says.

About 70 percent of the Tasmanian devil population has disappeared as a result of the disease, and if the current rate of decline continues, devils could become extinct in the wild in 30 to 50 years, says Elizabeth Murchison, now a postdoctoral researcher at the Wellcome Trust Sanger Institute in Hinxton, England. Murchison, a native of Tasmania who grew up seeing devils in the wild, led the project while working in Hannon’s lab at Cold Spring Harbor. “I didn’t want to sit back and let the devils disappear,” she says.

Health - Canadian research alters view of breast tumours

CBC News - Health - B.C. research alters view of breast tumours

Not all cells in a breast cancer tumour contain the same mutations, researchers in British Columbia have found.

The finding that changes occur in tumours over time could change how scientists think about developing new breast cancer drugs and deciding which patients would benefit most from treatments.

In Wednesday's issue of the journal Nature, Samuel Aparicio and his colleagues at the BC Cancer Agency charted the genetic mutations that occurred in the 3 billion letters of the DNA sequence from an estrogen-receptor-alpha-positive breast tumour.

"The impact is going to be in the way that cancer researchers look at developing therapies and applying therapies in the short term," said Aparicio, chair of breast cancer research at the BC Cancer Agency and Canada research chair in molecular oncology.

"Over the long term, we hope that being able to decode the sequence of tumours on a routine basis will eventually lead us to being able to better predict which combinations of medicines to use when treating a cancer. We're not quite at that point yet."

The team found 32 mutations after it had spread, nine years after the original biopsy of the lobular breast cancer, which accounts for eight to 15 per cent of all breast cancers, Aparicio said.


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Does Aspirin Reduce the Chance of Colon Cancer

People with a genetic susceptibility to colon cancer could cut their chances of developing the disease in half by taking a daily dose of aspirin, researchers said Monday.

The finding might lead to other treatments by helping researchers understand how aspirin combats colon cancer, one of the top three cancers in rich countries.

Though aspirin has been used widely for years to treat minor aches and to alleviate fevers, it can irritate the stomach and intestines and cause major bleeding.

European researchers followed more than 1,000 people with Lynch syndrome, a genetic mutation that makes them vulnerable to cancers in the colon, rectum, stomach, brain, liver, womb and elsewhere. The syndrome accounts for about 5 percent of all colon cancers.

About half of the study participants were given 600 milligrams, or two aspirin pills daily, while the other half got placebo pills for about four years.

In the group that got aspirin, six people developed colon cancer, versus 16 in the group that got placebos. "We are delighted," said John Burn of Newcastle University in Britain, who led the study.

"All the more so because we stopped giving the aspirin after four years, yet the effect is continuing," he said in a statement.

Burn presented the study results Monday in Berlin at a joint meeting of the European Cancer Organisation and the European Society for Medical Oncology.

Experts said the finding would have no immediate impact on the general public.

"This doesn't mean that everyone should start taking aspirin if they're worried about bowel cancer," said Henry Snowcroft of Cancer Research United Kingdom.

"Aspirin can cause significant side effects if not used as directed by a doctor," Snowcroft said.

Previous studies have found patients who already have colon cancer and are being treated with chemotherapy and surgery may further reduce their risk of dying by up to 30 percent by taking aspirin. The cheap drug is also taken by millions of people worldwide to prevent heart attacks and strokes.