Friday, April 20, 2012

Aspirin and Cancer Prevention

Aspirin has been around for a long time. Salicylic which is from will bark was recorded as early as 300 B.C. I was used to relieve aches and pains. The official drug called aspirin in the year of 1899. Acetyl-salicylic acid became the new chemical combination.

In recent years it has been advised for people with heart problems to take a baby aspirin regularly to prevent blockages in the cardiac system.
Now the subject of aspirin helping prevent cancer is in the news.  There are new statistics of the use of aspirin in clinical trials have been promising.  Here are the results:

A combined analysis of 51 randomized trials found that daily aspirin use reduces the risk of new cancer diagnoses as well as the risk of cancer death. These results were published in The Lancet.
A growing body of evidence suggests that aspirin may reduce the risk of several types of cancer, with particularly strong evidence for colorectal cancer. Not all studies have found a benefit, however, and any potential benefits of aspirin must be weighed against risks such as bleeding.
To further explore the relationships between daily aspirin and cancer, researchers conducted a combined analysis of 51 previous randomized trials. The trials were originally designed to evaluate the effect of daily aspirin on outcomes such as heart disease, but information about cancer was also available.
  • Daily aspirin reduced cancer deaths. After five years, aspirin users had a 37 percent reduction in risk of cancer death.
  • Aspirin also reduced the likelihood of developing cancer. From three years onward, aspirin users had a 24 percent reduction in the risk of being diagnosed with cancer.
  • As expected, aspirin carried a risk of major bleeding, but this risk appeared to diminish over time.
Another study published in the same issue of The Lancet evaluated the effect of daily aspirin on cancer metastasis (the spread of cancer from its original site to other parts of the body). The study focused on 987 people who were diagnosed with cancer while participating in one of five trials of aspirin use. Those who were taking aspirin were less likely to have metastatic cancer than those who were not taking aspirin.
These results suggest that regular aspirin use may reduce cancer incidence and mortality, but concerns remain about the risks of regular aspirin use in healthy individuals. People who are considering using aspirin on a regular basis are advised to discuss the risks and benefits with their physician.

http://news.cancerconnect.com/aspirin-continues-to-look-promising-for-cancer-prevention/

Thursday, April 19, 2012

Lung Cancer Personalized Treatment

The new direction of cancer treatment is becoming personalized to the characteristics of individual patients. Instead of treating specific cancers the same way for all patients researchers are focusing on the characteristic's of each patient and their tumors.
These new ways of treatment was presented at the Third European Lung Cancer Conference in Geneva.

A major goal of lung cancer treatment is to tailor the treatment to the individual," says Dr Fiona Blackhall from The Christie NHS Foundation Trust in Manchester, UK. "The studies that will be presented at ELCC 2012 are important practical steps to achieving this in the clinic. Methods ranging from convenient blood-based molecular tests, detailed genetic analysis of tumors and functional imaging techniques have been applied in patient populations receiving a range of treatments. These findings provide impetus to continue developing a personalized medicine approach to lung cancer with the overall aim of selecting the most effective treatment for the individual."


Proteins provide clues to outcomes

An international group of researchers report promising results with a test that may identify patients likely to benefit from first-line therapy with a particular drug combination.
Dr Oliver Gautschi from the Swiss Group for Clinical Cancer Research (SAKK), and collaborators from The Netherlands and the US company developing the test, conducted a retrospective analysis of two phase-II trials with a serum proteomic classifier called VeriStrat-. Their aim was to evaluate the prognostic value of the test in patients with advanced non-small cell lung cancer receiving first-line treatment with bevacizumab and erlotinib.
VeriStrat- uses mass spectrometry to measure proteins in pre-treatment blood and assigns a result that correlates with outcome from treatment with a class of drugs known as EGFR inhibitors, which includes erlotinib and gefitinib. The test was initially developed and validated in patients who had already been treated with chemotherapy, and who then received an EGFR inhibitor in second line, Dr Gautschi explains.
"We conducted this project to see if the test is also prognostic in untreated patients who received an EGFR inhibitor in the first line. Until now, this has not been clear."
The researchers used VeriStrat- to analyze blood samples from 117 patients previously enrolled in two phase II trials and compared the results to the patients' progression-free survival and overall survival. The analysis showed that those classified by the test as likely to have better outcomes on EGFR inhibitor therapy did indeed live longer.
"The difference in overall survival between patients classified by the test as likely to have better or worse outcomes when receiving EGFR inhibitors was clinically relevant," Dr Gautschi said. However he noted that definitive conclusions about the use of this test in previously untreated patients requires further studies.
"There is an unmet need for reliable blood-based markers in patients with lung cancer, because lung tumors are harder to biopsy than breast tumours for example. The current study indicates that modern technologies, such as proteomics, are promising tools, which need further validation in large trials," he said. In this context, the European Thoracic Oncology Platform (ETOP) is currently launching a prospective phase-III trial to futher validate this test in patients with lung cancer.

                                            Gene Based Lung Cancer Treatment

For more information:
http://www.news-medical.net/news/20120419/New-studies-on-personalized-lung-cancer-treatment-presented-at-3rd-ELCC.aspx

Tuesday, April 17, 2012

Brain Cancer Vaccine Results Are Provocative

Lengthening the life of a patient with brain tumors is wonderful news. Phase 2 of the clinical trials paves the way for testing a new therapy that combines a brain cancer vaccine with the oncology drug, Avastin






A new report of this news was reported today by the University of California, San Francisco.

This vaccine is individualized by using tissue from the patient's tumor. This procedure has proven effective in a multicenter phase 2 clinical trial at extending their lives by several months or longer. The patients suffered from recurrent glioblastoma multiforme—which kills thousands of Americans every year.

These results, to be announced Tuesday, April 17 at the American Association of Neurological Surgeons (AANS) meeting in Miami, compared the effectiveness of the vaccine for more than 40 patients treated at UCSF’s Helen Diller Family Comprehensive Cancer Center, at the Seidman Cancer Center at University Hospitals Case Medical Center in Cleveland and at New York-Presbyterian Hospital/Columbia University Medical Center in New York City.

The trial found the vaccine could extend survival for the patients by several months when compared to 80 other patients who were treated at the same hospitals and received standard therapy—47 weeks compared to 32 weeks. Several of the patients who received the cancer vaccine have survived for more than a year.
“These results are provocative,” said UCSF neurosurgeon Andrew Parsa, MD, PhD, who led the research. “They suggest that doctors may be able to extend survival even longer by combining the vaccine with other drugs that enhance this immune response.”

The next step, he said, will be a more extensive, randomized clinical trial to look at the effectiveness of the vaccine combined with the drug Avastin, a standard therapy for this type of cancer, compared to the effectiveness of Avastin alone. Those trials, to be run by the National Cancer Institute, will begin enrolling patients later this year.

To read more of this article:
http://www.newswise.com/articles/brain-cancer-vaccine-proves-effective?ret=/articles/list&category=medicine&page=1&search%5Bstatus%5D=3&search%5Bsort%5D=date+desc&search%5Bsection%5D=10&search%5Bhas_multimedia%5D=

Monday, April 16, 2012

Thyroid Nodule Testing By Molecular Cytology

Many people have thyroid problems.  Due to the instability of trying to control the function of the thyroid nodules can develop. An endocrinologist will need to do a biopsy if calcification is seen from an ultrasound
report. The doctor will take an aspiration needle and extract tissue from the nodules to be put on slide and prepared by the histology lab for the pathologist to view to determine carcinoma.






Genzyme and Veracyte have a great announcement concerning diagnosing cancer from thyroid nodules . These companies are the leaders in molecular cytology as tool for diagnosis.

The following are excerpts from a recent news article on the web about a testing product and how it really can be better than a microscopic view under a microscope.

Genzyme, a Sanofi company , and Veracyte, Inc., a molecular diagnostics company pioneering the emerging field of molecular cytology, today announced that the Afirma(R) Thyroid FNA Analysis, an innovative approach for improved thyroid nodule diagnosis, is now available to patients across the United States.

The Afirma(R) Thyroid FNA Analysis combines expert cytopathology assessment of thyroid nodule fine needle aspiration (FNA) samples, with the Afirma(R) Gene Expression Classifier, a novel genomic test, used to resolve inconclusive results and thus help patients whose nodules are actually benign avoid unnecessary surgery. Two independent clinical studies to date have shown that the Afirma(R) Gene Expression Classifier can reclassify patients with indeterminate thyroid FNA results as "benign" with the same degree of accuracy as a benign cytopathology diagnosis.

Thyroid cancer is the fastest-growing cancer in the U.S., with an estimated 56,460 new cases expected in 2012, according to the American Cancer Society. An estimated 450,000 thyroid nodule FNAs -- a minimally invasive procedure to extract cells for examination under a microscope -- are performed in the U.S. each year to rule out cancer. Thyroid nodule FNAs are challenging to interpret, however, producing ambiguous results in up to 30 percent of cases. Current guidelines recommend that most patients with ambiguous results undergo thyroid resection for a definitive diagnosis. Post-surgical results, however, show that only 20-30 percent of these patients have cancer. 

"Until now, most patients with 'indeterminate' thyroid nodules based on cytology went to surgery to help ensure that a cancer was not missed," said Dr. Bryan Haugen, professor of medicine and pathology at the University of Colorado School of Medicine. "Now, the Afirma(R) Gene Expression Classifier can potentially help tens of thousands of patients with inconclusive thyroid nodules each year avoid unnecessary surgery and improve patient outcomes." 

Genzyme is an established leader in endocrinology globally, developing and marketing Thyrogen(R) (thyrotropin alfa for injection) for patients with well-differentiated thyroid cancer. Thyrogen(R) is used as an adjunctive diagnostic tool for serum thyroglobulin (Tg) testing with or without radioiodine imaging. Thyrogen(R) is also approved in the U.S. and Europe as an adjunctive treatment for radioiodine ablation of thyroid tissue remnants in patients who have undergone a near total or total thyroidectomy for well-differentiated thyroid cancer and who do not have evidence of metastatic thyroid cancer.

Friday, April 13, 2012

Wilm's Tumor In Children

Wilm's tumor is a rare type of cancer that is found mainly in children. Another name for Wilm's tumor is nephroblastoma and it is the most common cancer of the kidneys.  The age range of a child is 3-4 years old is when the Wilms tumor usually develops.  This specific tumor is usually seen on just one of the kidneys, but can be seen in both.

                                                     Wilms Tumor in kidneys of a child



Approximately 500 cases are seen every year in the United States. Fortunately, this type of tumor is highly responsive to treatment.


Wilms' tumor is a malignant tumor containing metanephric blastema, stromal and epithelial derivatives. Characteristic is the presence of abortive tubules and glomeruli surrounded by a spindled cell stroma. The stroma may include striated muscle, cartilage, bone, fat tissue, fibrous tissue. The tumor is compressing the normal kidney parenchyma.
The mesenchymal component may include cells showing rhabdomyoid differentiation. The rhabdomyoid component may itself show features of malignancy (rhabdomyosarcomatous Wilms).
Wilms' tumors may be separated into 2 prognostic groups based on pathologic characteristics:
  • Favorable - Contains well developed components mentioned above
  • Anaplastic - Contains diffuse anaplasia (poorly developed cells)

The symptoms that are typical of Wilm's tumor are an abnormally large abdomen, abdominal pain,fever,nausea and vomiting,blood in the urine and high blood pressure in some cases.

The diagnosis of this tumor requires several tests.

  • A physical examination. The doctor will look for possible signs of Wilms' tumor.
  • Blood and urine tests. Blood tests can't detect Wilms' tumor, but they can provide your child's doctor with an overall assessment of your child's health.
  • Imaging tests. Imaging tests that create pictures of your child's kidneys can help your doctor determine whether your child has a kidney tumor. Imaging tests may include ultrasound, computerized tomography (CT) and magnetic resonance imaging (MRI).
  • Surgery. If your child has a kidney tumor, your doctor may recommend removing the tumor or the entire kidney to determine if the tumor is cancerous. The removed tissue is analyzed in a laboratory to determine whether cancer is present and what types of cells are involved. This surgery may also serve as treatment for Wilms' tumor.
Once your child's doctor has diagnosed Wilms' tumor, he or she works to determine the extent (stage) of the cancer. Your child's doctor may recommend a chest X-ray, chest CT scan, chest MRI and bone scan to determine whether the cancer has spread beyond the kidneys. 

The growth of the cancer is usually described in Stages.  The following are the stages for Wilm's tumor.

  • Stage I. The cancer is found only in one kidney, and generally can be completely removed with surgery.
  • Stage II. The cancer has spread to the tissues and structures near the affected kidney, such as fat or blood vessels, but it can still be completely removed by surgery.
  • Stage III. The cancer has spread beyond the kidney area to nearby lymph nodes or other structures within the abdomen, and it may not be completely removed by surgery.
  • Stage IV. The cancer has spread to distant structures, such as the lungs, liver, bones or brain.
  • Stage V. Cancer cells are found in both kidneys.
·         Standard treatment for Wilms' tumor is surgery and chemotherapy. The stage of the tumor and appearance of the cancer cells under a microscope help determine whether your child also needs radiation therapy. At this point, your doctor may tell you the tumor appears to be either favorable or unfavorable (anaplastic) — the histology of the tissue. Children whose tumors have a favorable histology have better survival rates. However, many children with unfavorable histology also have good outcomes.
·         Because this type of cancer is rare, your doctor may recommend that you seek treatment at a children's cancer center that has experience treating this type of cancer.


Professor Frank Friedman explains Wilm's Tumor Kidney Cancer in Children

More information : www.mayoclinic.com, 

 



Wednesday, April 11, 2012

Dedicated Reseachers Are Committed to Tackling Liver Cancer

There are researchers that have dedicated their careers to finding cures for certain cancers. The following news story is one of hope for those persons who have liver cancer.



Ulla Hansen is a scientist who fell in love with a protein. She began studying it nearly three decades ago as a postdoctoral fellow at MIT because of its potential to solve the mystery of how cells grow. She continued those studies as a faculty member at the Dana-Farber Cancer Institute and Harvard Medical School. And now the College of Arts & Sciences biology professor has discovered that this same protein, transcription factor LSF, also referred to as late SV40 factor, appears to play a role in the growth of liver cancers. Understanding that role could be the key to a treatment for the deadly disease.

It’s incredibly gratifying personally that all of our basic science all these years has come to a position now where we may be able to translate it into the clinics,” says Hansen, director of BU’s program in molecular biology, cell biology, and biochemistry.

Liver cancer may not garner the media attention that other cancers do, but it is the fifth most common cancer and the world’s third leading cause of death from cancer. And while the rate of diagnosis for other cancers in the United States is declining, diagnosis of liver cancer is rising, largely because of its connection to an increasing incidence of hepatitis C.

“We’re still trying to figure out all the genes that LSF targets and turns on and off,” she says. “Most transcription factors target at least hundreds of genes, if not thousands.”
For many years, Hansen’s laboratory was the only one in the world to focus on LSF’s role in cell growth and division. It wasn’t unusual for her to get phone calls from scientists around the world wanting to share their own LSF-related discovery.
Devanand Sarkar was one. He called from the Virginia Commonwealth University Institute of Molecular Medicine to tell Hansen that he had found higher levels of LSF in cells after his lab turned on a gene that causes metastasis. “Usually there’s a few thousand LSF entities per cell, but this went up tenfold or twenty-fold,” Hansen says. And when Sarkar looked specifically at liver cancer cells, he saw that the more advanced the cancer had become, the more LSF was present. The two concluded that LSF not only encourages normal cell growth, but also liver cancer cell growth.

What she really needed, she decided, were some small-molecule inhibitors, or chemical torpedoes, that specifically targeted LSF and disabled it. She found a source in a Nevada company, Sierra Sciences. Researchers there have spent years working on a way to prevent aging (the company motto: Cure Aging or Die Trying) and had toyed with the idea that controlling LSF was key. They had screened 110,000 small-molecule inhibitors and found 80 strong candidates, none of which worked. So they put their work on ice, literally.
When Hansen got in touch with the company about a possible collaboration, the chief scientific officer offered to just send her everything they had.
“I couldn’t believe it,” Hansen says. “This is not the way companies usually act. But they’re not interested in money. They were happy to help.”
After plugging the compounds into liver cancer cells to see if they turned off LSF, Hansen and her team found several encouraging candidates. But they needed more of each compound. Sierra Sciences had included the chemical structures for each compound, but she had no idea how to buy more.
“I decided the best option in this nice interdisciplinary building,” Hansen says, referring to BU’s Life Sciences and Engineering Building, “was to go upstairs to ask some nice synthetic organic chemists how they would go about ordering more of these things.”

So she walked up to the chemistry department and started knocking on doors. Scott Schaus’ was the first to open. The two chatted about her research briefly as Schaus typed away on his computer. Then, Hansen recalls, he looked up and asked, “Do you want us to synthesize it for you?”
She accepted the offer immediately.
Schaus, a CAS associate professor of chemistry and bioinformatics, recruited two graduate students to work on the project. One synthesized compounds, the other tested them to see which were most effective at knocking down LSF. Those compounds were then passed along to Hansen’s team, which tested them in liver cancer cells. Together the labs have identified at least three highly effective small-molecule inhibitors, with FQI2 (dubbed “Ficky 2” by the graduate students) the most promising.
Hansen has since tested the compounds in mice with liver cancer cells and seen impressive results. “Our small-molecule inhibitors are in fact knocking LSF down to nothing,” she says. But that’s not the only good news. “We see absolutely no side effects in the mice.”
It now seems that liver cancer cells need LSF to grow, divide, and multiply. Normal cells do not, or at least have found other ways to work around the protein. Hansen is now trying to figure out why.

http://www.bu.edu/today/2012/taking-on-cancer-tackling-liver-cancer-in-the-lab/




Tuesday, April 10, 2012

Colorectal Cancer Patients Drug Resistance

Recent research has discovered in the lab a way to overcome drug resistance in colorectal cancer.  This recent article explains the the findings and it is great news!


The results, which highlight the use of a novel drug called ARI-4175, may eventually point to new approaches that can be used in treating other cancers
When combined with other treatments, the drug cetuximab—which works by slowing or stopping the growth of cancer cells—has been shown to extend survival in certain types of cancer, including metastatic colorectal cancers. Unfortunately, about 40 percent of colorectal cancer patients—specifically those who carry a mutated form of a gene called KRAS—do not respond to the drug. Researchers at Fox Chase Cancer Center in Philadelphia, however, have been working on a way to overcome this resistance to cetuximab by unleashing a second cetuximab driven mechanism using a novel drug called ARI-4175.
In mice that had KRAS mutated colorectal cancer, researchers found that ARI-4175 not only blocked tumor growth when used alone, but also when used in combination with cetuximab. They hypothesize that the new drug may work by enlisting "natural killer" cells of the body's own immune system to reject the tumor.
"We've discovered that ARI-4175 appears to increase the level of natural killer cells that could play a role in rejecting the tumor," Hossein Borghaei, DO, director of thoracic medical oncology at Fox Chase and lead author on the study says. He notes that this action—rallying the body's own immunologic defenses—may explain why ARI-4175 effectively stops the growth of tumors. "My theory is that this particular drug turns on the host's anticancer immune response, while cetuximab serves to help direct it toward the cancer."
Borghaei, along William W. Bachovchin, PhD, professor of biochemistry at Tufts Sackler School of Graduate Biomedical Sciences (also co-author on the study) and colleagues, tested ARI-4175 in colorectal cancer cell lines and in mice with two types of cetuximab-resistant colorectal tumors.
Neither cetuximab nor ARI-4175, separately or together, succeeded in killing the cells in lab dishes. In the mice, however, ARI-4175 blocked tumor growth, and was more successful at higher doses of the drug. The research shows an even stronger effect in mice that received ARI-4175 combined with cetuximab.
Cetuximab, which is FDA-approved for metastatic colorectal cancer and some head and neck cancers, works by blocking a crucial receptor on the surface of a cancer cell—causing the cell to die. In people carrying the mutated form of the KRAS gene, cetuximab is not effective, but ARI-4175 may open up a detour around that impasse.
Borghaei notes that a cancer treatment like the immune stimulator ARI-4175, which uses the body's own defenses, may be more effective than drugs targeting tumor oncogenes that are susceptible to mutations that lead to resistance. "Tumors often develop resistance to targeted therapies," he says, "but it's more difficult to find resistance to a patient's own immune system. Bringing in the activity of the immune system might be the most effective way to fight some of these cancers."
"Our immune system can actually be a very useful partner in the fight against cancer," he says.
The researchers say their results suggest ARI-4175 warrants further testing in clinical trials. Although the researchers investigated colorectal cancer, their findings may also point to new approaches to treating other types of cancer. "If we can show that the drug overcomes resistance to cetuximab, it can be used against head and neck cancers as well," says Borghaei.

http://www.bioresearchonline.com/article.mvc/Researchers-Uncover-A-Viable-Way-For-0001