DOI-10.1002-path.1711980102 - 1711980102 J Pathol 198-56A.pdf

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Husain, E; Miguel, M de; Blanes, A; Cerio, R; Pozo-Garcia, L; Diaz-Cano, Salvador J. (2012): DOI-10.1002-path.1711980102 - 1711980102 J Pathol 198-56A.pdf. figshare.
Retrieved 23:42, Dec 01, 2015 (GMT)


Introduction: Spitz tumors (ST) are poorly understood, their behavior can be unpredictable and their cell kineticis unknown.

Methods: We selected ST (42), malignant melanomas (42, 15 radial growth phase MM-RGP and 27 vertical growth phase MM- VGP), and conventional melanocytic nevi (15 junctional, 20 compound), the latter two grou s used as controls. lmmunostainingfor Ki-67, p53, p21WAF1 and p27KIP1 was scored by topographic compartments (junctional, and dermal superficial and deep to 0.76 mm), screening the whole compartment in each case. CD-31-stained slides were used to estimate microvessel density. The results were statistically compared using analysis of variance and Student t-test, and consideredsignificantif P<0.05. Results: Superficial-to-deep gradient was maintained for Ki-67 in all lesions, but significantly higher in MM. No differences in p53 immunoexpression were detected. ST revealed reverse pattern with significantly overexpressed p21WAF1 and p27KIP1 and increased microvessel density at the deep dermal compartment.

Conclusions: The kinetic profile suggests an overall regression for ST and a dissociated and ineffective deep vascular proliferation to maintain the cell growth.


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