[ON THE SO-CALLED "LATEROCERVICAL ABERRANT THYROID TUMORS". (LYMPH-NODE METASTASES OF CONFIRMED THYROID TUMORS)].
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Cystadenoma↗
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Results for “thyroid tumor”
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Incidence of malignant thyroid tumors in humans after exposure to diagnostic doses of iodine-131. II. Estimation of thyroid gland size, thyroid radiation dose, and predicted versus observed number of malignant thyroid tumors.
The size of the thyroid glands was analyzed for 10% of the patients in a selected group that had been exposed to diagnostic doses of 131I. The mean thyroid gland weight +/- SD was 50 +/- 33 g for patients 20 or more years of age and 10 +/- 5 g for patients less than 20 years of age. With the present follow-up, diagnostic doses of 131I appeared not to be associated with an increased risk for later development of malignant thyroid tumors. Possible reasons for the difference between the observed number of such tumors and the number expected (47-124) on the basis of risk estimates of the United Nations Scientific Committee on the Effects of Atomic Radiation are discussed.
Dose-Response Relationship, Radiation↗
Aerodigestive dysfunction secondary to thyroid tumors.
Although most thyroid tumors first manifest clinically by a neck mass, several patients with thyroid tumor have been treated whose initial complaint was a disturbance of the respiratory and digestive tracts. Because this association is not well recognized, the diagnosis of a thyroid tumor can be delayed, or even missed until the tumor grows much larger causing other symptoms. A series of 269 patients with thyroid tumors seen at UCLA from 1979-1980 was reviewed. Approximately 16% of these patients sought treatment because of aerodigestive dysfunction such as dyspnea, dysphagia, hoarseness, throat discomfort and hemoptysis. Such symptoms often indicate malignancy of substernal extension of tumor. The management of these tumors is discussed.
Deglutition Disorders↗
[Computed tomographic diagnosis of thyroid tumors--a new attempt to classify the pattern of thyroid tumors].
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Humans↗
The current management of thyroid tumors in childhood.
Thyroid cancer is a rare but intriguing malignancy when it occurs in childhood and adolescence. Although it often presents at a more advanced stage than similar adult thyroid tumors, the biologic behavior is more benign, accounting for improved survival. Therefore, pediatricians and surgeons have debated the wisdom of aggressive versus conservative surgical approaches. Although the final answers have not been achieved it has become increasingly clear that radical surgical approaches may be unnecessary. Further investigation of the tumor cell biology, genetics, and molecular biology of thyroid tumors may allow prospective classification of children so that the best operative and adjuvant management can be selected for each individual.
Child↗
Dipeptidyl peptidase IV (DPP IV/CD26) staining predicts distant metastasis of 'benign' thyroid tumor.
Because follicular thyroid carcinoma is extremely difficult to diagnose, several cases were encountered which have been rediagnosed as carcinoma due to distant metastasis. In the search for a method of correctly diagnosing 'benign' thyroid tumor, dipeptidyl peptidase (DPP) IV immunostaining was applied to 10 cases whose diagnoses had been corrected to follicular thyroid carcinoma because of distant metastases. The positive rate of immunostaining using paraffin sections in the rediagnosed follicular thyroid carcinoma group (7/10) was much higher than that of the control group (1/29), which consisted of 15 cases of follicular thyroid adenoma and 14 cases of nodular hyperplasia. These results suggested that pre- or postoperative DPP IV staining is useful for predicting distant metastasis of 'benign' thyroid tumor.
Adenocarcinoma, Follicular↗
[Possibilities and limits of radiologic diagnosis of thyroid tumors. (results of radio iodine diagnosis in 603 tumors of the thyroid)].
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Humans↗
Predictors of thyroid tumor aggressiveness.
Thyroid cancers are classified as papillary, follicular (including Hürthle cell), medullary, and anaplastic. Papillary cancers account for about 82% of all thyroid cancers, follicular about 8%, medullary about 6%, Hürthle cell 3%, and anaplastic 1%. The prognosis of patients with papillary thyroid cancer is usually favorable, whereas most patients with anaplastic cancer die within 6 months. The behavior of papillary thyroid cancer can be predicted by patient age, sex, tumor size, local invasion, angioinvasion, lymph node metastases, distant metastases, as well as tumor differentiation and ability to take up radioactive iodine. Thus, older male patients with larger or invasive tumors, with angioinvasion, lymph node or distant metastases, and with tumors that do not take up radioactive iodine or cannot be completely surgically resected have a worse prognosis. Anaploid tumors, tumors with a low adenylate cyclase response to thyroid-stimulating hormone tumors, tumors that are ras-and gsp-positive, and tumors that are p21-positive and p53-positive also appear to behave in a more aggressive manner. In contrast, lymphocytic thyroiditis associated with papillary thyroid cancer predicts fewer recurrences and an improved survival. The treatment of patients with papillary thyroid cancer is controversial primarily because most patients do well with relatively minimal therapy, and there are no prospective studies concerning the merits of various treatments. Much of the controversy relates to the safety of thyroidectomy versus other procedures and, to a lesser extent, when to do a central or modified radical neck dissection. The rate of recurrence is lower, and the death rate may also be lower when patients are treated initially by total thyroidectomy. The rationale for total thyroidectomy is that it enables one to use radioactive iodine to detect and treat local and distant metastases, and it makes serum thyroglobulin determination more sensitive for detecting persistent disease. Total thyroidectomy should be associated with a permanent complication rate of less than 2%. Thyroid-stimulating hormone suppression therapy is recommended by most experts for patients with differentiated thyroid cancer and supported by most clinical and laboratory studies. Central and lateral node selection is recommended for patients with palpable lymphadenopathy.
Adult↗
Somatic mutations of the PTEN tumor suppressor gene in sporadic follicular thyroid tumors.
The PTEN (MMAC1/TEP1) tumor suppressor gene was recently isolated and mapped to human chromosome band 10q23. Homozygous deletions and mutations of PTEN were observed in cell lines and sporadic cancers of the breast, kidney, and central nervous system. Germline mutations in PTEN were recently found in Cowden disease, an autosomal dominant inherited syndrome, previously mapped to chromosome bands 10q22-23. This disease is associated with a wide variety of malignancies and hamartomas of ectodermal, mesodermal, and endodermal origin. The most common neoplasms in Cowden disease patients arise in the breast, skin, and thyroid (follicular subtype). To determine the involvement of PTEN in sporadic follicular thyroid tumors, we first analyzed sporadic follicular adenomas and carcinomas for deletions of the PTEN gene. Loss of heterozygosity was found in 7/26 (27%) follicular carcinomas and 2/27 (7%) follicular adenomas, one of which was a small hemizygous deletion (approximately 3 cm). Sequence analysis of the entire PTEN coding region revealed two mutations in carcinomas with 10q loss. Our findings suggest that the PTEN tumor suppressor gene is occasionally inactivated in sporadic follicular thyroid tumors.
Adenocarcinoma, Follicular↗
Galectin-3, fibronectin-1, CITED-1, HBME1 and cytokeratin-19 immunohistochemistry is useful for the differential diagnosis of thyroid tumors.
The diagnosis of thyroid tumors is critical for clinical management; however, tumors with follicular architecture often present problems. We evaluated the diagnostic use of the protein expression of four genes that were found to be upregulated in papillary thyroid carcinoma compared to normal thyroid (LGALS3, FN1, CITED1 and KRT19), and of the mesothelial cell surface protein recognized by monoclonal antibody HBME1 in thyroid tumors. Tissues from 85 carcinomas (67 papillary, six follicular, eight Hürthle cell and four anaplastic) and 21 adenomas were evaluated by immunohistochemistry for the expression of these gene protein products, for example, galectin-3 (GAL3), fibronectin-1 (FN1), CITED1, cytokeratin-19 (CK19) and HBME1. Non-neoplastic thyroids (29 adenomatous and 14 thyrotoxic hyperplasia, and 59 normal) were also studied. The expression of all five proteins was significantly associated with malignancy, and highly specific (> or = 90%) for carcinoma compared to adenoma. GAL3, FN1 and/or HBME1 expression was seen in 100% of carcinomas (85/85) and in 24% of adenomas (5/21). Coexpression of multiple proteins was seen in 95% of carcinomas and only 5% of adenomas (P<0.0001). Coexpression of FN1 and GAL3 (FN1+ GAL3+, 70/85) or FN1 and HBME1 (FN1+ HBME1+, 53/85) was restricted to carcinomas, while their concurrent absence (FN1- GAL3- or FN1- HBME1-, 18/21 adenoma) was highly specific (96%) for benign lesions. Among non-neoplastic thyroids, adenomatous hyperplasia frequently expressed GAL3 (n=16), CK19 (n=9) and CITED1 (n=7), but the expression was predominantly focal in contrast to the diffuse expression in carcinomas. An immunohistochemical panel consisting of GAL3, FN1 and HBME1 may be useful in the diagnosis of follicular cell-derived thyroid tumors.
Adenoma↗
Absence of G(s)alpha gene mutations in childhood thyroid tumors after Chernobyl in contrast to sporadic adult thyroid neoplasia.
Heterotrimeric G proteins participate in the signal transduction cascade. Adult thyroid tumors have been shown to harbor specific point mutations in codons 201 and 227 of the G(s)alpha subunit of the adenylate cyclase stimulator. This protein affects the GDP/GTP turnover and finally results in an enhanced activation of G(s) and thus adenylate cyclase. We attempted to find out if G(s)alpha gene mutations were present in thyroid tumors of children from Belarus after the Chernobyl nuclear accident. Paraffin sections of 20 thyroid tumors were used for PCR amplification by oligonucleotide intron primers flanking exons 8 and 9, encompassing codon 201 and 227, respectively. By direct sequencing of the 274-bp amplification product, we did not detect any mutations of the G(s)alpha gene in codon 201 or 227. In contrast to thyroid neoplasia of adults, G(s)alpha gene mutations do not play a role in the development of childhood thyroid tumors after the Chernobyl reactor accident.
Carcinoma, Papillary↗
Apoptosis and proliferative activity in thyroid tumors.
To clarify the growth mechanisms of thyroid tumors, we examined apoptotic cells in 61 thyroid tumors, consisting of 14 adenomas, 35 papillary carcinomas, 4 follicular carcinomas, and 8 undifferentiated carcinomas, using terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate digoxigenin-nick end labeling (TUNEL). The proliferative activity was also evaluated immunohistochemically using the monoclonal antibody to Ki-67 antigen (MIB-1) in the same tumors. The apoptotic index (AI) was expressed as a percentage of the TUNEL-positive cells in the tumor cells, and a proliferation index (PI), being the percentage of Ki-67 positive cells, was calculated for each tumor. The overall level of AI was very low in all histotypes of the thyroid tumors analyzed, the mean AI being 0.5 +/- 0.4 in adenoma, 0.4 +/- 0.3 in differentiated carcinoma, and 1.8 +/- 1.5 in undifferentiated carcinoma. The PI in the thyroid tumor subtypes was significantly lower in adenoma and differentiated carcinoma, at 0.5 +/- 0.7 and 1.1 +/- 0.7, respectively, than that in undifferentiated carcinoma at 14.5 +/- 3.7 (P < 0.05). There was no correlation between clinicopathological factors and AI or PI in differentiated thyroid carcinoma. Our findings suggest that apoptosis occurs infrequently in thyroid tumors, and that proliferative activity markedly differs according to the thyroid tumor subtypes. Moreover, the ratio between proliferating cells and apoptotic cells may reflect thyroid tumor progression.
Adenocarcinoma, Follicular↗
The efficiency of performing ultrasound-guided fine-needle aspiration biopsy following mass screening for thyroid tumors to avoid unnecessary surgery.
Thyroid masses are a common clinical finding, and their management remains controversial. The purpose of this study was to evaluate the clinical effect of performing routine ultrasound (US) examinations and US-guided fine-needle aspiration biopsy (US-FNAB) in the management of diffuse or nodular goiter diagnosed by mass screening. Mass screening carried out from 1993 to 1996 revealed 444 women with goiter, 322 of whom had diffuse goiter and 122 had nodular goiter. All of these patients underwent US examination, the results of which determined that 169 should undergo US-FNAB to confirm an accurate diagnosis of their thyroid tumors. Histological examinations after surgical resection revealed that 12 of the 322 patients with diffuse goiter (3.7%) and 23 of the 122 with nodular goiter (18.9%) had malignant tumors. Among the 61 thyroid tumors surgically verified, US-FNAB yielded a sensitivity rate of 93%, a specificity rate of 81%, and an accuracy rate of 90%. Insufficient aspiration was obtained from 5%. Performing US-FNAB-resulted in an elevation in the percentage of malignant tumors yielded at surgery of up to 72%. Thus, ultrasonography followed by US-guided-FNAB could be a useful routine method of evaluating thyroid tumors detected by mass screening. Moreover, a greater number of unnecessary thyroid operations can be avoided by performing US-FNAB rather than FNAB alone.
Biopsy, Needle↗
Somatic deletions and mutations in the Cowden disease gene, PTEN, in sporadic thyroid tumors.
The majority of familial medullary thyroid neoplasms are associated with germ-line mutations of the RET proto-oncogene, yet very little is known about the mechanisms involved in the pathogenesis of familial and sporadic nonmedullary thyroid tumors. A subset of thyroid tumors have loss of heterozygosity of chromosome 10q22-23, a region harboring the gene responsible for Cowden disease, an autosomal dominant hamartoma syndrome associated with thyroid and breast tumors. PTEN/MMAC1/TEP1 codes for a dual-specificity phosphatase and is likely a tumor suppressor gene. We sought to determine the PTEN status in a series of epithelial thyroid neoplasms. We studied 95 sporadic thyroid tumors, of which 39 were papillary thyroid carcinomas (PTCs), 12 were follicular carcinomas, 9 were anaplastic carcinomas, 5 were Hürthle cell carcinomas, 21 were nonfunctioning follicular adenomas, and 9 were Hürthle cell adenomas. Direct sequencing of PCR-amplified products was performed for all nine exons of PTEN. Two polymorphic markers, one located in intron 8 and another, a dinucleotide repeat marker, AFMa086wg9, located within intron 2, were analyzed in paired blood-tumor DNA samples to assess hemizygous deletions of PTEN. We found a somatic frameshift mutation in one PTC, which was expected to generate a premature stop codon 2 amino acids downstream. Twenty-six % of informative benign tumors (four follicular adenomas and three Hürthle cell adenomas) and only 3 of 49 (6.1%) informative malignant tumors (one PTC, one follicular carcinoma, and one anaplastic carcinoma) showed evidence of hemizygous deletion of PTEN (P = 0.046). We conclude that a subset of thyroid tumors have somatic deletions of the PTEN gene, predominantly the benign forms, and that small intragenic mutations of PTEN are infrequent in thyroid tumors. We speculate that other mechanisms of PTEN inactivation, rather than small intragenic mutations, might occur in the hemizygously deleted samples and act as the "Knudson second hit." Alternatively, other tumor suppressor genes mapping to chromosome 10q22-23 could be the actual targets for such deletions and thus represent the various hits in the pathway of multistep carcinogenesis.
Adenocarcinoma, Follicular↗
Fractional allelic loss of tumor suppressor genes identifies malignancy and predicts clinical outcome in follicular thyroid tumors.
Thyroid follicular tumors can be challenging diagnostically and clinically, because the cytologic and histologic features can be subtle and prognosis is also difficult to predict. In this study, we analyzed thyroid follicular tumors with known long-term follow-up for a molecular panel of tumor suppressor genes to determine whether this molecular approach has prognostic significance. Microdissection and DNA extraction were performed from tumor and normal tissue. Polymerase chain reaction (PCR) was performed for 13 short tandem repeats at or near tumor suppressor genes. PCR product was detected using semiquantitative capillary gel electrophoresis and fractional allelic loss (FAL) was calculated. We included eight adenomas, three minimally invasive carcinomas, four angioinvasive carcinomas, and three widely invasive carcinomas with a mean follow-up of 77 months. Three patients died of disease and an additional two are alive with disease recurrence/metastasis. The mean FAL for benign tumors (14%) was significantly different from that of malignant tumors (56%, p < 0.001). Patients with a follicular tumor who had no evidence of disease recurrence had a mean FAL of 22% and those with disease recurrence or death from disease had a mean of 78% (p < 0.002). Based on these results, a tumor suppressor gene panel for allelic imbalance in follicular-derived tumors (FTT) may correlate with both malignancy and outcome in patients with follicular-derived carcinomas of the thyroid.
Adenoma↗
Production of thyroxine (T4) and triiodothyronine (T3) in nontoxic thyroid tumors. An immunohistochemical study.
Thyroid tissue specimens from 27 patients with thyroid tumors were examined for thyroxine (T4) and triiodothyronine (T3) by the peroxidase-labeled antibody method. The result revealed localization of T4 in 12 of the 14 follicular adenomas, in all the 8 papillary carcinomas and in 1 of the 3 follicular carcinomas studied, and of T3 in 13 of the 14 follicular adenomas, in all the 8 papillary carcinomas and in all the 3 follicular carcinomas. In the tumor tissue, the thyroid hormones were demonstrated in the colloid substance, on the luminal surface of tumor cells and in their cytoplasm. Compared with nontumorous thyroid tissue, the tumor tissue showed localization of the hormones predominantly in the cytoplasm and to a lesser extent in the colloid substance, with conspicuous variations in tissue distribution of positive areas and intensity of staining. This tendency was more marked in thyroid carcinomas. The demonstration of T4 and T3 in routine histological paraffin sections of formalin-fixed thyroid tissues in this investigation indicates potential usefulness of thyroid hormone detection by the peroxidase-labeled antibody technique. It is an effective diagnostic tool for evaluating the functional activity of the thyroid tumors as well as for determining whether a malignant growth under examination originates from the thyroid.
Adenocarcinoma↗
[A case of primary squamous cell carcinoma of the lung with a metastatic thyroid tumor improved following chemotherapy].
Metastatic thyroid tumor is rarely diagnosed clinically. We report here a case of a 59-year-old male of a primary squamous cell carcinoma of the lung with metastatic thyroid tumor diagnosed by an ultrasonography-guided aspiration cytology. A squamous cell carcinoma of the lung (c-T4N3M1 stage IV) was diagnosed in March 2001, and so chemotherapy using carboplatin and paclitaxel was tried initially. A partial response was obtained. Then, he was re-admitted to our hospital because his thyroid gland was swollen. Ultrasonography-guided aspiration cytology of the thyroid tumor was performed and revealed a metastatic squamous cell carcinoma from the lung cancer. The patient was given chemotherapy using gemcitabine and docetaxel as second line chemotherapy. This reduced the thyroid tumor size and improved the symptoms.
Antimetabolites, Antineoplastic↗
Loss of heterozygosity of the VHL gene identifies malignancy and predicts death in follicular thyroid tumors.
BACKGROUND: Follicular thyroid tumors (FTT) usually require resection to distinguish adenoma from carcinoma. Better markers that predict histologic subtype and prognosis are needed for FTT. METHODS: Seventeen benign and malignant FTT with follow-up were selected. Pathologic diagnosis was confirmed, tumor and normal tissue were microdissected, and DNA was extracted. Polymerase chain reaction (PCR) products for a microsatellite marker at the von Hippel Lindau gene (VHL) gene locus (3p26) were analyzed with semiquantitative capillary gel electrophoresis to detect loss of heterozygosity (LOH). Data were assessed for statistical significance with chi(2). RESULTS: Mean follow-up was 77 months (range 29 to 120 months). Four cases were uninformative (homozygous microsatellite). Among 13 evaluable patients (6 adenomas, 7 follicular cancers) LOH of VHL was present only in carcinomas (P=.013). LOH was present in 4/4 patients with recurrence and 0/3 patients without recurrence (P=.017). Death from disease has occurred in 3 patients. LOH of VHL was strongly associated with death from disease (P=.034). CONCLUSIONS: FTT can be analyzed for LOH at the VHL gene locus. In this initial study, LOH of VHL was highly specific for malignancy and predicted death from disease. The analysis of VHL may provide for preoperative detection in cytologic samples with potential impact on clinical management of FTT.
Adenocarcinoma, Follicular↗