Lymphocytic infiltration in juvenile thyroid carcinoma

Kamma, Hiroshi; Fujii, Keiji; Ogata, Takesaburo

doi:10.1002/1097-0142(19881101)62:9<1988::aid-cncr2820620919>3.0.co;2-0

Cited by 56 publications

(28 citation statements)

References 11 publications

(1 reference statement)

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“…The relationship between PTC or FTC and HT remains unclear because it is controversial whether HT is induced secondarily to the neoplasm or whether HT predisposes the patient to develop thyroid cancer [15,16]. Despite the difference in etiology of these disorders, the prevalence and severity of HT combined with adenomatous goiter, follicular adenoma, or PTC was defined by examination of surgically resected materials from three ethnic groups, and the findings illustrated that the incidence of autoimmune thyroiditis was significantly higher in patients with PTC than in patients with adenomatous goiters or follicular adenoma [17].…”

Section: Discussionmentioning

confidence: 99%

Well-Differentiated Thyroid Carcinoma with Concomitant Hashimoto’s Thyroiditis Present with Less Aggressive Clinical Stage and Low Recurrence

Huang¹,

Hseuh²,

Chao³

et al. 2011

Endocr Pathol

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Papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC) are the most common differentiated thyroid cancers. Previous studies report that Hashimoto's thyroiditis (HT) concomitant with PTC is unusual and improves prognosis compared to classical PTC. Few previous studies address FTC concomitant with HT. In this study, we retrospectively analyzed data from one institution and compared clinical presentations and results of treatment of PTC and FTC with and without HT. In addition, studies comparing presentation and long term follow-up prognosis in classical PTC and FTC were conducted. A total of 1,788 PTC patients and 209 FTC patients underwent thyroidectomy with or without lymph node dissection and follow-up at Chang Gung Medical Center in Linkou, Taiwan. All thyroid carcinomas were pathologically classified according to World Health Organization criteria. Histological patterns of PTC were categorized as classical PTC, or PTC with HT. Follicular thyroid carcinoma patients were categorized as FTC or FTC with HT. The dataset contained a total of 1,703 PTC cases categorized as classical PTC, 85 cases of PTC with HT, 201 cases of FTC and eight cases of FTC with HT. Analysis of Classification of Malignant Tumors (TNM) stage revealed a higher percentage of classical PTC in stage IV than HT group (12.03% vs. 4.70%). Mean tumor size of classical PTC was larger than HT group. Although 42.3% of FTC cases presented with distant metastases, no cases of FTC with HT presented with distant metastasis. Cancer-specific mortality was higher in classical PTC group than in PTC with HT. There was 53.2% of FTC without HT assigned recurrent status, and six of them died of thyroid cancer. No cancer mortality or recurrence in HT with FTC. PTC and FTC with HT presented with better clinical stage and better prognosis after same therapeutic modality. In conclusions, both PTC and FTC with HT have less aggressive clinical presentation and better prognosis.

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Section: Discussionmentioning

confidence: 99%

Well-Differentiated Thyroid Carcinoma with Concomitant Hashimoto’s Thyroiditis Present with Less Aggressive Clinical Stage and Low Recurrence

Huang¹,

Hseuh²,

Chao³

et al. 2011

Endocr Pathol

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“…Studies over the past decade suggest that the immune system plays an important role in preventing thyroid tumor metastasis and recurrence (3)(4)(5)(6). In particular, lymphocytic infiltration in PTCs is associated with lower-stage disease at diagnosis and reduced recurrence risk.…”

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confidence: 99%

Clinicopathological Significance of Major Histocompatibility Complex Class I-Related Chain A and B Expression in Thyroid Cancer

Xu¹,

Rao²,

Gaffud³

et al. 2006

The Journal of Clinical Endocrinology & Metabolism

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“…The importance of MHC expression by tumor cells in mounting an effective antitumor immune response has been shown in animal models for T-cell-mediated immunotherapy 14 -16 and is corroborated by the notion that tumors expressing high levels of both MHC class I and class II molecules display abundant lymphocytic infiltration. [17][18][19] Notably, patients with high tumorlytic lymphocyte infiltrates generally have a better prognosis. [17][18][19] Several tissues have been shown to exhibit a significantly reduced membrane expression of MHC class I molecules.…”

mentioning

confidence: 99%

“…[17][18][19] Notably, patients with high tumorlytic lymphocyte infiltrates generally have a better prognosis. [17][18][19] Several tissues have been shown to exhibit a significantly reduced membrane expression of MHC class I molecules. In particular, certain reproductive and developmental tissues lack expression of MHC class I molecules, including sperm, 20 oocytes, 21 preimplantation embryos 22 and villous trophoblast cells.…”

mentioning

confidence: 99%

Lack of ifn‐γ‐mediated induction of the class II transactivator (CIITA) through promoter methylation is predominantly found in developmental tumor cell lines

Stoep

Biesta

Quinten

et al. 2001

Intl Journal of Cancer

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The class II transactivator (CIITA) plays a pivotal role in the expression of major histocompatibility complex (MHC) class II and accessory genes (invariant chain [Ii] and HLA-DM), whereas it has an ancillary function in the expression of MHC class I and ␤ 2 -microglobulin (␤ 2 m) genes. 1-9 The MHC is a large multigene family that encodes cell surface glycoproteins involved in binding and presentation of antigenic peptides to T lymphocytes. The products of the ␤ 2 m, Ii and HLA-DM genes are also essential proteins in MHC class I-and class II-mediated antigen presentation function, respectively. For this reason CIITA-mediated MHC expression is central in the generation of an antigen-specific immune response by presenting antigenic peptides to the T-cell receptor (TCR) on T lymphocytes. 10,11 MHC class I molecules are expressed on almost all nucleated cells. In contrast, the constitutive expression of MHC class II molecules is restricted to specific immune cell types that include antigen-presenting cells such as dendritic cells, B lymphocytes, macrophages and thymic epithelial cells. Nonimmune cells lack constitutive expression of MHC class II; however, in most of these cells MHC class II expression can be induced by interferon-␥ (IFN-␥). 12,13 Notably, expression of MHC class I molecules can also be enhanced by IFN-␥. Together, the upregulated expression of MHC class I and class II molecules results in an increase in the immunogenic potential of cells. The importance of MHC expression by tumor cells in mounting an effective antitumor immune response has been shown in animal models for T-cell-mediated immunotherapy 14 -16 and is corroborated by the notion that tumors expressing high levels of both MHC class I and class II molecules display abundant lymphocytic infiltration. [17][18][19] Notably, patients with high tumorlytic lymphocyte infiltrates generally have a better prognosis. [17][18][19] Several tissues have been shown to exhibit a significantly reduced membrane expression of MHC class I molecules. In particular, certain reproductive and developmental tissues lack expression of MHC class I molecules, including sperm, 20 oocytes, 21 preimplantation embryos 22 and villous trophoblast cells. 23 The absence of MHC molecules from fetal and embryonic tissues creates an immune privilege for these cells during gestation and may be of functional significance during development. Also, several malignant cell types have been shown to lack the expression of MHC molecules. This reduced expression of MHC molecules will contribute to a decreased recognition by T cells, allowing an escape from immunosurveillance. 24 -26 Interestingly, most of the MHC-deficient tumor cells have originated from fetal or embryonic tissues. Downregulation of MHC gene expression in these embryonic or developmental tumors may therefore not result from the neoplastic transformation event but may instead reflect the characteristic silent state of MHC class I and class II genes during early development.To understand the mechanisms of downregulat...

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Lymphocytic infiltration in juvenile thyroid carcinoma

Cited by 56 publications

References 11 publications

Well-Differentiated Thyroid Carcinoma with Concomitant Hashimoto’s Thyroiditis Present with Less Aggressive Clinical Stage and Low Recurrence

Well-Differentiated Thyroid Carcinoma with Concomitant Hashimoto’s Thyroiditis Present with Less Aggressive Clinical Stage and Low Recurrence

Clinicopathological Significance of Major Histocompatibility Complex Class I-Related Chain A and B Expression in Thyroid Cancer

Lack of ifn‐γ‐mediated induction of the class II transactivator (CIITA) through promoter methylation is predominantly found in developmental tumor cell lines

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