Thyroid Cancer and Dental X-rays are Unrelated - Dental Health Magazine

Many individuals believe that dental X-rays can increase the risk for developing thyroid cancer. However, here are a few things you should know right before you start dwelling on the same question:

One of the most important things is not to rely on your medical/health education from what is being said on TV shows. These are most of the times sensational in nature only, many times presenting topics and hypotheses that are meant to scare the average viewer.

According to chief medical officer of the American Cancer Society, Dr. Otis W. Brawley, the technology of cancer detection has gotten so professional and reliable that today it is possible to spot cancer types that 15 years ago would not even be diagnosed as health conditions.

This is the main reason why there are so many types of thyroid cancers available today.

It has been already medically proven that there is no link existent between mammograms or dental X-rays and the apparition of thyroid cancer. It is simply technology that evolved so much, it is able to pick up and recognize a greater variety of cancers in the human body.

The doctor further reveals that nowadays they even find types of cancers that do not pose any kind of health risk for the patients, so advanced these technologies have gotten.

Further, this fact is also backed by Dr. Leonard Wartofsky who is a thyroid cancer specialist and who has conducted a JAMA Study back in 2006. He advises the following:

• People should choose a dentist who uses the digital X-ray technology (less exposure to radiation)
• Also to choose dentists that can offer a lead apron with thyroid collar during the X-ray

He further states, that indeed there might be a very slight chance, almost inexistent of developing thyroid cancer from too much exposure to dental X-rays, but then how about thinking more about the risks that are there with you everyday?

These include over eating, smoking, drinking and not making any physical exercise, all of which are by far a greater risk of developing the disease than from an X-ray examination.

Fingerprint of radiation exposure discovered in thyroid cancer | Bioscience Technology Online

Fingerprint of radiation exposure discovered in thyroid cancer

Neuherberg, 24. Mai 2011. Scientists from the Helmholtz Zentrum München have discovered a genetic change in thyroid cancer that points to a previous exposure of the thyroid to ionising radiation. The gene marker, a so-called „radiation fingerprint“ was identified in papilliary thyroid cancer cases from Chernobyl victims, but was absent from the thyroid cancers in patients with no history of radiation exposure. The results are published in the current issue of PNAS.

The research team, led by Prof. Horst Zitzelsberger and Dr. Kristian Unger from the Radiation Cytogenetics Unit of the Helmholtz  Zentrums München, in collaboration with Prof. Geraldine Thomas, Imperial College London, studied thyroid cancers from children exposed to the radioiodine fallout from the Chernobyl nuclear reactor explosion. The team compared the genetic information from these tumours to that found in the same type of tumour that arose in children born more than one year after the explosion, after the radioactive iodine had decayed away. The number of copies of a small fragment of chromosome 7 was found to be increased only in the tumours from the irradiated children, establishing this as one of the first genetic markers that indicate a radiation aetiology of cancer.

This breakthrough is the first time since the reactor accident in 1986 that scientists have been able to discriminate between the cancers caused by the radioactive contamination and those that arise naturally.  Prof. Zitzelsberger ascribes the success of this study to the careful collection, documentation and storage of thyroid cancers from the Chernobyl region in the Chernobyl Tissue Bank. He noted that this unique collection of materials made it possible for the team to compare for the first time tumours from children of the same age and regional background. The availability of the genetic marker, according to Prof. Zitzelsberger, will improve both the clinical diagnosis of thyroid cancer and our understanding of how radioactive iodine causes the disease to develop. In future studies funded by EURATOM in the project „EpiRadBio“ the group will extend the study to determine if the genetic fingerprint is able to indicate the level of radiation exposure that is required to cause the cancer.

Additional Information

Original Publication:

Hess, J. et al Gain of chromosome band 7q11 in papillary thyroid carcinomas of young patients is associated with exposure to low-dose irradiation. Proceeding of the National Academy of Sciences USA (PNAS); Link to publication

Caption:
picture above: Julia Heß, Prof. Dr. Horst Zitzelsberger, Dr. Kristian Unger

picture below: In papillary thyroid carcinomas, more copies of the CLIP2 gene (red) are detected than of a reference gene (green)

About Helmholtz Zentrum München

The Helmholtz Zentrum München is the German Research Centre for Environmental Health. The leading research facility in this field, it conducts research into chronic and complex diseases caused by the interaction of environmental factors and an individual’s genetic disposition. The Helmholtz Zentrum München has about 1,700 staff members and is headquartered in Neuherberg in the north of Munich on a 50-hectare research campus. The Helmholtz Zentrum München is a member of the Helmholtz Association, Germany’s largest scientific organization, a community of 17 scientific-technical and medical-biological research centers with a total of 30,000 staff members. www.helmholtz-muenchen.de

Contacts for media representatives

Sven Winkler, Helmholtz Zentrum München – German Research Centre for Environmental Health (GmbH), Ingolstädter Landstrasse 1 85764 Neuherberg, Germany. Phone.: +49  89-3187-3946 . Fax +49 89-3187-3324, Email: presse@helmholtz-muenchen.de

Scientific contact

Prof. Dr. Horst Zitzelsberger, Abteilung für Strahlenzytogenetik, Helmholtz Zentrum München - Deutsches Forschungszentrum für Gesundheit und Umwelt (GmbH), Ingolstädter Landstraße 1 85764 Neuherberg. Phone.: + 49 89-3187-3421 .
Email: zitzelsberger@helmholtz-muenchen.de

Radioactive iodine therapy associated with increased second malignancies in low-risk thyroid cancer | HemOncToday

Radioactive iodine therapy associated with increased second malignancies in low-risk thyroid cancer 

Iyer NG. Cancer. 2011;doi:10.1002/cncr.26070.

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Patients with well-differentiated thyroid cancer developed excess cases of salivary gland malignancies and leukemia after treatment with radioactive iodine, according to an analysis of more than 37,000 patient records collected in the SEER database.

Because well-differentiated thyroid cancer is rarely fatal, the researchers said these results suggest that the use of radioactive iodine should be rationed in this patient population.

Researchers at Memorial Sloan-Kettering Cancer Center reviewed data on 37,176 patients diagnosed with low-risk thyroid cancer from 1973 to 2007. During that time, use of radioactive iodine as first-course therapy increased from 6.1% to 48.7%. Among patients aged younger than 45 years with low-risk tumors, use of radioactive iodine increased from 3.3% in 1973 to 38.1% in 2006. However, the OS rate has remained constant during that time.

Approximately 15,000 patients were treated with radioactive iodine. Researchers expected to find 3,029 secondary primary malignancies; however, they discovered 3,223 secondary primary malignancies.

“During the era when radioactive iodine use was uncommon, there was no statistically significant elevated risk of secondary primary malignancies among patients who were diagnosed with well-differentiated thyroid cancer,” they wrote. “However, the risk of secondary primary malignancies subsequently has increased in parallel with the escalating frequency of radioactive iodine use.”

The overall risk for secondary primary malignancies at any site increased from 1.00 (95% CI, 0.94-1.16) during 1973 to 1981 to 1.22 (95% CI, 1.10-1.35) during 1999 to 2006 for all patients. At the same time, excess absolute risk increased from 0 to 14.3 excess cases per 10,000 person-years at risk.

Risk for hematologic malignancies had the greatest increase. For leukemia, the standarized incidence ratio increased from 1.09 (95% CI, 0.72-1.57) during 1973 to 1981 to 2.40 (95% CI, 1.40-3.85) during 1999 to 2006. There was a corresponding increase in excess absolute risk, from 0.2 to 2.0 excess cases per 10,000 person-years at risk.

Among all patients in the cohort who received radioactive iodine from 1973 to 2007, SIR for secondary primary malignancies at any site was 1.18 (95% CI, 1.10-1.25). There was no increased risk for patients who did not receive radioactive iodine therapy (SIR=1.02; 95% CI, 0.98-1.06). There was an excess absolute risk for 11.9 excess cancers per 10,000 person-years at risk among patients assigned to radioactive iodine.

Studies summarize promising innovations in molecular diagnosis of thyroid cancer

Two recently released studies, one written by a pair of Greek endocrinologists and the other by an American pathologist, summarize the latest advancements made into the molecular analysis and diagnosis of thyroid cancer.


In a report appearing in the Journal of Thyroid Research (JTR), researchers from Athens noted that a number of genetic mutations, molecular markers and epigenetic modifications can help doctors detect an increased risk of abnormal thyroid cell growth.


The other paper, written by a physician at the University of Pittsburgh Medical Center and published in the journal Modern Pathology, addressed similar subject matter, though its scope was limited to genetic mutations.


Both papers pointed to chromosomal rearrangement as a budding field of thyroid cancer-related inquiry. For instance, researchers have found that the REarranged during Transfection (RET) proto-oncogene confers a substantial risk of medullary or papillary thyroid cancer.


The RET proto-oncogene is a strip of DNA that, when spontaneously rearranged, can increase the growth, differentiation and migration of thyroid cells. RET rearrangements often occur after exposure to intense radiation, according to the JTR report.


Both studies also discussed the molecular detection of RAt Sarcoma (RAS) oncogenes. When mutations occur in a specific area of a person's DNA that controls RAS subfamily proteins, cells can experience radical growth. This phenomenon occurs because RAS proteins help control the signals between a cell's nucleus and its organelles. Point mutations in the genes that control these proteins can increase the risk of thyroid cancer, although these same mutations may be detected through genetic testing.


Finally, the JTR study touched on epigenetic modifications. All DNA is coiled into a tight structure called chromatin. Molecules called methyl groups, which lie on the outside of DNA strands, help keep genes bunched together in this way.


However, accidental modifications to the placement of these methyl groups can lead to whole sections of DNA being inaccessible to transcribing proteins. These epigenetic changes can prevent thyroid cells from limiting their own growth.

Medicines may one day target papillary thyroid cancer based on its genetic source

Given that thyroid cancer is a disease that originates in mutations of DNA, an Italian researcher recently reviewed the state of genomic medicine, a healthcare field that has the potential to treat malignancies based on their genetic origins.

Mario Vitale, an oncologist and endocrinologist at the University of Naples Federico II, published an editorial in the Journal of Clinical Endocrinology and Metabolism (JCEM) stating that medications targeting particular enzymes may be able to mitigate papillary thyroid cancer (PTC) growth in patients with mutations of the serine/threonine-protein kinase B-Raf (BRAF) gene.

This gene encodes information that regulates the creation of proto-oncogene c-Raf, an enzyme that plays a crucial role in the molecular chain of events controlling cell growth, division and death in many thyroid cancers.

Previous studies have linked dozens of mutations in the BRAF gene to common forms of cancer. A report appearing in a 2003 issue of the JCEM found that one specific mutation, known as V599E, was found in 49 out of 170 cases of PTC, making it a particularly vulnerable "hot spot" for cancer-causing genetic variation.

In the new report, Vitale stated that chemotherapies that inhibit specific molecular targets - like tyrosine kinase receptors, kinases or oncogenes - may be able to more effectively dampen the growth of PTC caused by changes to the BRAF sequence.

As an example, the researcher indicated that in laboratory rodent models, c-Raf inhibitors have been found to slow the growth of cancer cells carrying BRAF mutations.

Vitale also pointed to other cellular mechanisms that can be pharmacologically influenced in order to reduce tumor cell survival. He noted that for any PTC site to grow beyond a couple of millimeters in diameters, the tissue area must create new blood vessels to feed the tumor, a process known as neoangiogenesis.

The oncologist stated that medications like bevacizumab, which targets signaling proteins that stimulate vascular growth, have been shown to significantly limit the proliferation of PTC. Vitale concluded that genomic medication and targeted protein inhibition lies on the frontier of PTC treatment.

At least 70 percent of all diagnoses of thyroid cancer are PTC, according to the Columbia University Department of Surgery.