Ask Thry'vors Archive Categories
- Beginnings
- Pathology and Cytology
- Surgery
- Treatment and Follow-up
- Radioactive Iodine
- Low Iodine Diet
- Thyroid Hormone Replacement and TSH Level
- Psychological impact of Thyroid Cancer
- Other Related Health Issues
- Women's Issues
- Men's Issues
- Children and Youth Issues
Beginnings
- How does a patient find a thyroid cancer specialist?
Ezzat (July 1/05)
Check with major cancer treatment centres. Most current studies are multi-centre in nature with involvement from major Canadian centres.
Driedger (July 1/05, revised Sept 26/08)
There is not a Consumers' Guide to thyroid cancer specialists. Most oncologists, surgeons, endocrinologists and nuclear physicians can treat these conditions adequately most of the time.
Some patients may think that they receive better care when it is delivered by a physician who has achieved a public profile on the subject; I'm not certain that this is true. I do know that physicians practicing in many communities are providing the best care they can to thyroid cancer patients and that these physicians regularly consult with acknowledged experts concerning the care to be provided to specific patients. What patients need to do to is ask all their questions of their primary and referral physicians and to satisfy themselves of the care they are seeking.
- Are there any new drugs such as chemotherapy agents being tested for use with differentiated thyroid cancer?
Ezzat (July 1/05)
Unfortunately, current chemotherapeutic agents are not useful for most types of metastatic thyroid cancer. However, newer agents are currently being tested in phase ii and iii clinical trials. Most such agents act by specifically inhibiting cancer cell growth. These agents are selected on the basis of their relative specificity to a cancer utilizing signalling (information) pathway. Their long-term safety and effectiveness is now being examined.
Driedger (July 1/05, revised Sept 26/08)
Up to now, there is not an established role for chemotherapy of differentiated thyroid cancers. There are some interesting, mostly phase II, clinical trials in progress.
- What specifically can thyroid cancer survivors do to support thyroid cancer research?
Driedger (Mar 1/06, revised Sept 26/08)
A couple of things:
i) ask your physician about his/her participation in clinical trials and about trials that might be appropriate for your clinical situation. From my experience, participation in available trials is one way to ensure the best possible personal care while also helping to improve the care of future patients.
ii) Research is always a costly undertaking and financial support is appreciated. We appreciate those who undertake to raise funding support. While I will always fondly remember the old gentleman who charged an entry fee of $2 of everyone who came to his 80th birthday party and brought me his take for my research, it is best that contributions be made to a body with procedures for financial accountability, such as the Thyroid Foundation, so that there will be proper scrutiny of research proposals and the best possible use made of the available resources.
Ezzat (Mar 1/06)
Make your interests and concerns known. Advocate your cause and the importance of thyroid cancer to major research funding agencies such as the National Cancer Institute of Canada (NCIC) and the Canadian Institutes of Health Research (CIHR).
- What research is being conducted in the field of thyroid cancer study? Do Canadian thyroid cancer MDs work together to study this cancer?
Driedger (Mar 1/06, revised Sept 26/08)
The major areas of research in thyroid cancer have to do with our inadequate understanding of the origin of thyroid cancers (including the genetic factors) and studies of thyroid cancer populations in regard to the outcomes of various accepted treatments.
(In regards to specialists networking) there is a large informal component to networks; it has a lot to do with where one trained, who one knows or meets at specialty society meetings. We have been trying to raise the level of formality a bit in order to use our shared energies to better effect. Specifically, a small number of us recently formed an open group that we call the Canadian Thyroid Cancer Consortium; our shared objective is to develop a common database from which we will be able to evaluate long term outcomes of participating centres. We anticipate that more than a thousand new patients will be recruited annually and followed-up. We should not forget the critical role that industry plays in network building.
Ezzat (Mar 1/06)
(In regards to specialists networking) admittedly communication is quite limited. The relatively small number of specialists in Canadatypically meet at major international conferences in the U.S..
Ezzat (Oct 1/05)
Angiogenesis inhibitors are now being used for some forms of lung cancer. They appear to be promising in retarding tumor progression. However, they have not yet been tested in any systematic manner in the treatment of thyroid cancers. I would check with major cancer centres to determine if any on-going or proposed research studies are underway.
- What are the possible effects of radiation of the development of thyroid cancer? What are the possible genetic predispositions to developing thyroid cancer? What are the effects 1950-1960s nuclear testing fallout?
Driedger (Aug 1/07, revised Sept 26/08)
There have been many reviews over the past 60 years or so to assess what impact any of several sources or radiation exposure might have on thyroid cancers. We know that radiation treatments given to newborns before about 1950 in a mistaken attempt to shrink the thymus gland, which lies close to the thyroid, and prevent crib deaths caused many thyroid cancers in later life.
We also know that high radiation exposures to children, but not so much to adults, in the Chernobyl area have increased the subsequent incidence of thyroid cancers in that part of the world. So far, more than 5,000 thyroid cancers have been diagnosed in that region.
Patients who have had radiation therapy (high doses) for other head and neck cancers have an increased occurrence of thyroid cancer in the following years.
The situation is not so clear in regard to lower doses of radiation. Natural background radiation levels vary by a factor of about 50 around the world and have not been clearly shown to link to thyroid cancers. In Ontario, the incidence of thyroid cancer seems to be lower in northern Ontariowhere the natural radiation level is about 3 times that of the southwest. Medical diagnostic and dental x-ray exposures are not clearly linked to any cancer by evidence although there is a theoretical basis to think that they might be.
The medical community that cares for thyroid cancers is recognizing that there are familial occurrences of papillary cancer in about 6-8% of cases. If these cancers occurred only by chance, the lifetime odds for any one of us to develop one are about 1 in 200. If the familial occurrences that we see occurred only by chance, then they would have a frequency of only 1 in 40,000 cases. And the occurrence of two such families would be 1 in 1.6 billion. However, we have data on about 60 families in London alone, some with as many as 5 cases of the disease. There is no reasonable probability that this could occur by chance; there is a genetic factor in some cases, although it is not obvious that inheritance plays a role in most cases.
Driedger (March 1/11)
(In regards to Ameican nulear testing, and its effects in Canadian provinces...) it's a really great question. The map that the questioner refers to appeared in the report of an American Senate Committee hearing on the subject of radiation-induced cancers from the atmospheric bomb tests that were conducted in the American midwest in the post-war era until about 1963. The isodose curves on the map were drawn only over American territory as though their activities had no effect outside of their borders. I too lived in Saskatchewan during those years.
The American Senate hearings were conducted to determine whether the US Government was in any way liable for the health consequences of their bomb tests and the question of consequences outside of their borders never came up.
We do not have exactly replicating documentation as to how Canadians were affected but we do have other documentation. I used to have access to a Canadian website that used both the CIHI cancer statistics and the national census data (back when we had a census!) to create maps of the distribution of the different cancers across Canada. I've lost the website but I can tell you that the last data I saw showed that the incidence of thyroid cancers in the southern prairies is lower than it is in more places more remote from the explosions, such as Ontario.
The American data were really not very useful; they concluded that the fallout might result in something between 7,000 and 70,000 cases of thyroid cancers over the ensuing 50 years. We have better data from the lifelong monitoring of Japanese bomb survivors; here we can say that radiation exposures that ranged from the just barely survivable to trivial resulted in a statistical excess of some 600 cancer cases, this in a population which experienced 300,000 'naturally occurring' cancers in the same time. What this teaches us is that radiation, though greatly feared, is a very inefficient carcinogen compared to pollutants and certain chemicals and especially to tobacco smoke.
The point of all this is that, knowing what I know, I do not worry at all about the effects of my own childhood exposure to radioactive fallout on the Canadian prairies and I would urge your readers to maintain a balanced perspective of that sorry experience. - Does being overweight and eating too many carbs raise the risk of thyroid cancer and/or raise the risk of a recurrence?
Cheng (Nov. 1/08)
A recently published review of dietary and other risk factors for thyroid cancer concluded that there appears to be an association between higher body mass index and risk of thyroid cancer in women. However, this association was not found in men. Interestingly, there was also a weak association between height, particularly in men, and medullary thyroid cancer. As for diet, high intake of vegetables (other than cruciferous vegetables such as cabbage, brussel sprouts, cauliflower, broccolis) appears to be protective and is associated with a decreased risk of thyroid cancer. As for carbohydrates, some studies have shown an increased risk of developing thyroid cancer among those with a diet high in refined carbohydrates with a high glycemic index compared to a diet that consists of low glycemic index carbohydrates. However, it is important to bear in mind that the associations are suggestive but not definitive. There are many health benefits to maintaining a healthy body weight and eating a well-balanced diet with lower glycemic index carbohydrates. Therefore, irrespective of the potential impact on thyroid cancer, these are still worthy interventions for all.
Ref:
- Why did I get thyroid cancer? Is there a genetic link? Does exposure to radiation increase one's chances of developing thyroid cancer?
Drucker (Aug 1/07) (for full text with article reference please see Dr. Drucker's website: http://www.mythyroid.com/whythyroidcancer.html)
Many patients naturally want to know "Why did I get thyroid cancer?" Most patients have no known risk factors or family history and were often previously in good health. Scientists and physicians do not have good answers to this question yet, but many research programs are looking into this issue. A substantial number of thyroid cancers appear to exhibit genetic abnormalities in one or more chromosomes, but the reason for these types of chromosomal abnormalities remains obscure. Importantly, dozens of studies have demonstrated that the vast majority of patients with well differentiated thyroid cancer (papillary thyroid cancer) have an excellent prognosis.
A very common mutation detected in papillary thyroid cancer is activation of the Ret or Trk signalling pathways, leading to enhanced cell growth. Similarly, mutations have also been detected in BRAF, a cell signalling molecule whose activities are coupled to stimulation of cell growth. BRAF mutations appear to be detected in papillary but not follicular thyroid cancer. Furthermore, the presence of BRAF mutations appears to be associated with an increased risk of extrathyroidal tumour extension, and a higher risk of recurrence. In contrast, specific genetic mutations have also been identified in follicular thyroid tumours. 3p25 rearrangements of the peroxisome proliferator-activated receptor gamma (PPARgamma) gene have been detected in follicular epithelial tumours of the human thyroid gland. Eleven of 42 (26%) low-stage follicular carcinomas, 0 of 40 follicular adenomas, 1 of 30 Hurthle cell carcinomas, 1 of 90 papillary carcinomas, and 0 of 10 nodular goitres had 3p25 rearrangements by interphase fluorescence in situ hybridization. Hence, this abnormality likely contributes to the development of follicular thyroid cancer.
Molecular genetic studies suggest that exposure to ionizing radiation is associated with specific genetic changes that activate oncogenes, or cancer-causing genes, in thyroid tissue. More recent studies have demonstrated that intrachromosomal rearrangements involving the BRAF oncogene also play an important role in the development of radiation-induced thyroid cancer in many patients. The majority of patients with non-medullary thyroid cancer, including patients with well differentiated thyroid cancers (WDTC) such as papillary or follicular thyroid cancers, do not have a familial component to their disease, and usually do not pass on a markedly increased risk of cancer to their children. Nevertheless, a small percentage of even WDTC patients do appear to develop the disease as a result of an as yet unknown genetic predisposition. Many patients have more than one papillary carcinoma within the removed thyroid, often referred to as multifocal disease. Genetic analysis of the tumours in some studies indicates that the different tumours appear to arise from independent events, and are not genetically related or derived from the same original tumour. However, these results have not been universally confirmed, as similar studies have concluded that multifocal tumours often arise from a single common primary lesion.
Several studies suggest that survivors of bone marrow transplants may also have a slightly increased risk of thyroid cancer. For example, children receiving allogeneic BMT clearly exhibit an increased number of thyroid cancers several years after treatment, and should be followed closely with regular thyroid assessments. Analysis of patients treated with high dose radiotherapy at Memorial Sloan-Kettering Cancer Center revealed 13 patients with well differentiated thyroid cancer. The median interval from the time of radiation therapy until the recognition of thyroid disease was 13.0 years (range, 6.2-30.1 years). Similarly, transplant patients receiving prolonged immunosuppression appear to be a greater risk for development of thyroid cancer. Furthermore, patients with radioactive iodine exposure during childhood also exhibit an increased risk of thyroid cancer years later during adulthood as outlined in Patients exposed to radiation have an increased risk of developing benign thyroid nodules as well as thyroid cancer. Nevertheless, the majority of patients with thyroid cancer have no history of radiation exposure.
Genetic Syndromes and Thyroid Cancer
Patients with Medullary Thyroid Cancer (MTC) will frequently have a genetic mutation that is responsible for development of the cancer. A substantial proportion of patients with MTC will have a mutation in the ret oncogene, and such patients should have genetic screening of their families to identify other potential gene carriers. Some patients with MTC may also have other endocrine tumours, such as adrenal tumours (pheochromocytomas) (or parathyroid hyperplasia) that comprise a genetic syndrome known as the Multiple Endocrine Neoplasia II syndrome (MEN 2). Patients with MEN 1, a different genetic disease, may also have parathyroid disease but generally do not get thyroid cancer as an associated feature of the MEN 1 syndrome. Patients with familial adenomatous polyposis (FAP) also appear to have an increased incidence of papillary thyroid cancer. In one studies, multiple thyroid tumours developed, each harbouring a different mutation in the FAP gene. In patients with FAP that underwent a screening ultrasound, thyroid cancer was ultimately detected in 12% of the patients. Patients with Cowden's Syndrome have an increased risk of several malignancies, and exhibit an increased risk of benign and malignant thyroid disease. Cowden\'s syndrome patients have a mutation in the gene designated PTEN, that encodes a protein tyrosine phosphatase.
Thyroid cancer may cluster in isolated families in about 2% of all cases. The genetic basis for these syndromes remains unknown, but is under active investigation. Indeed, experts have suggested that the incidence of familial papillary carcinoma may be higher than 2%, as high as 9% in some centers.
A new syndrome, transmitted in an autosomal dominant manner with incomplete penetrance has been described that links papillary thyroid cancer, nodular thyroid disease, and papillary renal neoplasia (kidney tumours) in certain families. The putative gene has been localized to chromosome 1q21, but the gene has not yet been definitively identified. There may also be a slightly increased risk of premenopausal breast cancer in patients with this mutation. Independent analysis of families of women who had either breast or ovarian cancer also indicate a slightly increased risk of thyroid cancer in the children.
The incidence of thyroid cancer, especially well differentiated thyroid cancer, has increased over the past few decades, as documented in several cancer registries in both North America and Europe. The Canadian Cancer Society Epidemiology Statistics are also provided in an easy to use Web-based format. Examine the changing trends in thyroid cancer incidence by region, age, sex, or compare variables.
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