A Contribution to the Question of Heredity of Malignant Melanomas

Salamon, T; Schnyder, U. W.; Storck, H

doi:10.1159/000254910

Cited by 15 publications

(4 citation statements)

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“…Hereditary cutaneous malignant melanoma has been defined as the presence of at least 2 cases of cutaneous mel anoma within a kindred [1][2][3][4][5][6][7][8][9]. Familial dysplastic melano cytic nevi (DMN) are reported to share the same mode of inheritance and gene locus as hereditary melanoma [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of Nonfamilial and Familial Melanoma

et al. 1992

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There has been concern that individuals with nonfamilial melanoma and dysplastic melanocytic nevi (DMN) are not directly comparable to patients with hereditary melanoma and DMN. Because we have conducted a comprehensive study of nonfamilial melanoma over the past several years, we have addressed the above issue by directly comparing the characteristics of 145 nonfamilial patients, 6 patients with familial melanoma and the information available for familial melanoma in the literature. All 6 patients with familial melanoma had at least one first-degree blood relative with cutaneous melanoma. A large number of clinical and histologic variables were compared for both groups. Some pertinent variables included mean age at melanoma diagnosis 46.7 versus 52.3 years, mean Breslow thickness 2.11 versus 1.54 mm, mean total body nevi per patient 20.6 versus 18.3, mean total clinically atypical nevi per patient 2.0 versus 1.7 and total histologically confirmed DMN per group 22 (18.3%) versus 2 (33%), for patients with nonfamilial versus familial melanoma, respectively. No substantial differences were observed between the two groups. A review of the medical literature failed to reveal any quantitative data for melanocytic nevi, either clinical or histologic, at present that would allow distinction of patients with sporadic versus familial melanoma. We conclude that studies concerning the clinical characteristics of patients with DMN and nonfamilial melanoma are relevant to other persons with DMN including familial melanoma.

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Section: Introductionmentioning

confidence: 99%

“…We have recently reviewed published descriptions of patients with familial melanoma (summarized in table 1) and have found almost no data quantifying the clinical or histologic features of mclanocytic nevi in these individuals [4. 5.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Nonfamilial and Familial Melanoma

et al. 1992

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“…Indeed, dark-skinned, dark-haired individuals may also develop UV-induced cancer (indeed, not as o en as pale-skinned people). It is common for the pa ents with familial predisposi on for melanoma to have fair complexion, o en with freckles, blue or green eyes and numerous nevi (moles) on the face and the body [634,635]. The moles are usually somewhat larger than average size, with irregular borders, pink to brown in colour.…”

Section: Translated By F Lambornmentioning

confidence: 99%

DNA repair systems

Chakarov¹,

Petkova²,

Russev³

2014

Biodiscovery

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This paper provides detailed insight into the mechanisms of repair of different types of DNA damage and the direct molecular players (enzymes repairing the damage or tagging the damaged site for further processing; damage sensor molecules; other signalling and effector molecules). The gene c bases of diseases and condi ons associated with defec ve DNA repair are comprehensively reviewed, from the 'classic' severe diseases such as xeroderma pigmentosum and Cockayne syndrome to the much more subtle UV sensi vity syndromes. The review analyses the basic molecular mechanisms underlying the rela vely rare monogenic diseases of DNA repair and management of genome integrity as well as the common mul factorial diseases and condi ons with late onset that are associated with increased levels of oxida ve stress (metabolic syndrome, diabetes type 2, cardiovascular disease) and with accumula on of 'errors' in DNA (normal and pathological ageing phenotypes, various cancers). The role of cell cycle checkpoints in dividing cells and the mechanisms of decision-making for the fate of a damaged cell are discussed with regards to the cell homeostasis in normal and cancerous ssues. The role of major DNA damageassociated signalling and effector molecules (p53, ATM, poly-(ADP-ribose)-polymerase, DNA-dependent protein kinase, BRCA proteins, re noblastoma protein, and others) is discussed and illustrated with examples in the context of health and disease. DNA repair and programmed cell death are viewed together as a unified mechanism for limi ng the presence of damaged cells and cells with poten ally oncogenic transforma on in mul cellular organisms. Special a en on is paid to ageing as a natural phenomenon and an adap ve evolu onary mechanism, with a brief outline of 'successful ageing'. The differen al rates of repair of DNA in transcribed and nontranscribed regions of the genome and the specifici es of DNA repair profile in some types of cells (terminally differen ated cells, pluripotent stem cells, etc.) and in certain taxonomic groups (e.g. 'the rodent repairadox') are discussed with regards to replica ve ageing and the evolu onary processes on microand macroscale. The role of mutagenesis as a 'hit and miss' mechanism and the 'leakiness' of DNA repair for increasing gene c diversity in the course of individual life and on evolu onary scale and the phenomenology of ongoing molecular evolu on are extensively reviewed. Conflict of Interests:No poten al conflict of interest was disclosed by any of the authors. Types of DNA repair systemsIf you wish for peace, prepare for war.Publius Flavius Vege us Renatus, De Re Militari (circa 380 AD).DNA damage is a very broad term, encompassing many different types of lesions in DNA.Accordingly, DNA repair comprises many different types of pathways and mechanisms covering virtually every possible type of injury to the sequence or the structure of DNA.Accep ng Lewin's defini on of DNA damage "... any change that introduces a devia on from the usual double-helical structure" [1] , we may pre...

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“…31, 409 47, 54 Familial malignant melanoma originating in sites other than the eye was first reported by Cawley8 in 1952 when he described a 61-year-old man with a melanoma on the left arm whose 24-year-old son and 31-year-old daughter had cutaneous malignant melanoma. Since that time, 57 additional examples in which two or more family members were affected have been reported by Von Greifelt,21 Mo~chella,~' Miller and Pack, 36 Salamon et a1., 42 The present communication describes a set of triplets in whi.ch monozygous twins were concordant for cutaneous malignant melanoma which appeared simultaneously at nearly identical sites. T o our knowledge, the existence of this type tumor in monozygous twins has not previously been reported.…”

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confidence: 92%

Melanoma in twins.Cutaneous malignant melanoma in identical twins from a set of triplets

St-Arneault

Nagel

Kirkpatrick

et al. 1970

Cancer

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Identical twins and a fraternal triplet were studied because the identical twins developed malignant melanoma at age 53. Each had a preexisting mole, nearly identically placed on the left chest, which began to grow within 2 months of one another. The homozygosity of the twins was established with high probability by appearance, behavior, psychologic testing, deficiency of color vision, red cell typing, haptoglobin typing, dermatoglyphics, lymphocyte typing, mixed lymphocyte culture, lymphocyte transfer, and skin grafting. The concordance for cutaneous malignant melanoma as well as the congruence for the site and identity of age of onset of this tumor in these monozygotic twins clearly indicates the predominant role of genetic rather than environmental factors in the development of their cancers (congruent contemporaneous concordance). Furthermore, the observation suggests that the initial phenomenon eventually leading to malignant melanoma occurred in the conceptus prior to twinning. This finding is relevant to understanding the etiopathogenesis of malignant melanoma in man.

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A Contribution to the Question of Heredity of Malignant Melanomas

Cited by 15 publications

References 0 publications

Comparison of Nonfamilial and Familial Melanoma

Comparison of Nonfamilial and Familial Melanoma

DNA repair systems

Melanoma in twins.Cutaneous malignant melanoma in identical twins from a set of triplets

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