Not lazy my friends, just busy... now that I have a toddler! Here is my latest news copied and pasted from my yahoo 360 blog of September 28, 2006:

This week has been a challenging one for me. As it was last year. Two years ago (while pregnant) I was diagnosed with Papillary Thyroid Cancer and 2004 became a whirlwind for me, much of which happened that year has thankfully been lost in my swiss cheese of a brain.

Last September I had my first post-removal and post-treatment scan. It was CLEAR. That was a surreal and happy moment for me. Of course, any ThyCa cancer patient will tell you that they really don't give you something to cheer about until you have had at least two clean scans, i.e., two years post. So this week is my second scan.

It's no simple deal, the process literally takes all week. I had to go into the Nuclear Medicine department of my local hospital to get Thyrogen injections on Monday and Tuesday morning at 8AM. Thyrogen alters the levels in my body to the degree so that when they gave me a small dose (approx 4 millicuries) of Radioactive Iodine, or I-131 on Wednesday morning, my body would absorb it correctly and then Friday morning brings the Gamma Camera SCAN!

The big bummer is spending time away from my little girl. She is in the loving care of her Daddy who has been just great with her. They are having fun running around town, hitting the park and all... also tonight is FREE ice cream night at COLDSTONE CREAMERY nationwide! He has plans to take her there too.

The government assures its employees and everyone that this stuff is "safe" when handled properly and that those of us with small children should "just make an effort to keep little children away from our neck area where the destructive I-131 might concentrate." Yeah Sure. They also told those poor men who stood in the desert of Nevada in the 1950s that it was safe to stand a few feet from where they detonated atomic bombs ABOVE GROUND that they were "safe" and that any nuclear fallout could be washed off in a shower. Sadly, most of them died of Cancer.

uhhhhhhhhhh.... don't mind me if I err on the side of caution and take a few days away from my little girl. I feel bad enough that I might have passed on weak thyroid genes to her, why complicate things by exposing her to something that could destroy her thyroid totally if I can help it?

So where am I now? in Purgatory. Waiting. Waiting. Waiting. waiting for more radioactive material (technetium 99) to be injected into me tomorrow morning.

the scan.

then more waiting for the results.

I really don't feel negatively about it, I think it will be a clear test. but just re-experiencing this crap brings it back to reality for me. cancer takes me to a dark place. it's scary and ugly and lonely.

my friends, I hope you NEVER have to go there.

Here is the follow-up posting of October 3, 2006 with said pending results:

some of you know me well enough to know that I am not a patient patient when it comes to waiting for test results. True to my nature, I didn't wait for my doctor's appointment scheduled for Oct 5th. I went to the hospital - straight to the records department and requested copies of all records from my visit including lab reports.

The scan report says there is no visible uptake of the iodine in my neck or in remote sites of the body, i.e. chest, lungs, bones, etc... which means NO CANCER! YEAH! NO CANCER TWO YEARS IN A ROW, PEOPLE. yahoooooooooooooo!

Okay. good news is always welcome. thanks again to all of you who have been supportive. I surely do appreciate it.

Now I return you to your regularly scheduled programming.

Major Guidelines for Managing Thyroid Cancer Published in Thyroid Journal

As you know by now, I stay on top of the latest findings regarding thyroid cancer. Google's News service has a subscription service so any new info posted anywhere gets sent to my mailbox directly. This is a recent find.... very good info to have as a ThyCa patient!

January 20, 2006 08:01 AM US Eastern Timezone

Major Guidelines for Managing Thyroid Cancer Published in Thyroid Journal

NEW ROCHELLE, N.Y.--(BUSINESS WIRE)--Jan. 20, 2006--The American Thyroid Association has released updated, official guidelines for the management of patients with thyroid nodules and thyroid cancer, which reflect a decade of improved strategies for identifying, evaluating, and treating thyroid disorders. The new management guidelines have been pre-published online (www.liebertpub.com/thy) and will be available in print in the February 2006 (Volume 16, Number 2) issue of Thyroid, a peer-reviewed journal published by Mary Ann Liebert, Inc. (www.liebertpub.com).

Prepared by the ATA's Guidelines Taskforce, comprised of a team of experts in endocrinology, surgery, and nuclear medicine from leading academic and research institutions from across the U.S., the guidelines present recommendations for many controversial treatment issues. These include identifying the most cost-effective approach for diagnostic evaluation of thyroid nodules, the extent of surgery needed for small thyroid cancers, the appropriate use of thyroxine suppression therapy, the role of recombinant human thyrotropin, and the use of radioactive iodine to ablate remnant tissue following thyroidectomy.

Led by taskforce Chair David S. Cooper, M.D., Director, Division of Endocrinology, Sinai Hospital of Baltimore (Maryland), and Professor of Medicine, Johns Hopkins University School of Medicine, the taskforce focused on the importance of the timely and accurate diagnostic evaluation of thyroid nodules to rule out thyroid cancer and on therapeutic strategies for differentiated thyroid cancer, which represents approximately 90% of the estimated 26,000 cases of thyroid cancer diagnosed each year in the U.S.

The guidelines also include hands-on information on the follow-up and treatment of thyroid nodules, including the role of medical therapy. They outline the goals of therapy for differentiated thyroid cancer, strategies for staging thyroid tumors, the role of adjunctive external beam radiation and chemotherapy, and long-term management issues.

"I am gratified that the ATA had the foresight to develop evidence-based guidelines that will enable physicians who care for patients with thyroid disease to do so rationally, judiciously, and cost-effectively," says Dr. Cooper.

Thyroid, edited by Terry F. Davies, M.D. , of the Division of Endocrinology, Diabetes & Bone Diseases at Mount Sinai School of Medicine (New York, NY), is an authoritative peer-reviewed journal published monthly in print and online. As the Official Journal of the American Thyroid Association, Thyroid publishes original papers and timely reviews that reflect the rapidly advancing changes in our understanding of thyroid physiology and pathology, from the molecular biology of the cell to clinical management of thyroid disorders. A complete table of contents and free sample issue may be viewed online at www.liebertpub.com/thy

Mary Ann Liebert, Inc., is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Diabetes Technology & Therapeutics and Journal of Women's Health. Its biotechnology trade magazine, Genetic Engineering News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 60 journals, books, and newsletters is available at www.liebertpub.com.

Gene Mutation and Poor Outcomes in People with Thyroid Cancer

Newswise — Scientists at Johns Hopkins have found that a mutation in the gene that triggers production of a tumor growth protein is linked to poorer outcomes for patients with papillary thyroid cancer (PTC).

A report on the study is published in the December issue of The Journal of Clinical Endocrinology and Metabolism.

Mingzhao Xing, M.D., Ph.D., an assistant professor in the Division of Endocrinology and Metabolism at The Johns Hopkins University School of Medicine, led the multi-center study. “This discovery should help physicians rate risk levels for patients with PTC,” he says.

The gene, called BRAF, is part of a signaling pathway that, when activated, is known to cause tumor growth, and mutations in BRAF have been linked to a variety of human cancers, the researchers say.

For the study, Xing and colleagues looked at information from 219 PTC patients from 1990 to 2004. The relationship among BRAF mutations, initial tumor characteristics, cancer recurrence and clinical outcomes was analyzed.

Results showed a “significant association” between BRAF mutation and spread of the cancer from the thyroid, lymph node metastasis, and advanced tumor stage at the time of surgery to remove the cancerous thyroid gland. The thyroid, a gland located beneath the voice box (larynx) that produces thyroid hormone, helps regulate body cell growth and metabolism.

Results also showed that, given an average follow-up of three to four years, 25 percent of patients with BRAF mutations experienced tumor recurrence compared to 9 percent without evidence of BRAF mutations.
BRAF mutation was also an independent predictor of recurrence in patients with early disease, with 22 percent recurrence in those who had BRAF mutations versus only 5 percent in patients without the mutation.
Finally, BRAF mutation was more frequently associated with treatment failure in recurrent disease, according to the study.

“By illustrating a higher risk of poorer outcomes and recurrence, these results should help physicians perform better risk analysis of patients with PTC, which in turn will lead to more tailored treatment of the disease,” Xing said.

PTC is the most common thyroid cancer, accounting for 80 percent or more of thyroid malignancies. Although PTC is usually curable with surgical removal of the gland, often followed by radioiodine treatment, many cases recur and are fatal.

The ability to predict outcome has traditionally been based on such factors as patient age and gender, tumor size and the nature of the spread of disease. However, these criteria often leave uncertainty regarding the risk of tumor progression and recurrence. “What we have is a novel molecular diagnostic tool that will improve existing clinical efforts,” Xing said.

The study patients were recruited from The Johns Hopkins University School of Medicine; The Yale University School of Medicine; The Hospital for Endocrine Surgery in Kiev, Ukraine; and The University of Bologna Hospital in Bologna, Italy.
Other contributors from Hopkins include William H. Westra, M.D., professor in the Department of Pathology; Ralph P. Tufano, M.D, assistant professor in the Department of Otolaryngology -- Head and Neck Surgery; David Sidransky, M.D., professor in the Department of Otolaryngology -- Head and Neck Surgery, and Paul W. Ladenson, M.D., director of the Division of Endocrinology and Metabolism.

The study was supported by grants from the National Institutes of Health and the Flight Attendant Medical Research Institute.
© 2006 Newswise.

Role Of MicroRNA Identified In Thyroid Cancer

24 Dec 2005:

The presence of only five tiny strands of RNA is enough to clearly distinguish cancerous thyroid tissue from otherwise normal tissue, scientists say.

The findings provide more evidence that an emerging set of RNA genes called microRNA (miRNA) is a powerful regulatory force in the development of cancer and other diseases. The study is published online in the Dec. 19 Proceedings of the National Academy of Sciences.

Scientists already know that some people inherit a predisposition to developing papillary thyroid cancer (PTC), the most common form of thyroid cancer, representing about 80 percent of all cases. Although changes in key cell-signaling systems and gene translocations are sometimes present in thyroid tumors, no specific gene mutations have yet been identified that are directly linked to the predisposition of this type of cancer.

That led researchers in The Ohio State University Comprehensive Cancer Center to conclude that while genetic mutations may indeed cause some people to be more likely to develop PTC than others, the mutations may not occur often enough to be readily detectable. They hypothesized that any predisposition to PTC might be more reasonably linked to a more subtle, complex interaction among several genes - suggesting a possible role for miRNAs.

MiRNAs are smidgens of genetic material no longer than 22 or so nucleotides in length. A gene, in comparison, can be tens of thousands of nucleotides long. Scientists used to think miRNAs were parts of long stretches of functionless, "junk" DNA in the genome. But Dr. Huiling He, a research scientist in the Human Cancer Genetics Program at Ohio State and the lead author of the study, says researchers are now beginning to understand how important they may be.

"The identification of miRNA 'signatures' in cancer and other diseases has really changed the way we think about the process of malignant growth," says He.

Old dogma held that a gene carries a recipe for a molecule of messenger RNA which, in turn, carries a blueprint for the creation of a particular protein. Any mutation in the gene could affect the production of the protein. But recent studies have shown that protein production can also be manipulated indirectly through miRNAs.

"MiRNAs can latch on to part of the messenger RNA and scramble its ability to properly carry out its original coding instructions," says He.

Under the direction of Dr. Albert de la Chapelle, a professor in the department of molecular virology, immunology and medical genetics at Ohio State, He and other researchers examined samples of malignant tissue from 15 patients diagnosed with PTC and compared them with normal appearing tissue adjacent to the tumors.

They found 23 miRNAs that were significantly altered in the cancerous tissue when compared with the normal samples, with three of the miRs - miR-146, miR-221 and miR-222 - dramatically overexpressed, or "turned on," registering 11-to-19-fold higher levels of expression in the tumors than in the unaffected tissue nearby.

Further investigation revealed that two additional miRs - miR-21 and miR-181a - when coupled with the three that showed dramatic overexpression, formed a "signature" that clearly predicted the presence of malignant tissue.

"We also discovered miR-221 expression in all of the apparently normal tissue of the patients with PTC, but it was significantly overexpressed in a subset of three of the samples, suggesting that increased activity of miR-221 may be one of the earliest signs of carcinogenesis," says de la Chapelle.

Some scientists believe miRNAs act like oncogenes, molecules that promote cell growth, and they also feel they may be tumor and tissue specific. For example, in many other forms of cancer, miRNA activity is suppressed, but in PTC, researchers found just the opposite: 17 of the 23 miRNAs they discovered were overexpressed.

According to the American Cancer Society, the incidence of thyroid cancer has been increasing slightly over the past several years. It estimates that about 25,000 new cases will be diagnosed in the United States this year.

"This is just the beginning of our work identifying the role of miRNAs in thyroid cancer," says He. "But we are encouraged by these findings. We feel that they help point the way toward new options in diagnosis and treatment for this disease."

A grant from the National Institutes of Health supported the research team, which included Drs. Krystian Jazdzewski, Wei Li, Stefano Volinia, George Calin, Carlo Croce and Chang-gong Liu, all of the Ohio State Human Cancer Genetics Program; Dr. Saul Suster, from OSU's department of pathology; Dr. Richard Kloos from OSU's departments of internal medicine and radiology; Rebecca Nagy, a genetic counselor in the Human Cancer Genetics Program; Sandra Liyanarachchi, a biostatistician in the Ohio State Human Cancer Genetics Program; and Dr. Kaarle Franssila, from the department of pathology at Helsinki University Central Hospital, Finland.

Michelle Gailiun
gailiun.1@osu.edu
Ohio State University Medical Center
http://www.osumedcenter.edu