Evolution of Spitz Nevi

Emiroğlu, Nazan; Yıldız, Pelin; Özkaya, Dilek Bıyık; Bahalı, Anıl Gülsel; Su, Özlem; Onsun, Nahide

doi:10.1111/pde.13184

Cited by 11 publications

(2 citation statements)

References 26 publications

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“…Rarely, multiple and agminated (multiple grouped) lesions can occur (Morgan et al 2006;Böer et al 2001). The lesions can be pigmented or nonpigmented (Emiroglu et al 2017;Kittler 2016). A nonpigmented or lightly pigmented variant is seen as a rapidly growing pink/reddish or skin- colored papule (Fig.…”

Section: Spitz Nevusmentioning

confidence: 99%

Dermoscopy

Tiodorović

Mijušković

Kasumagić-Halilovic

et al. 2021

Atlas of Dermatology, Dermatopathology and Venereology

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Section: Spitz Nevusmentioning

confidence: 99%

Dermoscopy

Tiodorović

Mijušković

Kasumagić-Halilovic

et al. 2021

Atlas of Dermatology, Dermatopathology and Venereology

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“…Spitz nevi have an intrinsic tendency to evolution. A recent study based on the follow-up of 27 Spitz nevi provided evidence that only seven remained stable over time, while 20 exhibited an evolution; therefore, the most common biologic behavior for Spitz nevi is evolution [ 99 ]. Few studies have characterized the mutational spectrum of spitzoid tumors.…”

Section: Molecular Abnormalitiesmentioning

confidence: 99%

Melanoma: Genetic Abnormalities, Tumor Progression, Clonal Evolution and Tumor Initiating Cells

Testa

Castelli

2017

Medical Sciences

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Melanoma is an aggressive neoplasia issued from the malignant transformation of melanocytes, the pigment-generating cells of the skin. It is responsible for about 75% of deaths due to skin cancers. Melanoma is a phenotypically and molecularly heterogeneous disease: cutaneous, uveal, acral, and mucosal melanomas have different clinical courses, are associated with different mutational profiles, and possess distinct risk factors. The discovery of the molecular abnormalities underlying melanomas has led to the promising improvement of therapy, and further progress is expected in the near future. The study of melanoma precursor lesions has led to the suggestion that the pathway of tumor evolution implies the progression from benign naevi, to dysplastic naevi, to melanoma in situ and then to invasive and metastatic melanoma. The gene alterations characterizing melanomas tend to accumulate in these precursor lesions in a sequential order. Studies carried out in recent years have, in part, elucidated the great tumorigenic potential of melanoma tumor cells. These findings have led to speculation that the cancer stem cell model cannot be applied to melanoma because, in this malignancy, tumor cells possess an intrinsic plasticity, conferring the capacity to initiate and maintain the neoplastic process to phenotypically different tumor cells.

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