Genetic Aspects of Malignant Melanoma

Cawley, Edward P.; Kruse, William T.; Pinkus, Hermann

doi:10.1001/archderm.1952.01530230064006

Cited by 130 publications

(24 citation statements)

References 6 publications

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“…47 As in the Cancer Family Syndrome and heredo-familial breast cancer, phys ical markers of the preneoplastic state have been lacking. Recently, however, a hereditary, premelanotic cutaneous phe notype (characterized by multiple large moles, irregularly shaped, reddish-brown to pink in color, and with evidence of 49 This phenotoype is illustrated in a member of a family we have studied (Fig.…”

Section: Familial Atypical Multiple Mole-melanoma Syndrome (Fammm)mentioning

confidence: 99%

Hereditary Cancer: Ascertainment and Management

Lynch

Albano

et al. 1979

CA: A Cancer Journal for Clinicians

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Section: Familial Atypical Multiple Mole-melanoma Syndrome (Fammm)mentioning

confidence: 99%

Hereditary Cancer: Ascertainment and Management

Lynch

Albano

et al. 1979

CA: A Cancer Journal for Clinicians

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“…that certain families have a higher incidence of melanoma than that expected in the general population, and that this appears to be attributable to hereditary factors (Cawley, 1952; Anderson, 1971;Wallace & Exton, 1972). Patients in these families tend to develop melanoma at an earlier age, have a higher frequency of multiple melanomas and a greater incidence of other malignancies.…”

mentioning

confidence: 98%

Low natural-killer-cell activity in familial melanoma patients and their relatives

Hersey¹,

Edwards²,

Honeyman³

et al. 1979

Br J Cancer

133

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Summary.-Patients with melanoma who had one or more close relatives with melanoma were studied for their natural-killer-cell (NK) activity against cultured melanoma cells and Chang cells. A high proportion of the patients and their relatives were found to have low NK activity against these target cells. In most of the patients this could not be attributed to general depression of their immune function, since Band T-cell numbers and the mitogenic response to PHA were within normal limits. The levels of NK activity of the patients and their relatives were found to be significantly correlated, suggesting that the NK activity in these families may have been genetically (or environmentally) determined. Several genetic markers were examined in the patients and their relatives for association with the disease state and NK activity. No association with HLA antigens or ABO blood groups was detected, but there was a low incidence of the Rhesus negative phenotype in the patients (the Rh phenotype had previously been associated with high NK activity).The present results indicate that NK activity has a familial association in families with a high incidence of melanoma, and raise the question whether low NK activity may be one of the predisposing factors in the development of familial melanoma.

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“…In the first kindred the karyotype of all three melanoma sufferers was 46XX 9qh +, while six unaffected members had a normal karyotype. BamHI polymorphism of the Ha-ras gene does not identify the affected members in the HM/DNS families studied.A familial form of malignant melanoma has long been recognised (Norris, 1820;Cawley, 1952) for analysis, and of the selected members of a second kindred. We were unable to show any linkage between melanoma occurrence and particular BamHI Ha-ras alleles.…”

mentioning

confidence: 99%

“…A familial form of malignant melanoma has long been recognised (Norris, 1820;Cawley, 1952) for analysis, and of the selected members of a second kindred. We were unable to show any linkage between melanoma occurrence and particular BamHI Ha-ras alleles.…”

mentioning

confidence: 99%

“…A familial form of malignant melanoma has long been recognised (Norris, 1820;Cawley, 1952) and approximately 5% of melanoma patients have an affected first degree relative (Anderson, 1971;Scheibner et al, 1981). The closely related preneoplastic condition, familial dysplastic naevus syndrome (DNS) (Greene et al, 1985b) and hereditary melanoma (HM) itself probably represent pleiotropic effects of a single highly penetrant autosomal dominant gene (Greene et al, 1985a).…”

mentioning

confidence: 99%

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Harvey-ras oncogene restriction fragment alleles in familial melanoma kindreds

Sutherland¹,

Shaw²,

Roberts³

et al. 1986

Br J Cancer

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Summary Unique and uncommon BamHI allelic restriction fragments of the Ha-ras locus have been reported in the genomes of patients with cancer and of three affected members of a familial melanoma kindred (Krontiris et al., 1986). Analysis of the BamHI and Msp/HpaII restriction fragments of peripheral blood leucocyte DNA from the members of two families with hereditary melanoma (HM)/familial dysplastic naevus syndrome (DNS) revealed that the only Ha-ras allele common to four affected members of one kindred and two from a second kindred, was the 6.7kb allele which is found in 66% of the normal population. This allele was found equally in affected and non-affected family members, and in one affected case was inherited from an unaffected homozygous parent. It was absent in two affected sisters in a third kindred. In the first kindred the karyotype of all three melanoma sufferers was 46XX 9qh +, while six unaffected members had a normal karyotype. BamHI polymorphism of the Ha-ras gene does not identify the affected members in the HM/DNS families studied.A familial form of malignant melanoma has long been recognised (Norris, 1820;Cawley, 1952) for analysis, and of the selected members of a second kindred. We were unable to show any linkage between melanoma occurrence and particular BamHI Ha-ras alleles. Materials and MethodsThe registry of familial melanoma in the Sydney Melanoma Unit was searched for families in which three or more affected members in two generations were still living. The natural history of melanoma makes the availability of such a related group a rarity, and despite our large register of affected families only three suitable kindreds were identified of which one has been studied in detail. The original excision biopsy specimens of affected family members were reviewed by one histopathologist (JG). The authenticity of the kindred was established by paternity studies using blood group phenotypes.DNA was isolated from peripheral blood leukocytes (Kunkel et al., 1977) (Southern, 1975). The probe, a 6.6 kb BamHI fragment containing the EJ/T24 bladder carcinoma ras oncogene cloned into pBR322 (Shih & Weinberg, 1982), was nick translated (Rigby et al., 1972) to a

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Genetic Aspects of Malignant Melanoma

Cited by 130 publications

References 6 publications

Hereditary Cancer: Ascertainment and Management

Hereditary Cancer: Ascertainment and Management

Low natural-killer-cell activity in familial melanoma patients and their relatives

Harvey-ras oncogene restriction fragment alleles in familial melanoma kindreds

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