PubMed HealthSearch

PubMed · 8964151

[Lymph node excision in thyroid carcinoma].

Abstract

The prognostic value of lymph node metastases in thyroid cancer has been a matter of controversy for many years. However, during the past decade most multivariate analyses have shown a prognostic influence of lymph node metastases in papillary as well as medullary thyroid carcinoma constituting the basis for a standardized concept of lymphadenectomy oriented to the lymph node classification of the UICC (1993). Due to the frequency of lymph node metastases in the ipsilateral cervicocentral compartment (42-86%), in the ipsilateral cervicolateral compartment (32-68%), in the contralateral cervicolateral compartment (12-24%), and in the mediastinal compartment (3-20%), these compartments can be defined as the lymph node regions of the first, second, third and fourth order, respectively. Cervicocentral systematic lymphadenectomy should be part of the en bloc resection of the thyroid gland and the first lymph node region in any thyroid cancer. Cervicolateral as well as mediastinal lymphadenectomy should be performed according to the extent of lymph node involvement, i.e. systematically when multiple lymph node metastases are present, otherwise selectively. One exception is in medullary thyroid carcinoma, where a four-compartment lymphadenectomy is recommended in any patient with positive lymph nodes. Performing a gentle technique using magnifying glasses and bipolar coagulation forceps, systematic lymphadenectomy does not increase the rate of complications, can decrease the recurrence rate and improve survival.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Dralle, O Gimm. 1996. [Lymph node excision in thyroid carcinoma].. https://doi.org/10.1007/pl00002519

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

KEEP EXPLORING

Related citations

Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin release.

The G12 subfamily of heterotrimeric G proteins, comprised of the alpha-subunits Galpha12 and Galpha13, has been implicated as a signaling component in cellular processes ranging from cytoskeletal changes to cell growth and oncogenesis. In an attempt to elucidate specific roles of this subfamily in cell regulation, we sought to identify molecular targets of Galpha12. Here we show a specific interaction between the G12 subfamily and the cytoplasmic tails of several members of the cadherin family of cell-surface adhesion proteins. Galpha12 or Galpha13 binding causes dissociation of the transcriptional activator beta-catenin from cadherins. Furthermore, in cells lacking the adenomatous polyposis coli protein required for beta-catenin degradation, expression of mutationally activated Galpha12 or Galpha13 causes an increase in beta-catenin-mediated transcriptional activation. These findings provide a potential molecular mechanism for the previously reported cellular transforming ability of the G12 subfamily and reveal a link between heterotrimeric G proteins and cellular processes controlling growth and differentiation.

Adenocarcinoma

Human papillomavirus infection and esophageal cancer: a nationwide seroepidemiologic case-control study in Sweden.

BACKGROUND: Infection with human papillomavirus (HPV) type 16 has been implicated as a risk factor for esophageal squamous cell carcinoma in three seroepidemiologic studies. We conducted a larger, population-based study to verify this association and to investigate possible confounding factors. METHODS: We performed a nationwide case-control study in Sweden of HPV16 or HPV18 infection and risk of esophageal squamous cell carcinoma or esophageal/gastroesophageal adenocarcinoma. Tumors were strictly classified by their location and histologic type. Case subjects with incident cancers and population-based control subjects donated blood samples and were interviewed in person about potential confounding factors. An enzyme-linked immunosorbent assay was used to detect HPV seropositivity. Multivariate analyses were conducted to study relationships between HPV seropositivity, level of education, smoking (all tobacco) status, alcohol consumption, and cancer risk. RESULTS: We compared 121 case subjects with esophageal squamous cell carcinoma and 173 case subjects with adenocarcinoma of the esophagus or gastroesophageal junction with 302 population-based control subjects. The age- and sex-adjusted odds ratios (ORs) for squamous cell carcinoma were 1.0 (95% confidence interval [CI] = 0.5-2.0) for persons seropositive for HPV16 and 0.5 (95% CI = 0.2-1.1) for persons seropositive for HPV18 in comparison with seronegative individuals. The corresponding ORs for adenocarcinoma were 1.2 (95% CI = 0.7-2.2) and 0.2 (95% CI = 0.1-0.7), respectively. Adjustments for smoking status, alcohol consumption, and level of education did not alter the results. CONCLUSIONS: We found no evidence of a positive association between HPV16 or HPV18 infection and either form of esophageal cancer. Our results do not support conclusions from previous studies.

Adenocarcinoma

Sp1 phosphorylation by Erk 2 stimulates DNA binding.

EGF stimulates gene expression through a variety of signal transduction pathways that include the ras-Erk pathway. We have shown previously that EGF receptor activation stimulates gastrin gene expression through a GC-rich element called gERE. This element binds Sp1 family members and raises the possibility that the ras-Erk signal transduction cascade may target this novel EGF responsive element. Moreover, it is known that Erk 2 is capable of phosphorylating other mitogen-inducible transcription factors, e.g., Elk, Sap suggesting that Erk may also inducibly phosphorylate Sp1. To test this hypothesis directly using cotransfection experiments, we show that ras and Erk 2 activation indeed target the gERE element. The Mek 1 kinase inhibitor, PD98059, blocks 50% of EGF-inducible gastrin promoter activity. Pretreatment of the extracts with recombinant Erk2 stimulated Sp1 binding; whereas dephosphorylation reduced but did not eliminate Sp1 binding. Together, these studies demonstrate the novel finding that inducible binding of Sp1 is regulated by its state of phosphorylation. Further, gastrin promoter activation is mediated in part by the ras-Erk signaling cascade that targets Sp1.

Adenocarcinoma