Cytoarchitectural and kinetic features in the histological evaluation of follicular thyroid neoplasms

Şanlı, Arif; Patel, Jinesh; Blanes, Alfredo; Diaz-Cano, SJ

doi:10.1111/j.1365-2559.2007.02680.x

Cited by 10 publications

(5 citation statements)

References 29 publications

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“…1,6,17,27,28,44,45 This progression would be related to the accumulation of genetic abnormalities and selective segregation of tumor cells with invasive capabilities, which are frequently topographically distributed. 20,23,46 A progressive and significant reduction in marker expression from junctional to deep dermal compartments was a general finding mirrored by the microsatellite profile. These findings proved a significant topographic heterogeneity present in all types of melanocytic lesions, even in early lowgrade superficial ones, and features of intraepithelial malignancy for high-grade atypical melanocytic nevi.…”

Section: Discussionmentioning

confidence: 91%

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

et al. 2011

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Atypical (dysplastic) melanocytic nevi are clinically heterogeneous malignant melanoma precursors, for which no topographic analysis of cell kinetic, cell cycle regulators and microsatellite profile is available. We selected low-grade atypical melanocytic nevi (92), high-grade atypical melanocytic nevi (41), melanocytic nevi (18 junctional, 25 compound) and malignant melanomas (16 radial growth phase and 27 vertical growth phase). TP53, CDKN2A, CDKN1A, and CDKN1B microsatellite patterns were topographically studied after microdissection; Ki-67, TP53, CDKN2A, CDKN1A, and CDKN1B expressions and DNA fragmentation by in situ end labeling for apoptosis were topographically scored. Results were statistically analyzed. A decreasing junctional-dermal marker expression gradient was observed, directly correlating with atypical melanocytic nevus grading. High-grade atypical melanocytic nevi revealed coexistent TP53-CDKN2A-CDKN1B microsatellite abnormalities, and significantly higher junctional Ki67-TP53 expression (inversely correlated with CDKN1A-CDKN1B expression and in situ end labeling). Malignant melanomas showed coexistent microsatellite abnormalities (CDKN2A-CDKN1B), no topographic gradient, and significantly decreased expression. Melanocytic nevi and low-grade atypical melanocytic nevi revealed sporadic junctional CDKN2A microsatellite abnormalities and no significant topographic kinetic differences. High-grade atypical melanocytic nevi accumulate junctional TP53-CDKN1A-CDKN1B microsatellite abnormalities, being progression TP53-independent and better assessed in the dermis. Melanocytic nevi and low-grade atypical melanocytic nevi show low incidence of microsatellite abnormalities, and kinetic features that make progression unlikely.

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Section: Discussionmentioning

confidence: 91%

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

et al. 2011

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“…It would not be surprising to find similar control for the tumor cell capabilities in both steps (stromal invasion and metastasis) [4]. This progression would be related to the accumulation of genetic abnormalities and selective segregation of tumor cells with invasive capabilities, which are frequently topographically distributed [9,22,23,170]. Clinicopathological studies have demonstrated lymph node metastases associated with histologically intraepithelial malignancies ( i.e.…”

Section: Tumor Componentsmentioning

confidence: 99%

Tumor Heterogeneity: Mechanisms and Bases for a Reliable Application of Molecular Marker Design

Díaz‐Cano

2012

IJMS

143

105

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Tumor heterogeneity is a confusing finding in the assessment of neoplasms, potentially resulting in inaccurate diagnostic, prognostic and predictive tests. This tumor heterogeneity is not always a random and unpredictable phenomenon, whose knowledge helps designing better tests. The biologic reasons for this intratumoral heterogeneity would then be important to understand both the natural history of neoplasms and the selection of test samples for reliable analysis. The main factors contributing to intratumoral heterogeneity inducing gene abnormalities or modifying its expression include: the gradient ischemic level within neoplasms, the action of tumor microenvironment (bidirectional interaction between tumor cells and stroma), mechanisms of intercellular transference of genetic information (exosomes), and differential mechanisms of sequence-independent modifications of genetic material and proteins. The intratumoral heterogeneity is at the origin of tumor progression and it is also the byproduct of the selection process during progression. Any analysis of heterogeneity mechanisms must be integrated within the process of segregation of genetic changes in tumor cells during the clonal expansion and progression of neoplasms. The evaluation of these mechanisms must also consider the redundancy and pleiotropism of molecular pathways, for which appropriate surrogate markers would support the presence or not of heterogeneous genetics and the main mechanisms responsible. This knowledge would constitute a solid scientific background for future therapeutic planning.

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“…FCs showed several nuclear features of high nuclear‐cytoplasmic ratio, nuclear atypia, coarse granular and/or dense chromatin, or intranuclear cytoplasmic inclusion more frequently than follicular adenomas. Follicular lesions with nuclear atypia were significantly likely to be malignant,10, 11 and 60% of follicular neoplasms with nuclear atypia were malignant 12. In our follicular neoplasms, 70% of high nuclear–cytoplasmic ratio, 73% of nuclear atypia, and 82% of coarse granular or dense chromatin were FCs.…”

Section: Discussionmentioning

confidence: 51%

Improving the diagnostic accuracy of thyroid follicular neoplasms: Cytological features in fine‐needle aspiration cytology

Maruta

Hashimoto

Suehisa

et al. 2010

Diagnostic Cytopathology

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Cytological diagnosis in follicular neoplasms of the thyroid has to surmount some difficulties. Capsular/vascular invasions or metastasis are the histological criteria for follicular carcinoma (FC), and, on fine-needle aspiration (FNA) samples, marked cytological atypias are only observed in moderately to poorly differentiated FC, while they may be completely lacking in well differentiated angio- or capsulo-invasive FC. To clarify the cytological features and to improve the accuracy and reliability of aspiration cytology, 892 follicular adenomas and 82 FCs were reviewed. A macrofollicular pattern or large sheet pattern of follicular cells with thin colloid in the background were found to be indicators of follicular adenoma. Crowding or irregular arrangement of follicular cells were found to indicate microfollicular lesions but could not discriminate between benign and malignant conditions. High nucleo-cytoplasmic ratio, nuclear atypia, and coarse granular or dense chromatin were more important criteria for malignancy than nuclear grooves or intranuclear cytoplasmic inclusions. The cytomorphologic features of the follicular neoplasms of the thyroid are described, and the difficulties encountered in the cytodiagnosis of follicular lesions are discussed at length.

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Cytoarchitectural and kinetic features in the histological evaluation of follicular thyroid neoplasms

Abstract: Follicular carcinomas show up-regulation of proliferation markers and the distinctive topographical kinetic profiles provide a basis for the distinction between benign and malignant and an explanation for the circumscription and encapsulation of benign lesions.

Cited by 10 publications

References 29 publications

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

Heterogeneous topographic profiles of kinetic and cell cycle regulator microsatellites in atypical (dysplastic) melanocytic nevi

Tumor Heterogeneity: Mechanisms and Bases for a Reliable Application of Molecular Marker Design

Improving the diagnostic accuracy of thyroid follicular neoplasms: Cytological features in fine‐needle aspiration cytology

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