Page 2 of 2: LIBRARY : ONCOLOGY RESEARCH, NEWS & REVIEWS

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A relatively new, minimally invasive treatment was 93 percent successful in eradicating malignant kidney tumors, according to a recent study conducted by researchers from Wake Forest University Baptist Medical Center in Winston-Salem, NC.

"I have performed many radiofrequency ablations of renal tumors and the results looked promising," said Ronald J. Zagoria, MD, lead author of the study. "I wanted to scientifically review the data to better assess the results and look for patterns that might predict success or complications," he said.

The study consisted of 104 patients with a total of 125 tumors ranging from 0.6 cm to 8.8 cm. In all patients, a biopsy confirmed the presence of renal cell carcinoma (RCC), the most common type of kidney cancer. Of the 125 tumors, 95 were smaller than 3.7 cm and were completely eradicated in one treatment. Fourteen larger tumors were also eradicated after one treatment. Of the 16 remaining larger tumors, seven were eradicated after a second treatment.

"Patients who are not good operative candidates, usually due to co-existing illnesses, and those with multiple renal tumors, now have an excellent option for curing their tumors," said Dr. Zagoria. "Surgery should be the first option, since the long-term results of this procedure have not been substantiated," he said.

"There was a very low rate of serious complications and ablation was uniform and complete throughout the treated area, with no evidence of recurrence within the margins of the treated tumors," said Dr. Zagoria. "Also, ninety-five percent of patients were treated with minimal discomfort and they were able to go home the same day the procedure was completed," he said.

The full results of this study appear in the August issue of the American Journal of Roentgenology, published by the American Roentgen Ray Society.

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Main Category: Dermatology News
Article Date: 05 Aug 2007 - 0:00 PDT

Over the past several decades, the incidence of melanoma the most serious form of skin cancer has steadily increased in the United States. From 1995 to 2004, melanoma has increased by more than 1 percent per year in this country in sharp contrast to overall cancer rates that have steadily decreased by 0.6 percent per year during this time. While dermatologists and other public health officials work together to try to reverse this alarming trend, key findings from a successful multi-faceted intervention program designed to increase sun-safe behavior in children could play an important role in decreasing melanoma in future generations.

Speaking today at the American Academy of Dermatology 's Summer Academy Meeting 2007, dermatologist Martin A. Weinstock, MD, PhD, FAAD, professor of Dermatology and community health at Brown University in Providence, R.I., and chief dermatologist at Veterans Affairs Medical Center in Providence, presented a summary of recently published research on the rising incidence of melanoma and trends in sun exposure.

"While the increase in melanoma rates from 1995 to 2004 was not specific to one age group, we did notice an increase in the youngest age group (from ages 15 to 30) and in the age 60 and older age group," said Dr. Weinstock. "The possible reasons for this increase in younger and older Americans are not documented, but one possible explanation could be more exposure to UV radiation which we know is the most preventable risk factor for melanoma."

Youth and Sun Exposure

One population-based study published in the September 2006 issue of the journal Pediatrics found that although there was not a significant change in the proportion of youths that reported getting sunburned from 1998 to 2004, there were some interesting distinctions between the younger and older youths. For example, the 16 - 18 age group had more sunburns during that time period compared to the 11 13 and 14 15 age groups including an increase in the reported number of sunburns over the six-year study period. In 2004, 70 percent of the 16- to 18-year-olds reported getting sunburned, an increase from 64 percent reported by this age group in 1998.

In contrast, the study found that the younger age groups (ages 11 - 15) reported fewer sunburns and a decrease in the number of sunburns from 1998 to 2004. Specifically, the youngest age group studied (ages 11 13) fared the best in terms of the fewest sunburns dropping from 75 percent in 1998 to 67 percent in 2004. Those in the 14 15 age group also reported a decrease in the number of sunburns from 1998 to 2004 from 79 percent in 1998 to 70 percent in 2004.

"The study did not provide a definitive explanation as to why the younger age groups had fewer sunburns than their older counterparts, but one possible reason is that younger adolescents are more responsive to parental guidance than older teens who tend to be influenced more by their peers," explained Dr. Weinstock. "This trend, however, is worth noting in future public education campaigns geared toward teens and adolescents."

Another study published in the January 2007 issue of the journal Pediatrics found that a multi-component community-based intervention successfully increased sun-protection behaviors in adolescents entering 6th to 8th "SunSafe in the Middle Years" program, designed as a randomized, controlled trial. The intervention used a broad range of role models including school personnel, coaches, pediatricians, teen peer advocates and lifeguards who actively encouraged adolescents to practice proper sun protection in different environments.

"The study found that there was significant improvement in the areas of the body protected by sunscreen, clothing or shade in the adolescents in the 10 communities randomly selected for the intervention versus those in the control towns," said Dr. Weinstock. "From previous research, we know that compliance with sun-protective behaviors goes down between 6th to 8th grades. I think this study demonstrates that a multi-component program which involves a variety of people influential to this age group can have a positive impact on sun protection behavior and should be considered a model for future educational efforts aimed at adolescents."

Adults and Sun Exposure

Adults also failed to heed the warnings of dermatologists when it comes to practicing proper sun protection. A new article published in the June 1, 2007, issue of the Centers for Disease Control and Prevention's (CDC's) Morbidity and Mortality Weekly Report presented data showing an upward trend in the incidence of sunburns in U.S. adults. From 1999 to 2004, there was a 2 percent increase in the number of adults 18 years and older who reported getting sunburned (32 percent to 34 percent, respectively). While this represents only a slight increase, Dr. Weinstock pointed out that the data demonstrates that the occurrence of sunburns in the adult population is not decreasing.

"Dermatologists are concerned that melanoma and other skin cancers will continue to increase as long as sun exposure does," said Dr. Weinstock. "Since we know that overexposure to UV radiation is the most preventable risk factor for developing skin cancer, it's critical for dermatologists to emphasize that people should practice proper protection when engaging in outdoor activities."

The Academy recommends that people of all ages Be Sun Smart™ by following these tips:

-- Generously apply sunscreen with a Sun Protection Factor (SPF) of at least 15 that provides broad-spectrum protection from both ultraviolet A (UVA) and ultraviolet B (UVB) rays. Re-apply every two hours, even on cloudy days, and after swimming or sweating. Look for the AAD Seal of Recognition™ on products that meet these criteria.

-- Wear protective clothing, such as a long-sleeved shirt, pants, a wide-brimmed hat and sunglasses, where possible.

-- Seek shade when appropriate, remembering that the sun's rays are strongest between 10 a.m. and 4 p.m.

-- Use extra caution near water, snow and sand as they reflect the damaging rays of the sun which can increase your chance of sunburn.

-- Protect children from sun exposure by applying sunscreen.

-- Get vitamin D safely through a healthy diet that includes vitamin supplements. Don't seek the sun.

-- Avoid tanning beds. Ultraviolet light from the sun and tanning beds can cause skin cancer and wrinkling. If you want to look like you've been in the sun, consider using a sunless self-tanning product, but continue to use sunscreen with it.

-- Check your birthday suit on your birthday. If you notice anything changing, growing, or bleeding on your skin, see a dermatologist. Skin cancer is very treatable when caught early.

According to current estimates, there will be about 108,230 new cases of melanoma diagnosed in 2007 48,290 noninvasive and 59,940 invasive. For more information about skin cancer, visit

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and click on "SkinCancerNet."

Headquartered in Schaumburg, Ill., the American Academy of Dermatology (Academy), founded in 1938, is the largest, most influential, and most representative of all dermatologic associations. With a membership of more than 15,000 physicians worldwide, the Academy is committed to: advancing the diagnosis and medical, surgical and cosmetic treatment of the skin, hair and nails; advocating high standards in clinical practice, education, and research in Dermatology ; and supporting and enhancing patient care for a lifetime of healthier skin, hair and nails.

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Main Category: Liver Disease / Hepatitis News
Article Date: 05 Aug 2007 - 13:00 PDT

After lung and stomach cancer, liver cancer is the third largest cause of cancer deaths in the world. A new study on the relationship between coffee drinking and the risk of hepatocellular carcinoma (HCC) confirmed that there is an inverse association between coffee consumption and HCC, although the reasons for this relationship are still unresolved.

The results of this study appear in the August 2007 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD). Published by John Wiley & Sons, Inc., Hepatology is available online via Wiley InterScience at

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At least eleven studies conducted in southern Europe and Japan have examined the relationship between coffee drinking and the risk of primary liver cancer. The current study, led by Francesca Bravi of the Istituto di Ricerche Farmacologiche Mario Negri in Milan, Italy, was a meta-analysis of published studies on HCC that included how much coffee patients had consumed. Researchers combined all published data to obtain an overall quantitative estimate of the association between coffee consumption and HCC.

The results showed a 41 percent reduction of HCC risk among coffee drinkers compared to those who never drank coffee. "Moreover, the apparent favorable effect of coffee drinking was found both in studies from southern Europe, where coffee is widely consumed, and from Japan, where coffee consumption is less frequent, and in subjects with chronic liver diseases," the researchers state.

They point out that animal and laboratory studies have indicated that certain compounds found in coffee may act as blocking agents by reacting with enzymes involved in carcinogenic detoxification. Other components, including caffeine, have been shown to have favorable effects on liver enzymes. Coffee has also been related to a reduced risk of liver diseases and cirrhosis, which can lead to liver cancer.

"Despite the consistency of these results, it is difficult to derive a causal inference on the basis of the observational studies alone," the authors note. It may be that patients with digestive tract diseases, including liver disorders, naturally reduce their coffee consumption, even though avoidance of coffee is not routinely recommended. Also, they note that the assessment of coffee intake was based on patients' self-reporting, although recall of coffee drinking has been shown to be accurate. The fact that the inverse relationship between coffee drinking and HCC was shown in both southern Europe and Japan suggests a lack of bias in these studies. Allowance for other confounding factors, such as hepatitis B and C, cirrhosis, social class indicators, alcohol use and smoking, also suggests that such factors did not influence the results.

"In conclusion, the results from this meta-analysis provide quantitative evidence of an inverse relation between coffee drinking and liver cancer," the authors state. "The interpretation of this association remains, however, unclear and the consequent inference on causality and worldwide public health implications is still open for discussion."

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On The Development Of Pancreatic Cancer

Main Category: Cancer / Oncology News
Article Date: 05 Aug 2007 - 9:00 PDT

Nimesulide, a cyclooxygenase-2 (COX-2) inhibitor, delays the progression of precancerous pancreatic lesions in mice, according to researchers at David Geffen School of Medicine at UCLA. While inflammation has been shown to be a factor in many forms of cancer, the researchers say this is the first study to demonstrate the effect of an anti-inflammatory COX-2 inhibitor on the development of pancreatic cancer.

The study, published in the August 1 issue of Cancer Research, a journal of the American Association for Cancer Research, suggests a potential role for COX-2 inhibitors in pancreatic cancer prevention among high-risk patients. Pancreatic cancer is one of the leading causes of cancer death in America -- over 33,000 Americans will likely die from the disease in 2007, according to projections from the American Cancer Society.

"By inhibiting COX-2 in human patients, we may have an option to delay the progression of lesions," said lead author Guido Eibl, M.D., scientific director of the Hirshberg Laboratory of Pancreatic Cancer Research and adjunct assistant professor at UCLA .

Researchers believe pancreatic cancer arises from abnormal tissues, or lesions in the pancreas, known as pancreatic intraepithelial neoplasias (PanINs). By stalling the growth of PanINs, researchers hope to slow the development of or prevent pancreatic cancer.

COX-2, an enzyme which causes inflammation, is no stranger to cancer researchers. Studies of breast, colon, and pancreatic cancers have led researchers to believe COX-2 plays a key role in the development and growth of tumors.

To study the effects of COX-2 on PanIN progression, Dr. Eibl and colleagues focused on the KrasG12D mouse, an animal model that mimics the early stages of pancreatic cancer. In the KrasG12D mouse, low-grade PanINs (stage I or II) begin to appear in the pancreas of mice at one month. Starting at six months, high-grade PanINs (stage III) can be found in the mouse pancreas. According to Dr. Eibl, most researchers agree that stage III PanINs are a direct precursor to pancreatic cancer in humans as well as mice. Between 12 and 15 months, Dr. Eibl says the majority of KrasG12D mice will develop pancreatic tumors.

The UCLA researchers divided the mice into two groups -- one set received a nimesulide-enriched diet for 10 months; the other was offered only regular mouse chow. Their analyses revealed that the nimesulide diet greatly reduced the number of late-stage PanINs in KrasG12D (10 percent of pancreatic ducts had PanIN-2 or -3 in KrasG12D mice on nimesulide diet versus 40 percent of pancreatic ducts had PanIN-2 or -3 in KrasG12D mice on normal diet).

Because the pancreases of mice were analyzed at 10 months, before the typical appearance of pancreatic tumors, additional studies will be needed for researchers to conclude whether or not nimesulide can delay the onset of or prevent pancreatic cancer.

"With these results, I certainly wouldn't say everyone should be taking COX-2 inhibitors to protect against cancer," said Eibl. "However, with additional studies, we may find COX-2 inhibitors could help prevent pancreatic cancer in high risk populations."

"Pancreatic cancer is so deadly because it often goes undetected until it's too late," said Dr. Eibl. "If a patient is at a high-risk for developing pancreatic cancer, a COX-2 inhibitor may offer some protection."

In the future, Dr. Eibl and others plan to study the long-term effects of nimesulide and additional COX-2 inhibitors on the onset and progression of pancreatic cancer.

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A well-known inflammatory protein spawns an enzyme that inactivates two tumor-suppressing genes, ultimately triggering production of new blood vessels to nourish breast cancer cells, researchers at The University of Texas M. D. Anderson Cancer Center report in the August edition of the journal Cell.

"This is a completely new pathway for inflammation-induced cancer and may provide new targets for clinical intervention," senior author Mien-Chie Hung, Ph.D., professor and chair of M. D. Anderson's Department of Molecular and Cellular Oncology says of the chain of events described in the journal.

Inflammation is linked to breast cancer, liver cancer and cancers of the gastrointestinal tract. The research team set out to discover whether angiogenesis - the creation of new blood vessels - plays a role in cancer formation related to the inflammatory protein Tumor Necrosis Factor alpha (TNFa).

"What we found is a previously unrecognized role for IKKbeta, a protein kinase activated by TNFa," Hung says. IKKB inactivates a cancer-suppressing protein complex, which frees a cancer-inducing pathway to generate new blood vessels to supply tumors.

The chain of events, painstakingly worked out by Hung, first author and doctoral student Dung-Fang Lee, and colleagues works like this:

* TNFa activates IKKB, which as a kinase works by attaching phosphate groups to other proteins.

* IKKB phosphorylates tuberous sclerosis 1 (TSC1) blocking it from working with its ally, tuberous sclerosis 2, to repress the mammalian target of rapamycin (mTOR) pathway.

* With the tumor suppressors inactivated, mTOR is freed to produce vascular endothelial growth factor (VEGF), which creates new blood vessels to feed breast cancer.

The team confirmed the lab findings in mice. Mice with active IKKB had mean tumor volumes of 1,200 milimeters at 31 days, while those with inactive IKKB or with active IKKB and rapamycin injections to inhibit mTOR had mean volumes of less than 100 milimeters. Similar disparate tumor sizes were found when the tumor-suppressing TSC1 was inactivated. Tumors with TSC1 inactivated also were found to have greater blood vessel density - a measure of angiogenesis.

The researchers tested the theory by analyzing breast cancer tumors from 116 patients. They found breast cancer patients whose tumors had the TSC1/TSC2 tumor suppressor complex blocked by phosphorylation did not survive as long as those with an active TSC1/TSC2 (46 percent survival at 60 months vs. 65 percent).

Rapamycin is a powerful immune system suppressor used to protect organ transplant recipients against rejection of their new organs by suppressing mTOR. Rapamycin and similar mTOR inhibitors are in early clinical trials for a number of cancers at M. D. Anderson and elsewhere. One drug, temsirolimus, has been approved to treat renal cell carcinoma.

Hung's lab is exploring the possibility that this TNFa-driven activation of mTOR is the molecular link between obesity and heightened cancer risk. Obese mammals have high levels of TNFa secreted by their fat cells.

For Hung, the Cell paper is part of an ongoing effort to define the cancer-inducing activity of IKKB and its sibling, IKKa. He has found that the two, known to have a cancer-inducing affect working together, also have separate effects individually.

In the Cell paper, researchers show IKKB does its damage working in the cytosol of the cell, the internal fluid outside of the nucleus. Together, the two kinases previously were known to free the oncoprotein nuclear factor kappa B (NF"B) from the cytosol, allowing it to move to the nucleus and activate genes that promote cancer growth.

IKKa throws switch between tumor promotion and suppression

Earlier this year in a paper published in Molecular Cell, Hung's lab established that IKKa works individually by following NF"B into the nucleus, where IKKa plays the pivotal role in the oncogene's competition with the tumor-suppressing gene p53 for access to CREB-binding protein (CBP).

Both p53 and NF-kB covet CBP, an extremely popular activator of genes that interacts with hundreds of other proteins, Hung notes. In the case of the tumor suppressor and the oncogene, CBP will bind to only one at a time.

"You can think of them as a good guy, and a bad guy, with a gun lying between them. Who gets the gun" And how does one get it"" says Hung.

Hung and colleagues showed that IKKa phosphorylates CBP in the nucleus, switching CBP's binding preference to the NF"B oncogene, promoting cell growth. Unphosphorylated CBP helps p53 do its job suppressing cancer by forcing defective cells to kill themselves, programmed cell death known as apoptosis.

"If you can control IKKa, you get a double-dip effect," Hung says. "You not only activate p53, the good guy, you keep the bad guy out of the contest."

IKKa and IKKB together help NF"B escape into the nucleus, where it promotes cell growth and blocks programmed cell death. IKKa then works separately in the nucleus and IKKB in the cytosol to induce cancer through separate pathways.

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Gliomas are highly malignant and invasive tumors with tendrils that extend far from the primary tumor site, rendering conventional therapies ineffective and leading to an invariably poor prognosis. In a new study published online this week in the open-access journal PLoS Biology, Angela Johnston, Donna Senger, and colleagues at the University of Calgary injected immunocompromised mice with human gliomas and compared invasive cells (which left the primary tumor site) to noninvasive cells (which remained at the site of injection) in order to understand the molecular mechanisms underlying this invasive behavior.

They identified the neurotrophin receptor p75NTR, which normally functions during development to induce neurite outgrowth and promote neuronal cell death, as an important regulator of glioma invasion. The researchers present the first evidence that this neurotrophin receptor can also be a potent mediator of glioma invasion, and they show that the expression of this receptor is sufficient to impart a dramatic invasive behavior on genetically distinct tumors.

These data highlight a previously unknown function of this receptor and suggest it may be a novel therapeutic target in the treatment of this devastating cancer.

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New Treatment Option For Life Threatening Symptom Of Parathyroid Cancer

New research accepted for publication in the Journal of Clinical Endocrinology & Metabolism (JCEM) reveals that the drug cinacalcet HCl (cinacalcet) may effectively reduce the dangerous accumulation of calcium in the blood that typically accompanies parathyroid cancer.

This drug therapy could provide a new and effective medical treatment option for patients with inoperable parathyroid carcinoma (cancer).

"Patients with inoperable parathyroid cancer typically have to contend with extremely elevated levels of calcium in their blood, which can lead to mental confusion, dehydration, kidney damage and ultimately death," said Dr. Shonni Silverberg of the College of Physicians and Surgeons at Columbia University in New York City and senior author of the study.

Management of inoperable parathyroid carcinoma has been a challenge due to the lack of effective medical therapy. In addition to treating the cancer, doctors also often need to treat hypercalcemia, or excess calcium in the blood, which can be more harmful than the parathyroid cancer itself.

"Until now, the therapeutic choices for patients with inoperable parathyroid cancer have been extremely limited," said Silverberg. "Cinacalcet offers an important option for treating hypercalcemia in patients with metastatic disease after surgical options have been exhausted."

Cinacalcet is a drug that mimics how calcium acts on organ tissues. It is used to treat hyperparathyroidism, or elevated parathyroid hormone levels, because it reduces parathyroid cell hormone secretion by binding to the calcium-sensing receptor on parathyroid cells.

The study was conducted at 15 centers in the United States and Europe. Twenty-nine patients with parathyroid cancer were enrolled. The study design included a variable-length titration (treatment with varying doses) phase and a maintenance phase. During the titration phase, cinacalcet was administered to patients until their serum calcium concentration were within normal levels (<10 mg/dL), the dose reached 90 mg, or the patient experienced adverse effects.

During the maintenance phase, dose increases were administered if needed, and doctors were permitted to prescribe treatments deemed necessary to provide adequate supportive care.

Serum calcium was reduced by >1 mg/dL in 62 percent of patients. The greatest reductions in serum calcium were observed in patients with highest baseline calcium levels. Adverse effects of cinacalcet included nausea, vomiting, and headache.

Parathyroid glands are endocrine organs located behind the thyroid gland in the neck. They are necessary for proper bone development, and to control the level of calcium in the blood. The parathyroid glands make parathyroid hormone, which takes calcium from bones so that it will be available in the blood for nerve conduction and muscle contraction.

"This trial is an important milestone for patients suffering from this devastating form of cancer," said Dolores Shoback, Associate Editor of the Journal of Clinical Endocrinology and Metabolism. "Cinacalcet is the first agent to target the main control switch for parathyroid hormone secretion the calcium receptor. All prior therapies for this disease work on the bone and patients quickly become refractory to those treatments."

Other researchers working on the study include Drs. Mishaela Rubin and John Bilezikian of Columbia University, Dr. Charles Faiman of the Cleveland Clinic Foundation, Dr. Munro Peacock of the Indiana University School of Medicine, Dr. Dolores Shoback of the Department of Veterans Affairs Medical Center, Dr. Robert Smallridge of the Mayo Clinic College of Medicine, and Drs. Schwanauer, Olson, and Klassen from Amgen, Inc.

JCEM is a publication of The Endocrine Society. Dr. Silverberg's article "Cinacalcet Hydrochloride Reduces the Serum Calcium Concentration in Inoperable Parathyroid Carcinoma" will appear in the October issue of the journal.

Founded in 1916, The Endocrine Society is the world's oldest, largest, and most active organization devoted to research on hormones, and the clinical practice of endocrinology. Today, The Endocrine Society's membership consists of over 14,000 scientists, physicians, educators, nurses and students in more than 80 countries. Together, these members represent all basic, applied, and clinical interests in endocrinology. The Endocrine Society is based in Chevy Chase, Maryland. To learn more about the Society, and the field of endocrinology, visit our web site at

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Patients with micropapillary thyroid cancersmall tumors equal to or less than 1 centimeter and tumors even smaller, less than 1 millimeter (mm) are more common and not without a risk as previously thought, according to a new study presented on Fri., Oct. 5, at the 78th Annual Meeting of the American Thyroid Association (ATA) in New York.

This is contrary to the widely perceived belief that small papillary thyroid cancers are clinically insignificant and don't require active treatment. Papillary is the most common type of thyroid cancer, accounting for about 80% of all thyroid cancers.

The findings suggest that the size of the tumor itself may not be the sole determinant for the degree of the cancer's aggressiveness. Small papillary cancer can indeed metastasize or spread to other parts of the body. Ten percent of patients in the study with micropapillary cancer and six percent of those with less than 1 mm cancers had tumors that spread to nearby lymph nodes in the neck.

The study also shows that small papillary thyroid cancer can come back after the initial treatment. In the study, 12 percent of patients with micropapillary cancer who received radioactive iodine treatment after surgery required a second treatment of radioactive iodine, 11-60 months later because the cancer had come back. For those patients with less than 1 mm thyroid cancer, 19 percent of those who received the post-operative radioactive iodine treatment also required a second radioactive iodine treatment.

The standard treatment for papillary thyroid cancer is surgery to remove the thyroid gland (thyroidectomy). If the cancer is large, or has spread to lymph nodes, or if the patient is at a higher risk for cancer to come back, then radioactive iodine ablation therapy is often used to destroy any remaining thyroid cancer cells after surgery. Very frequently, radioactive iodine treatment is not given for small cancers, unless there are some clinical indications or suspicions for more aggressive disease, despite its small size.

Researchers also found that a substantial proportion of patients in their study had micropapillary and less than 1 mm thyroid cancers, suggesting that small papillary cancers are quite common. Close to half (45 percent) of papillary thyroid cancer patients in the study had micropapillary cancer, while over a quarter (26 percent) of these patients had less than 1 mm cancer.

"I hope our study will enhance the understanding of small papillary thyroid cancer, which seems to be increasing in number, yet the natural course or optimum treatment is not well known," said Haruko Akatsu Kuffner, M.D., author of the study and Assistant Professor of medicine, Division of Endocrinology and Metabolism at the University of Pittsburgh in Pittsburgh, Pa.

"We would like to be appropriately aggressive in treating small aggressive cancers. However, it is also important not to be aggressive in managing the majority of these patients with clinically insignificant small cancers. A better understanding of this disease will help us to better risk stratify these patients," added Dr. Kuffner.

This large, retrospective study involved reviewing the records from 1992 to 2004 of 888 papillary thyroid cancer patients with original Pathology records including the cancer size available through the use of the University of Pittsburgh Thyroid Cancer Database.

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Targeting Linchpin Gene For New Breast Cancer Therapies

University of Iowa researchers have discovered a gene that plays a linchpin role in the ability of breast cancer cells to respond to estrogen. The finding may lead to improved therapies for hormone-responsive breast cancers and may explain differences in the effectiveness of current treatments.

Estrogen causes hormone-responsive breast cancer cells to grow and divide by interacting with estrogen receptors made by cancer cells. Interfering with estrogen signaling is the basis of two common breast cancer therapies -- tamoxifen, which blocks estrogen's interaction with a primary estrogen receptor called ER-alpha, and aromatase inhibitors that reduce the amount of estrogen the body makes and therefore affect any pathway that uses estrogen.

The study, led by Ronald Weigel, M.D., Ph.D., professor and head of surgery at the University of Iowa Roy J. and Lucille A. Carver College of Medicine, reveals a central role for transcription factor AP2C (TFAP2C) in controlling multiple pathways of estrogen signaling. The findings are published in the Sept. 15 issue of Cancer Research.

"Estrogen binds to estrogen receptors and triggers a cascade of events including gene regulation," said Weigel, who also is a member of the Holden Comprehensive Cancer Center at the UI. "We found that elimination of the TFAP2C from the cell causes all of those cascades that we associate with estrogen to go away. The treated cancer cells were not able to respond to estrogen by any normal pathway."

The researchers found that silencing expression of TFAP2C in hormone-responsive breast cancer cells significantly decreased the amount of ER-alpha made by the cancer cell. This reduction in ER-alpha (down to 16 percent of the level normally made by breast cancer cells) also affected production of other "downstream" genes involved in cancer growth.

In addition, silencing the TFAP2C also knocked out expression of another estrogen receptor called GPR30 that is found at the cancer cell membrane.

Importantly, the team also showed that these effects inhibited tumor growth. Specifically, the treated cancer cells did not grow in response to estrogen and establishment of tumors in mice was delayed.

The finding suggests that there are many pathways that allow cells to respond to estrogen, and that TFAP2C is a central player in controlling hormone response.

"Targeting this gene may be a better way to develop drugs to treat hormone-responsive breast cancers because it targets multiple different pathways," Weigel said.

The results also may explain why tamoxifen, which targets a single pathway, is less effective that aromatase inhibitors, which likely affect many estrogen pathways.

Weigel noted that advancing understanding of estrogen regulation and hormone-response in breast cancer is just one part of a larger focus on breast health at the UI.

"The UI has a great interest in breast cancer. Within the next couple of months, the UI Breast Health Clinic will be open and part of its mission is advancing both basic and clinical research in breast cancer," he said. "This study is one example of how we are moving forward in unlocking the mysteries behind what controls the ability of a breast cancer to respond to estrogen."

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Linchpin Gene May Be Useful Target For Breast Cancer Therapies

University of Iowa researchers have discovered a gene that plays a linchpin role in the ability of breast cancer cells to respond to estrogen. The finding may lead to improved therapies for hormone responsive breast cancers and may explain differences in the effectiveness of current treatments.

Estrogen causes hormone responsive breast cancer cells to grow and divide by interacting with estrogen receptors made by cancer cells. Interfering with estrogen signaling is the basis of two common breast cancer therapies -- tamoxifen, which blocks estrogen's interaction with a primary estrogen receptor called ER alpha, and aromatase inhibitors that reduce the amount of estrogen the body makes and therefore affect any pathway that uses estrogen.

The study, led by Ronald Weigel, M.D., Ph.D., professor and head of surgery at the University of Iowa Roy J. and Lucille A. Carver College of Medicine, reveals a central role for transcription factor AP2C (TFAP2C) in controlling multiple pathways of estrogen signaling. The findings are published in the Sept. 15 issue of Cancer Research.

"Estrogen binds to estrogen receptors and triggers a cascade of events including gene regulation," said Weigel, who also is a member of the Holden Comprehensive Cancer Center at the UI. "We found that elimination of the TFAP2C from the cell causes all of those cascades that we associate with estrogen to go away. The treated cancer cells were not able to respond to estrogen by any normal pathway."

The researchers found that silencing expression of TFAP2C in hormone responsive breast cancer cells significantly decreased the amount of ER alpha made by the cancer cell. This reduction in ER alpha (down to 16 percent of the level normally made by breast cancer cells) also affected production of other "downstream" genes involved in cancer growth.

In addition, silencing the TFAP2C also knocked out expression of another estrogen receptor called GPR30 that is found at the cancer cell membrane.

Importantly, the team also showed that these effects inhibited tumor growth. Specifically, the treated cancer cells did not grow in response to estrogen and establishment of tumors in mice was delayed.

The finding suggests that there are many pathways that allow cells to respond to estrogen, and that TFAP2C is a central player in controlling hormone response.

"Targeting this gene may be a better way to develop drugs to treat hormone responsive breast cancers because it targets multiple different pathways," Weigel said.

The results also may explain why tamoxifen, which targets a single pathway, is less effective that aromatase inhibitors, which likely affect many estrogen pathways.

Weigel noted that advancing understanding of estrogen regulation and hormon -response in breast cancer is just one part of a larger focus on breast health at the UI.

"The UI has a great interest in breast cancer. Within the next couple of months, the UI Breast Health Clinic will be open and part of its mission is advancing both basic and clinical research in breast cancer," he said. "This study is one example of how we are moving forward in unlocking the mysteries behind what controls the ability of a breast cancer to respond to estrogen."

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Prostate Cancer Prevention Trial Study Reanalyzed

Reanalysis of data from the first long-term randomized trial of a chemopreventive agent for prostate cancer shows that the excess prevalence of high-grade prostate cancer in the drug-treated group may be attributable to shrinkage of the prostate at the time of biopsy.

The study of the Prostate Cancer Prevention Trial, led by University of Illinois at Chicago professor of Pathology Dr. Peter Gann, is published in the Journal of the National Cancer Institute.

The Prostate Cancer Prevention Trial evaluated the drug finasteride, which blocks production of a male hormone within the prostate and is proven effective in treating benign prostatic hyperplasia, or enlargement of the prostate. The trial was stopped in 2003 when finasteride was found to reduce the risk of prostate cancer by nearly 25 percent. However, men assigned to the finasteride group had a greater prevalence of high-grade cancer.

Gann said the results were confusing for clinicians and patients because the drug appeared to retard the development of prostate cancer and decrease its prevalence, but the increased risk of high-grade cancer was unexplained and worrisome.

Researchers reasoned one possible explanation was that because finasteride shrinks the prostate gland, it increases the likelihood that a biopsy will detect high-grade cancer.

"It's logical that if you shrink the size of the gland and then stick needles in it, you're more likely to find cancer if it exists," Gann said.

A second possible source of bias in the trial that may have contributed to overestimation of prostate cancer risk in the finasteride group is that the drug lowers the blood level of prostate-specific antigen by approximately 50 percent. The PSA level is a biological marker doctors use to detect disease, so PSA levels measured in men taking finasteride are routinely adjusted upward. This calculation may have led to overestimation of baseline PSA levels among men in the finasteride group who were already harboring high-grade tumors at the start of the study.

"This is a very unusual situation -- though it will become more common in the future -- where the drug affects the marker we use to find the cancer," said Gann.

Using data from the Prostate Cancer Prevention Trial study, Gann and colleagues developed statistical models that took into account the size of the prostate gland and the number of needle cores that were taken during biopsy. In essence, the researchers compared finasteride to placebo among men with an equivalent number of needle samples per unit of gland volume.

The analyses showed that adjusting for changes in gland size due to the drug could account for all of the excess high-grade tumors.

"Once we did this adjustment, all the excess high-grade went away, and the effect of the drug on low-grade cancer was even stronger, as we would expect," Gann said.

"This drug may have been much better than people thought," Gann said, "and the fears about its impact on high grade tumors may have been exaggerated based on this bias alone."

However, he said, the findings must be interpreted cautiously, and the new results alone do not justify definitive changes in clinical practice or widespread use of the drug.

"Our goal is to improve scientific understanding of what happened in this very important and expensive trial."

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Cancer Death Rates Still Declining

By Amanda Gardner
HealthDay Reporter
Wednesday, February 20, 2008; 12:00 AM

WEDNESDAY, Feb. 20 (HealthDay News) -- Good news continues to come forth from the cancer front: U.S. death rates from the disease have declined by 18.4 percent among men and by 10.5 percent among women since mortality rates first started going down in the early 1990s.

In 2008, an estimated 1,437,180 new cancers will be diagnosed, and 565,650 people will die of the disease, according to a report released Wednesday from the American Cancer Society (ACS). Death rates were at their highest for men in 1990, and for women in 1991.

Although the rate of cancer deaths decreased from 2004 to 2005, there was an increase in number of actual deaths (5,424) in 2005 compared to 2004, the report showed.

"We do not know why the declines in death rate from 2004 to 2005 slowed,compared to the previous two years," said Ahmedin Jemal, strategic director for cancer surveillance at the ACS. "But we can say that this occurred for almost all of the major cancer sites for men and women, which include colon and rectum in both men and women, breast cancer in women, and prostate cancer in men."

"Death rates from cancer continue to decrease because of prevention, early detection and treatment," Jemal added. "These have been decreasing from the early '90s and, really, because of this decrease, over half a million deaths from cancer have been avoided."

Jemal is first author ofCancer Statistics 2008, which is published in the March/April issue ofCA: A Cancer Journal for Clinicians. The report has been an annual fixture since 1952.

"This is both good news and bad news," said Dr. Louis Weiner, director of the Lombardi Comprehensive Cancer Center at Georgetown University in Washington, D.C. "The good news is that cancer rates continue to decline, and that the lives of hundreds of thousands of Americans have been saved over past 15 or 16 years as a result of this improvement in cancer death rates."

"The bad news is that more than a half a million Americans can be anticipated to die of cancer this year," Weiner continued. "That's equivalent to nearly the entire population of Washington, D.C., and losing more than the entire population of New Orleans in 2003. Viewed from that perspective, we have a long way to go."

According to Jemal, "smoking is a big part [of the decline.] Smoking rates have been decreasing for the last 30 to 40 years, when the Surgeon General came out with his report."

Screening for colorectal, breast and cervical cancer have also contributed to the decrease, he added.

Today, about one-quarter of deaths in the United States today are due to cancer, killing more people under 85 than heart disease.

Some specifics from this year's report:

In men, cancers of the prostate, lung, colon and rectum represented about half of all newly diagnosed cancers. Prostate cancer alone accounted for one-quarter of the total cancer cases in men.In women, the three most commonly diagnosed cancers in 2008 will be breast, lung and colorectal. These account for about half of all cancer cases in women. Breast cancer alone accounts for 26 percent of new cancer cases among women (although the incidence decreased by 3.5 percent per year from 2001 to 2004, part of which may be due to declines in the use of postmenopausal hormone replacement therapy). About one-quarter of all deaths from cancer in women in 2008 will be from lung cancer.In men aged 40 and younger, leukemia is the most common cause of cancer death, while lung cancer is the leading killer in men over the age of 40.Leukemia is also the leading cause of cancer death among females under 20, while breast cancer takes the greatest toll in women aged 20 to 59. Lung cancer is the biggest cancer killer in women over 60.The incidence of cancer is 19 percent higher and the death rate 37 percent higher among black men compared with white men. For black women, the incidence rate is 6 percent lower, but the death rate is 17 percent higher than for white women.The five-year survival rate for children with cancer has improved from 58 percent for those diagnosed between 1975 and 1977 to 80 percent for those diagnosed between 1996 and 2003.

This year's report also includes a special section that discusses the impact of health insurance status on cancer prevention, diagnosis, treatment and outcomes. Earlier this week, researchers from the American Cancer Society reported that people who either have no health insurance or rely on Medicaid are more likely to be diagnosed with advanced cancers.

SOURCES: Ahmedin Jemal, DVM, Ph.D., strategic director, cancer surveillance, American Cancer Society, Atlanta; Louis Weiner, M.D., director, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, D.C.;Cancer Statistics 2008

MY OPINION : A very nice, detailed generic report has been filed in this article. Although cases of cancer have been increasing, not only in USA, but everywhere else, mortality rates have decreased due to good diagnostic measures and early detection and screening methods. Previously released Gardasil, a vaccination for Cervical Cancer, may prove to be beneficial as well.
A similar study should be taken out in specific regions in India as well. Attention should be given to incidence rate of particular cancer in a particular region and in a particular gender. Specificity should be given attention to in the above mentioned study.
More detailed and profiling studies of specific regions and specific population of India or any other country can reveal the type of cancer the particular populace is prone too, and screening methods should be improved or implemented likewise. [/b]

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Australian researchers reveal how cancers become more aggressive

A team of Australian scientists have discovered how some cancers are able to mutate into more aggressive and potentially fatal cancers in the human body.

The scientists from Monash University have found that a family of enzymes play a role in changing benign or less aggressive tumours into more deadly cancers.

The discovery provides a important clue into how cancer cells develop and mutate, and could ultimately lead to different treatment options for cancer victims.

The team of scientists led by Associate Professor Tony Tiganis, from the Department of Biochemistry and Molecular Biology, say the enzymes known as protein tyrosine kinases (PTKs) had a greater role than previously thought in the rate of growth and tumour change over time.

Professor Tiganis says it was already know that PTKs are linked with several types of aggressive cancers, including colon, breast and lung cancers, but they have now discovered that PTKs also have an important role to play as cancer cells grow and mutate to become potentially more aggressive tumours.

Tiganis says the more there is known about how tumours develop will mean the more able we are to prevent their growth in the future.

The researchers say there are already drugs that inhibit particular PTKs in the late stages of treatment and their discovery could change the timing of when and how those or similar drugs are administered.

Professor Tiganis says all cells routinely divide and duplicate during growth and an entire genome is replicated and divides equally into two daughter cells - but sometimes things go awry.

In an attempt to prevent this, Tiganis says nature has installed key cell checkpoints where molecular 'wardens' slow down DNA replication to try and correct mistakes and get the cell duplication back on track.

As a rule PTKs are turned off in the face of compromised DNA replication, but when PTK pathways remain on, unscheduled cell division can take place where cells distribute their DNA unevenly between the two resulting daughter cells and as a result, tumour cells can accumulate or lose genes and chromosomes, and gain a growth and survival advantage.

Professor Tiganis says their research has shown that PTK pathways are intimately associated with the regulation of checkpoint responses during DNA replication and they have identified one mechanism by which PTKs may remain activated and allow cancer cells to bypass the molecular warden of DNA replication.

Professor Tiganis says they may lack a key enzyme called TCPTP.

The Monash team now intend to apply their laboratory findings to human cancer samples to see if they contain low levels of TCPTP and hopefully cement the role of this protein in cancer formation and development.

The research is published in the international journal Cancer Cell.

My extra notes: The human protein tyrosine phosphatase TCPTP exists as two forms: an endoplasmic reticulum-targeted 48-kDa form (TC48) and a nuclear 45-kDa form (TC45). TCPTP is expressed in a wide variety of tissues, with a possible role in hematopoietic and inflammatory disease.It has been shown to be a critical regulator of CSF-1 signaling and mononuclear phagocyte development in hematopoiesis, apart from the functions as phosphatase mentioned above.

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