The Cutaneous Evolution of Nevi in a Patient with Familial, Atypical, Multiple‐mole Melanoma Syndrome

Lynch, Henry T.; Fusaro, Ramon M.; Treger, Calvin L.; Pester, Judith; Lynch, Jane F.

doi:10.1111/j.1525-1470.1985.tb00467.x

Cited by 15 publications

(3 citation statements)

References 12 publications

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“…The finding that the DN patients were significantly younger than the control group was expected. Dysplastic nevi are evident in young adulthood 24,38 . Patients concerned about these lesions would seek advice early in life, especially if other family members informed them about the syndrome.…”

Section: Discussionmentioning

confidence: 99%

Skin Types in Dysplastic Nevus Syndrome

Kopf

Goldman

Rivers

et al. 1988

The Journal of Dermatologic Surgery and Oncology

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In order to determine if individuals with dysplastic nevi (DN) are relatively more sun-sensitive than controls who do not have DN, the sun-reactivity skin types (based on the Harvard classification) were determined in these two groups. Compared with controls, sun-sensitive types were significantly overrepresented in the DN group. This is consistent with the hypothesis that the fundamental defect in the dysplastic nevus syndrome is the genetically unstable melanocyte, which is susceptible to neoplastic transformation induced by sunlight.

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Section: Discussionmentioning

confidence: 99%

Skin Types in Dysplastic Nevus Syndrome

Kopf

Goldman

Rivers

et al. 1988

The Journal of Dermatologic Surgery and Oncology

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“…Little, however, is known about the pl integrin expression in benign nevomelanocytes (NMC) and dysplastic nevus (DN) cells. Clinical and histopathological features of dysplastic nevi have been studied extensively (Ackerman and Mihara, 1985;Clark et al, 1978;Elder, 1985;Elder et al, 1982;Greene et al, 1980;Greene et al, 1978;Kraemer, 1983;Kraemer and Greene, 1985;Lynch, F'richot, and Lynch, 1978;Lynch et al, 1985;Mihm and Googe, 1990). These nevi are present in the general population (Elder et al, 1980;Rahbari and Mehregan, 1981), and are regarded as possible precursors of malignant melanoma.…”

Section: Discussionmentioning

confidence: 99%

Role of β1 Integrins in Cell Spreading and Migration of Human Nevomelanocytes and Dysplastic Nevi Cells on Collagen Type IV and Laminin

Vink

Dekker

Leeuwen

et al. 1994

Pigment Cell Research

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We characterized beta 1 integrin subunit expression on three different cultures of benign human nevomelanocytes (NMC) and on four different cell cultures of human dysplastic nevus (DN) cells by flow cytometry analysis and examined their role in mediating cell spreading and migration on collagen type IV (CN IV) and laminin (LN) coated substrates by using a quantitative video image analysis system. The seven human NMC and DNC cultures expressed heterogeneous levels of beta 1, alpha 2, alpha 3 and alpha 6 integrin subunits. Image analysis showed that a significant increase (P < 0.001) in cell spreading and migration of the DN cells was induced on increasing coating concentrations of CN IV and LN. However, the NMC did not show an increase in cell spreading or migration on these substrates when compared to the substrates coated with denatured BSA only. The CN IV-induced cell spreading of the DN cells was significantly inhibited by anti-beta 1 mAb (AIIB2), anti-alpha 2 mAb (P1E6), or anti-alpha 3 mAb (P1B5), but not by mAb against alpha 6 integrin subunit (GoH3). The DN cell spreading on LN was not significantly inhibited by these mAbs. In contrast, the migration of the DN on CN IV and LN was significantly inhibited by anti-beta 1 mAb, anti-alpha 2 mAb, anti-alpha 3 mAb and anti-alpha 6 mAb. These data suggest that the alpha 2 and alpha 3 subunit are important for cell spreading of the DN on CN IV, although they are less important in cell spreading on the extracellular matrix component LN.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…These were not biopsied to verify their normal or possibly dysplastic histology. The atypical nevi were identified most easily in the younger members of the pedigree (under 40 years), as the atypical nevi, along with normal moles, tend to disappear in the older age group (over 50 years) (Lynch et al, 1985).…”

Section: Methodsmentioning

confidence: 99%

Phenotypic Variation and Systemic Cancer in the FAMMM Syndrome

Fusaro

Lynch

et al. 1988

Pigment Cell Research

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Familial atypical multiple mole melanoma (FAMMM) syndrome, a cancer‐associated genodermatosis, is a dominantly inherited heterogeneous disorder with variable expressivity of both its cutaneous and cancer phenotypes. By using a verified historical review technique of cancer documentation (idout patient health records, pathology reports/slides, autopsy reports/slides, and death certificates) of all anatomic sites in all members of a modified nuclear pedigree (first‐degree relatives plus maternal and paternal grandparents, aunts, and uncles) over several generations, we showed that the FAMMM syndrome is similar to the majority of autosomal dominant inherited cancer‐associated genodermatoses and has excessive risk for cancer of multiple anatomic sites. With respect to the FAMMM syndrome, these cancers involved the breast, respiratory tract, gastrointestinal system, the eye (intraocular melanoma), and the lymphatic system. These FAMMM pedigrees showed some of the following distinctive characteristics of hereditary cancer: 1) integral patterns of cancer within and between pedigrees; 2) early age of onset of cancer; 3) prolonged survival of some pedigree members with cancer; and 4) an excess of multiple primary melanomas and cancers of variable anatomic sites. The presence of these features indicates that these cancers of variable anatomic sites may be etiologically associated with the FAMMM syndrome. Heterogeneity should be investigated in FAMMM pedigrees with attention to consistent differences in size and distribution of atypical lesions, age at cancer onset, and pattern of tumor occurrences. The occurrence of FAMMM pedigrees in the general population or among pedigrees of probands with atypical nevi is not known. The occurrence of systemic cancers in these FAMMM pedigrees requires the development of cancer surveillance programs that are specifically modified to the particular cancer pattern of each pedigree.

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The Cutaneous Evolution of Nevi in a Patient with Familial, Atypical, Multiple‐mole Melanoma Syndrome

Cited by 15 publications

References 12 publications

Skin Types in Dysplastic Nevus Syndrome

Skin Types in Dysplastic Nevus Syndrome

Role of β1 Integrins in Cell Spreading and Migration of Human Nevomelanocytes and Dysplastic Nevi Cells on Collagen Type IV and Laminin

Phenotypic Variation and Systemic Cancer in the FAMMM Syndrome

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