Cell cycle and apoptosis regulators in Spitz nevi: Comparison with melanomas and common nevi

Stefanaki, Christina; Stefanaki, Kalliopi; Antoniou, Christina; Argyrakos, Theodoros; Patereli, Amalia; Stratigos, Alexander J.; Katsambas, Andreas

doi:10.1016/j.jaad.2006.09.015

Cited by 37 publications

(26 citation statements)

References 35 publications

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“…Immunohistochemical results were quantified considering the percentage of cells expressing nuclear positivity, counting 1,000 cells per slide. Immunoreactive cells were counted randomly with a minimum of 10 high-power fields (9400) according to Stefanaki et al [6]. The staining intensity was subjectively classified as weak (?…”

Section: Methodsmentioning

confidence: 99%

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Immunohistochemical Expression of p16, p21, p27 and Cyclin D1 in Oral Nevi and Melanoma

Andrade

León

Carlos³

et al. 2012

Head and Neck Pathol

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The acquisition of abnormalities at G1/S is considered a crucial step in the genesis and progression of melanoma. The expression of cell cycle regulators has also been used in various neoplasms as an adjunct to diagnosis. The aim of this study was to compare the expression of p16, p21, p27 and cyclin D1 in oral nevi and melanomas. Expression of these cell cycle regulatory proteins was evaluated by immunohistochemistry in 51 oral melanocytic lesions, including 38 intramucosal nevi and 13 primary oral melanomas. p16 and p27 were highly expressed in intramucosal nevi, whereas p21 and cyclin D1 expression was higher in oral melanomas. The results indicate that p21 and cyclin D1 may be involved in the development of oral melanomas, and eventually they may be useful in the differential diagnoses of oral benign and malignant melanocytic lesions.

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Section: Methodsmentioning

confidence: 99%

“…Among the cell cycle regulators, some studies have focused on the expression of p16, p21, p27 and cyclin D1 in cutaneous melanocytic lesions and melanomas, but little is known of their expression in oral melanoma and there are no data about oral nevi [1,6,7]. These proteins are involved in the retinoblastoma protein (pRb) and p53 pathways.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Expression of p16, p21, p27 and Cyclin D1 in Oral Nevi and Melanoma

Andrade

León

Carlos³

et al. 2012

Head and Neck Pathol

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“…The expression of cyclin B1 (P < 0.0001) is significantly higher in melanomas in comparison with Spitz nevi (Stefanaki et al, 2007).…”

Section: Diseasementioning

confidence: 90%

CCNB1 (cyclin B1)

Perez‐Stable¹

2011

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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IdentityOther names: CCNB HGNC (Hugo): CCNB1 Location: 5q13.2 DNA/RNA Description 9 exons; 2,087 bp; 433 residues CCNB1 transcript 1. 8 exons; 1,833 bp; 397 residues CCNB1 transcript 2. TranscriptionTwo alternative transcripts resulting from distinct transcription initiation sites. One is constitutively expressed and the other is G2/M cell cycle-regulated. PseudogeneNo verified pseudogenes. Protein DescriptionCyclin B1 (48.337 kDa) is a member of the cyclin family of proteins whose levels vary during the cell cycle in order to activate specific cyclin-dependent kinases (CDKs) required for the proper progression through the cell cycle. Cyclin B1 protein begins to increase during G2, peaks in mitosis, and is rapidly degraded before the cell cycle is completed. Cyclin B1 interacts with CDK1 to form a complex known as the maturation-promoting factor (MPF), which is essential for cell cycle progression through mitosis. When chromosomes are properly aligned during anaphase, rapid degradation of cyclin B1 by anaphase-promoting complex/cyclosome (APC/C) is required for mitotic exit and completion of the cell cycle. ExpressionCyclin B1 is overexpressed in a variety of cancers compared to normal cells and tissues. In normal tissues, low levels of cyclin B1 is detected in testis, thymus, bone marrow, and smooth muscle (CCNB1 expression). In most primary tumors, the expression of cyclin B1 is "unscheduled" (unrestricted to particular phases of the cycle), whereas in normal lymphocytes, the expression of cyclin B1 is restricted to very late S and G2 + M phases of the cell cycle (Gorczyca et al., 1997). LocalisationDuring interphase, cyclin B1 is concentrated in the cytoplasm but can shuttle to the nucleus (Pines and Hunter, 1991).Diagram of sequence domains for cyclin B1. The destruction box (DB) is required for degradation of cyclin B1 at the metaphase-toanaphase transition. The cytoplasmic retention sequence (CRS) and the nuclear export signal (NES) are critical determinants of cyclin B1 localization during mitosis. The cyclin box is required for interaction with CDK1.

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“…[8][9][10] Although the interpretation of immunohistochemistry results remain subjective among pathologists and there is some sample selection bias, p16, Ki67, and HMB45 expression has shown relatively consistent differences between Spitz nevus and spitzoid melanoma ( Using array-based comparative genomic hybridization, Curtin et al 15 found that the most frequently lost genomic locus in melanomas was chromosome 9p. This gene locus was lost in 50% of conventional melanomas, and patients with familial melanoma syndrome are associated with a homozygous loss of the CDKN2A gene.…”

Section: Immunohistochemical Testsmentioning

confidence: 99%

A diagnostic algorithm for atypical spitzoid tumors: guidelines for immunohistochemical and molecular assessment

Cho‐Vega

2016

Modern Pathology

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Atypical spitzoid tumors are a morphologically diverse group of rare melanocytic lesions most frequently seen in children and young adults. As atypical spitzoid tumors bear striking resemblance to Spitz nevus and spitzoid melanomas clinically and histopathologically, it is crucial to determine its malignant potential and predict its clinical behavior. To date, many researchers have attempted to differentiate atypical spitzoid tumors from unequivocal melanomas based on morphological, immonohistochemical, and molecular diagnostic differences. A diagnostic algorithm is proposed here to assess the malignant potential of atypical spitzoid tumors by using a combination of immunohistochemical and cytogenetic/molecular tests. Together with classical morphological evaluation, this algorithm includes a set of immunohistochemistry assays (p16 Ink4a , a dual-color Ki67/MART-1, and HMB45), fluorescence in situ hybridization (FISH) with five probes (6p25, 8q24, 11q13, CEN9, and 9p21), and an array-based comparative genomic hybridization. This review discusses details of the algorithm, the rationale of each test used in the algorithm, and utility of this algorithm in routine dermatopathology practice. This algorithmic approach will provide a comprehensive diagnostic tool that complements conventional histological criteria and will significantly contribute to improve the diagnosis and prediction of the clinical behavior of atypical spitzoid tumors.

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Cell cycle and apoptosis regulators in Spitz nevi: Comparison with melanomas and common nevi

Cited by 37 publications

References 35 publications

Immunohistochemical Expression of p16, p21, p27 and Cyclin D1 in Oral Nevi and Melanoma

Immunohistochemical Expression of p16, p21, p27 and Cyclin D1 in Oral Nevi and Melanoma

CCNB1 (cyclin B1)

A diagnostic algorithm for atypical spitzoid tumors: guidelines for immunohistochemical and molecular assessment

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