In 1997 there were 860 new cases (incidence) and 71 deaths for thyroid cancer in Australia, making it the 16th most common incident cancer. Survival after treatment for thyroid cancer was 95% at 5 years in New South Wales for the period 1980 to 1995. This makes it the most curable cancer in Australia, after non-melanoma skin cancer (250,000 new cases and 324 deaths in 1995). Like cancers at most sites, there is more than one type of thyroid cancer. Papillary and follicular thyroid cancer made up more than 90% of all new cases, with anaplastic and medullary (C-cell) thyroid cancers accounting for most of the rest. In this review I will concentrate on papillary and follicular thyroid cancers. The thyroid gland is an endocrine gland, and makes two different hormones. Thyroxine is made by the cells which line the follicles of the thyroid gland. These cells are the source of papillary and follicular thyroid cancers. Thyroxine regulates the body's metabolic rate. If too much is produced, weight loss, palpitations, anxiety, sleeplessness, bulging eyes, tremulous hands and weakness result. If too little is produced then dry hair and skin, hair loss, lethargy, intolerance of cold and slow thinking results. Thyroxine hormone has iodine as part of its structure, and the thyroid gland takes up most of the iodine we absorb in our diet. Thyroxine production, and hence iodine uptake, by the thyroid gland is controlled by thyroid stimulating hormone (TSH), which is a hormone produced by the pituitary gland, a part of the brain. When TSH rises, more thyroxine is produced and this feeds back on the brain so TSH production falls. Most papillary and follicular thyroid cancers take up iodine under the influence of TSH, and some of them also produce thyroxine.

The second hormone is calcitonin, which is produced by C-cells or parafollicular cells which lie between the thyroid follicles. This hormone helps regulate the body's calcium. Cancers arising from these cells do occur but are rare. Anaplastic thyroid cancers are composed of cancer cells which are so abnormal it is not possible to know from which cells they arose. These cancers do not take up iodine and do not make hormones. These cancers generally have a "bad" prognosis (outcome).

The diagnosis and treatment of thyroid cancer has become standardised in recent years, and most patients are now managed by specialised units, or multi-disciplinary teams involving surgeons, pathologists, endocrinologists and nuclear medicine specialists. In contrast to the past, where thyroid scans and ultrasounds and other diagnostic tests were done, diagnosis of most patients today can be made by a simple fine needle aspiration biopsy (FNAB) of a thyroid lump, which is how almost all thyroid cancers present. Blood tests for thyroid hormones, and a general medical assessment are all that are usually necessary before a thyroid cancer operation is undertaken. In this operation part or virtually all of the thyroid gland is removed, depending upon the pathologist's report on the FNAB and the operative findings. Post-operatively a dose of radioactive iodine may be given, again depending upon the pathologist's report on the cancer removed and the operation performed. Patients may then have to take thyroxine tablets for a period of time, or for life, depending upon the treatment used for the cancer.

Many patients with papillary or follicular thyroid cancer will have total removal of the thyroid gland, followed by high doses of radioactive iodine (radio-iodine ablation), and then take thyroxine tablets for life. Using this approach the ten- year disease-free survival (cure rate) is in the range 90-100% for all patients under the age of 70 years, except for those with follicular cancer aged over 60 years. If the cancer is localised to the thyroid gland at the time of diagnosis the cure rate is almost 100%. Even if the cancer has spread to the local lymph nodes the cure rate is still at least 95%. For papillary and follicular thyroid cancer the cure rate for spread to other parts of the body is still about 80%, since most of these cancers take up radioactive iodine, which then destroys them.

Follow-up after the initial treatment includes adjusting thyroxine tablets so that the blood is "normal," and regular radioactive iodine total body scans to check that the cancer has not recurred. These are done at intervals decided by the specialist team. These diagnostic scans can detect thyroid cancer cells anywhere in the body. The scans are very taxing on individuals, who must stop their oral thyroxine for about six weeks before the scan, use a short-acting form of the hormone for about four weeks and then take no thyroxine for about two weeks before the scan. This is to ensure that the blood thyroxine is quite low as the time for the scan approaches. This will stimulate TSH production by the pituitary gland, so any thyroid cancer cells left in the body will take up the radiative iodine and be visible on the scan. If the thyroid cancer does recur more treatment with high-dose radioiodine may be given.

After the scan it can take many weeks of oral thyroxine before the blood level reaches normal. All in all, each of these scans takes about three months out of the patient's life. In these three months individuals will have a low metabolic rate and feel lethargic, drowsy, depressed, have memory problems and cannot drive a car. Because survival is so good after treatment for papillary and follicular thyroid cancer, treatment modifications which avoid total thyroidectomy and radioiodine ablation in very good risk patients, such as younger females with small localised cancers, are being explored. Because follow-up radioactive iodine whole body scans are so stressful for patients and their families, new approaches involving reducing the frequency of scans and directly stimulating thyroid cancer cells to take up iodine are also being explored.

In summary many improvements in the diagnosis, treatment and follow up of patients with papillary and follicular thyroid cancer have occurred over the last half century. Today these are the most curable of the potentially serious (non- melanoma) cancers which humans suffer from.

Professor Robert C. Burton is
Director Anti-Cancer Council of Victoria
His stepdaughter was treated for thyroid cancer in 1997

Further reading:

1. "Papillary and Follicular Thyroid Cancer", New England Journal of Medicine, Vol. 338, pages 297-306, 1998
2. "Prognostic Factors for Thyroid Carcinoma", Cancer, Vol. 79, pages 564-573, 1997

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