Comment on Clinical and Prognostic Relevance of Ret-PTC Activation in Patients with Papillary Thyroid Carcinoma

Cetta, Francesco; Gori, M.; Raffaelli, N.; Baldi, C.; Montalto, G.

doi:10.1210/jcem.84.6.5809-11

Cited by 8 publications

(6 citation statements)

References 5 publications

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“…If further confirmed, these data suggest that constitutive activation of ret in papillary cancers determines a different carcinogenetic pathway according to the different fused gene, with ret/PTC1 possibly having a better prognosis and ret/PTC3 a worse prognosis. 30 Our knowledge of the molecular genetics of PTC has grown significantly over the past few years. Flow cytometric data have revealed a correlation between aneuploid DNA patterns and poor outcomes for PTC patients.…”

Section: Risk-group Classificationsmentioning

confidence: 99%

Prognostic Indicators in Differentiated Thyroid Carcinoma

2000

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Section: Risk-group Classificationsmentioning

confidence: 99%

Prognostic Indicators in Differentiated Thyroid Carcinoma

2000

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“…19,20 If further confirmed, it may suggest that constitutive activation of ret in FAP PTCs determines a different carcinogenetic pathway, according to the different fused gene, with ret/PTC1 possibly having the better and ret/PTC3 the worse prognosis. 19,20 Conclusion FAP-associated PTC seems to be a specific type of thyroid carcinoma with a peculiar histological aspect that probably reflects cooperation among carcinogenetic genes different from that occurring in sporadic tumors. Recent findings have contributed to highlighting some aspects, but several questions still remain unanswered.…”

Section: Natural History Of Fap-associated Thyroid Carcinomamentioning

confidence: 99%

“…The accumulated data strongly suggest that in the same individual, germline APC mutations cooperate with ras for the progression of colonic polyps to carcinoma, whereas they cooperate with ret/PTC, but not with ras, for the occurrence of thyroid carcinoma. 19 Therefore, the mutagenic stimulus for neoplastic proliferation varies from one tissue to another in the same patient, leading to the activation of oncogenes that are both tissue-specific and stimulusrelated. 2,5…”

Section: Cooperation Among Genesmentioning

confidence: 99%

“…5 Most of the 110 patients with FAP-associated tumors reported in the literature did not produce distant metastases, and the patients had a mean survival of Ͼ15 years without recurrence. 5,19 The paper by Soravia et al is the first to give long-term information on follow-up of FAP PTCs, which included detection of both germline mutation of the APC gene and ret/PTC activation. On the basis of these observations, it seems important to screen for focal activation of ret/PTC3 in patients with tumor recurrence.…”

Section: Natural History Of Fap-associated Thyroid Carcinomamentioning

confidence: 99%

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Genetics and Clinicopathological Findings in Thyroid Carcinomas Associated with Familial Adenomatous Polyposis

Cetta

Pelizzo

Curia

et al. 1999

The American Journal of Pathology

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“…Previous studies have documented that the genes responsible for Cowden's disease (PTEN) and Gardner's disease or familial polyposis (APC) are not responsible for FNMTC (43, 48). Cetta et al have recently documented that most patients who have developed thyroid cancer who have familial polyposis not only have the germ line APC gene but also a RET/PTC somatic mutation in the thyroid (47, 48). Other possible candidate genes for FNMTC because of their association with sporadic papillary thyroid cancer including TRK, RAS, C‐MET have not been found to be responsible for FNMTC (8, 45).…”

Section: Genetics and Environmentmentioning

confidence: 99%

Familial Non Medullary Thyroid Cancer*

Clark¹

2002

European Surg

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Summary: Background: There have been an increasing number of articles regarding patients with familial non medullary thyroid cancer (FNMTC) in the past few years. FNMTC has been defined as families with two or more first degree relatives having papillary or Hurthle cell thyroid cancer.  Methods: The history and new aspects of genetics, environment, pathology, management and clinical outcome of FNMTC are reviewed.  Results: The familial occurrence of NFMTC was first noted in 1995. In families with three or more members with NFMTC there appears to be an autosomal dominant type of inheritance with incomplete penetrance. 99.9 % of these patients have familial disease. FNMTC without any other associated syndrome accounts for about 5 % of patients with thyroid cancer of follicular cell origin (prevalence ranges between 3.5 and 6.2 %). When two members of a family have thyroid cancer about 50 % will have a susceptibility gene for thyroid cancer. FNMTC is rare in patients with follicular thyroid cancer. To date, genetic testing to document whether an individual of a family with familial papillary or Hurthle cell cancer without other syndromes has a specific germ line mutation is not available. In 1998 a linkage site locus (thyroid cancer oxyophilia – TCO gene) on chromosome 19p13.2 in a single French family with oxyophilia and trabecular thyroid cancers was identified. Individuals with the TCO linkage site have a relatively characteristic histologic pattern with trabecular and oncocytic neoplasms. Patients with papillary thyroid cancers and familial polyposis also have a distinct architecture and primarily occur in women. An experienced pathologist can make or at least suggest that the patient with this particular histological pattern should be screened for FNMTC. When total thyroidectomy with removal of regional lymphadenopathy can be done safely this is the preferred approach for patients with nodules in families with FNMTC as recommended for patients with thyroid nodules and a history of radiation exposure. For individuals in families with two or more other members with papillary or Hurthle cell thyroid cancer and a normal thyroid gland to palpation a baseline ultrasound examination is recommended, to document whether there are any thyroid nodules present. If occult nodules are present they can be observed with a repeat ultrasound examination in six months and then yearly to be sure they are not growing, or they can be biopsied by FNA under ultrasound guidance. Although occult thyroid cancers are usually of little clinical significance this may not be true for patients with FNMTC. Occult thyroid cancers in patients with FNMTC seem more aggressive and may be lethal.  Conclusions: Several groups continue to try to identify the genes responsible for the majority of families with FNMTC. Such studies are relatively expensive, but seem necessary to improve the care of patients with FNMTC.

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Comment on Clinical and Prognostic Relevance of Ret-PTC Activation in Patients with Papillary Thyroid Carcinoma

Cited by 8 publications

References 5 publications

Prognostic Indicators in Differentiated Thyroid Carcinoma

Prognostic Indicators in Differentiated Thyroid Carcinoma

Genetics and Clinicopathological Findings in Thyroid Carcinomas Associated with Familial Adenomatous Polyposis

Familial Non Medullary Thyroid Cancer*

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