Sentinel lymph node dissection for thyroid malignancy.

P I Haigh; A E Giuliano

doi:10.1007/978-3-642-57151-0_17

Home/Archive/PubMed

PubMed · 10857173

Sentinel lymph node dissection for thyroid malignancy.

P I Haigh·A E Giuliano

View original source ↗Export metadata ↓

Abstract

Sentinel lymph node dissection (SLND) for melanoma and breast cancer has been validated as an accurate technique to assess the status of the lymph nodes in the regional drainage basin. The sentinel node concept has also been investigated in other solid tumors, and more recently, in thyroid carcinoma. SLND using a vital blue dye during thyroidectomy for suspected thyroid malignancy successfully identifies sentinel nodes, with minimal morbidity. Excised sentinel nodes can be examined for micrometastases, and if negative, then the rest of the cervical nodes are likely to be negative. The false negative rate of SLND for thyroid malignancy is unknown, however, because modified neck dissections have not accompanied all cases. The impact that lymph node metastasis in thyroid carcinoma has on prognosis is debatable, unlike breast cancer and melanoma, which therefore makes the utility of thyroid SLND less clear. The technique, results, and morbidity of SLND during thyroidectomy is presented, and its possible utility in well-differentiated and medullary thyroid carcinoma is discussed.

Explore related subjects

Adenocarcinoma, Follicular Carcinoma, Papillary Coloring Agents Feasibility Studies Humans Intraoperative Care Lymph Node Excision Lymphatic Metastasis Neck Dissection Sentinel Lymph Node Biopsy Thyroid Neoplasms Treatment Outcome Evaluation Study Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

P I Haigh, A E Giuliano. 2000. Sentinel lymph node dissection for thyroid malignancy.. https://doi.org/10.1007/978-3-642-57151-0_17

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Is there loss or qualitative changes in the expression of thyroid peroxidase protein in thyroid epithelial cancer?

There is disagreement concerning the expression of thyroid peroxidase (TPO) in thyroid cancer, some studies finding qualitative as well as quantitative differences compared to normal tissue. To investigate TPO protein expression and its antigenic properties, TPO was captured from a solubilizate of thyroid microsomes by a panel of murine anti-TPO monoclonal antibodies and detected with a panel of anti-human TPO IgGkappa Fab. TPO protein expression in 30 samples of malignant thyroid tissue was compared with TPO from adjacent normal tissues. Virtual absence of TPO expression was observed in 8 cases. In the remaining 22 malignant thyroid tumours the TPO protein level varied considerably from normal to nearly absent when compared to normal thyroid tissue or tissues from patients with Graves' disease (range less than 0.5 to more than 12.5 microg mg(-1) of protein). When expressed TPO displayed similar epitopes, to that of TPO from Graves' disease tissue. The results obtained by the TPO capturing method were confirmed by SDS-PAGE and Western blot analysis with both microsomes and their solubilizates. The present results show that in about two-thirds of differentiated thyroid carcinomas, TPO protein is expressed, albeit to a more variable extent than normal; when present, TPO in malignant tissues is immunologically normal.

Adenocarcinoma, Follicular↗

PubMed2001

Overexpression and overactivation of Akt in thyroid carcinoma.

Enhanced activation of Akt occurs in Cowden's disease, an inherited syndrome of follicular thyroid, breast, colon, and skin tumors, via inactivation of its regulatory protein, PTEN. Whereas PTEN inactivation is uncommon in sporadic thyroid cancer, activation of growth factor pathways that signal through Akt is frequently identified. We hypothesized that Akt overactivation could be a common finding in sporadic thyroid cancer and might be important in thyroid cancer biology. We examined thyroid cancer cells lines and benign and malignant thyroid tissue for total Akt activation and isoform-specific Akt expression. In thyroid cancer cells, Akt 1, 2, and 3 proteins were expressed, total Akt was activated by insulin phosphatidylinositol 3'-kinase, and inhibition of phosphatidylinositol 3'-kinase reduced cell viability. In human thyroid tissue, increased levels of phosphorylated total Akt were identified in follicular but not papillary cancers compared with normal tissue. Levels of Akt 1 and 2 proteins and Akt 2 RNA were elevated only in the follicular cancers. In paired samples, Akt 1, 2, 3, and phospho-Akt levels were higher in five of six cancers, including three of three follicular cancers. These data suggest that Akt activation may play a role in the pathogenesis or progression of sporadic thyroid cancer.

Adenocarcinoma, Follicular↗

PubMed2001

Bax expression in benign and malignant thyroid tumours: dysregulation of wild-type P53 is associated with a high Bax and P21 expression in thyroid carcinoma.

The purpose of our study was to determine the expression of the pro-apoptotic BAX protein in relation to the mutational status of BAX and p53 (as transcriptional activator of the BAX gene) in benign and malignant thyroid tissue. In 47 patients with thyroid tumours (14 follicular and 3 papillary carcinomas, 14 adenomas and 16 goitres), the DNA was screened for mutations of BAX (exon 1-6) and p53 (exon 5-8) by single-strand conformation polymorphism polymerase chain reaction (SSCP-PCR). Furthermore, the protein expression of BAX, p53 and p21 (which is also increased transcriptionally by p53) was investigated by immunohistochemistry. Surprisingly, we observed elevated BAX levels in patients with thyroid carcinomas compared with patients with adenomas (unpaired t-test: p<0.05) or with goitres (p<0.02). This is in clear contrast to other carcinomas where BAX is frequently inactivated which correlates to a poor prognosis (Sturm et al. J. Clin. Oncol. 1999;17:1364-74.). There were no significant differences of the BAX levels between goitres or the adenomas. In the SSCP-PCR analysis, no BAX mutations were detectable. P53 mutation analysis by SSCP-PCR did not reveal any functional p53 mutations in the patients with carcinomas, adenomas or goitres. Nevertheless, patients with carcinomas showed an overexpression (preferentially cytoplasmic) of p53 protein compared with patients with benign tumours (p<0.05). The absence of p53 mutations suggests that the overexpressed p53 is wild type. This is in line with the expression profile of BAX and p21, which showed a higher protein expression in these p53 positive tumours (p<0.05 in the carcinomas compared with the non-malignant lesions). Consequently, the overexpressed p53 might be a correlate for dysregulation without loss of function. This, in turn, might be a reason for the good outcome of some patients with thyroid cancer.

Adenocarcinoma, Follicular↗