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NCI CANCERLIT® Search: Hereditary Melanoma - August 2002
National Cancer Institute®
Last Modified: August 1, 2002
- Strength evaluation of transcriptional regulatory elements for transgene expression by adenovirus vector.
- Physical properties and in vitro transfection efficiency of gene delivery vectors based on complexes of DNA with synthetic polycations.
- Analysis of mutations and identification of several polymorphisms in the putative promoter region of the P34CDC2-related CDC2L1 gene located at
- Significant impact of promoter hypermethylation and the 540 C>T polymorphism of CDKN2A in cutaneous melanoma of the vertical growth
- Regulation of constitutive and induced NF-kappaB activation in malignant melanoma cells by capsaicin modulates interleukin-8 production and cell
- Update of familial pancreatic cancer in Germany.
- Prospective molecular profiling of melanoma metastases suggests classifiers of immune responsiveness.
- Circulating melanoma-associated markers detected by RT-PCR in patients with classic Kaposi's sarcoma.
- Detection of tyrosinase mRNA in tumor tissue microdissections from classic Kaposi's sarcoma.
- Degeneracy of antigen recognition as the molecular basis for the high frequency of naive A2/Melan-a peptide multimer(+) CD8(+) T cells in
- Molecular genetic analysis of malignant melanomas for aberrations of the WNT signaling pathway genes CTNNB1, APC, ICAT and BTRC.
- CD80-mediated induction of immunostimulation in two ocular melanoma cell lines is augmented by interferon-gamma.
- Detection of nodal micrometastases using immunohistochemistry and PCR in melanoma of the arm and trunk.
- Mutations in exon 3 of the beta-catenin gene are rare in melanoma cell lines.
- Loss of p14ARF expression in melanoma.
- Genetic and environmental factors in cutaneous malignant melanoma.
Table of Contents
1
UI - 11992688
AU - Xu ZL; Mizuguchi H; Ishii-Watabe A; Uchida E; Mayumi T; Hayakawa T
TI -
Strength evaluation of transcriptional regulatory elements for transgene
expression by adenovirus vector.
SO - J Control Release 2002 May 17;81(1-2):155-63
AD - Division of Biological Chemistry and Biologicals, National Institute of
Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, 158-8501, Tokyo, Japan.
In studies of both gene function and gene therapy, transgene expression
may be assisted considerably through the use of transcriptional
regulatory elements with high activity. In this study, we evaluated the
strength of various transcriptional regulatory elements both in vitro
(six types of cell line) and in vivo (mouse heart, lung, kidney, spleen,
and liver) by adenovirus-mediated gene transfer. In the case of the
promoter/enhancer (P/E), the activity of CMV P/E (from the human
cytomegalovirus immediate-early 1 gene) and hybrid CA P/E (composed of
the CMV enhancer and chicken beta-actin promoter) were investigated,
both of which are known to be strong and widely used. While hybrid CA
P/E showed a higher transgene expression activity than CMV P/E, the
addition of the intron A sequence (the largest intron of CMV) to CMV P/E
increased the activity of CMV P/E to the same or higher level than that
of hybrid CA P/E. Concerning the polyadenylation signal (P(A)) sequence,
one from the bovine growth hormone (BGH) gene was about two times more
efficient than that from the Simian virus 40 (SV40) late gene, both in
vitro and in vivo. In the context of the CMV P/E containing the intron A
sequence, a further increase in transgene expression was obtained by the
addition of a SV40 enhancer downstream from the P(A) sequence. The
combination of the SV40 P(A) and a SV40 enhancer showed almost
comparable activity to BGH P(A). This information would be helpful for
the construction of adenovirus vectors for studies regarding both gene
function and gene therapy.
2
UI - 11992692
AU - Reschel T; Konak C; Oupicky D; Seymour LW; Ulbrich K
TI -
Physical properties and in vitro transfection efficiency of gene
delivery vectors based on complexes of DNA with synthetic polycations.
SO - J Control Release 2002 May 17;81(1-2):201-17
AD - Institute of Macromolecular Chemistry, Academy of Sciences of the Czech
Republic, Heyrovsky Square 2, 16206 6, Prague, Czech Republic.
reschel@imc.cas.cz
Biophysical properties of polycation/DNA complexes designed for gene
delivery were studied with respect to the conditions of their
preparation, chemical structure and molecular weight of the polycations
involved. The polycations used included a variety of cationic polymers
and copolymers containing primary and tertiary amino or quaternary
ammonium groups. It was found that the molecular weight and the size of
these polyelectrolyte complexes (PECs) increase with increasing
temperature and pH of the buffer. By decreasing the molecular weight of
polycations used for PEC formation, the complexes become unstable
towards coagulation in aqueous solution at lower pH. The self-assembly
of DNA with low-molecular-weight polycations in water provides PECs with
the lowest molecular weight, smallest size and the lowest density but
their stability in NaCl solutions is very poor. Despite the complexity
of the multistep transfection process, a direct correlation between the
transfection efficiency in vitro and the stability of the complexes in
NaCl solutions and coagulation in 0.15 M NaCl solution was found. DNA
complexes with polycations containing primary amino groups showed the
best stability in saline solutions and also the best transfection
activity. PECs formed by polycations with quaternary ammonium groups
were the least resistant to destruction by the added salt and provided
the lowest activity in transfection assays. The highest transfection
activity was found for DNA complexes formed with a statistical copolymer
containing primary and tertiary amines.
3
UI - 12115485
AU - Feng Y; Shi J; Goldstein AM; Tucker MA; Nelson MA
TI -
Analysis of mutations and identification of several polymorphisms in the
putative promoter region of the P34CDC2-related CDC2L1 gene located at
1P36 in melanoma cell lines and melanoma families.
SO - Int J Cancer 2002 Jun 20;99(6):834-8
AD - Arizona Cancer Center, Tucson, AZ 85724, USA.
Chromosome 1 abnormalities are the most commonly detected aberrations in
many cancers including malignant melanoma. Partial deletions and an
allelic loss of the chromosome 1p36 region observed in melanoma indicate
the presence of putative tumor suppressor gene(s) in this region. A
candidate gene, CDC2L1, which encodes PITSLRE proteins related to
p34(cdc2), is mapped to 1p36. To determine whether CDC2L1 mutation is
involved in melanoma development, we examined 20 melanoma cell lines and
11 members of melanoma-prone families linked to chromosome 1p36.
Mutation analysis throughout the entire coding region of the CDC2L1 gene
revealed only 1 mutation (C-->T at nucleotide location 97 of exon 7,
Ser-->Leu) in the melanoma cell line UACC 903 out of 20 melanoma cell
lines and 6 melanoma cases. However, 4 polymorphic nucleotide changes,
C-48T, G-53C, T-103C and T-210C, in the putative promoter region of
CDC2L1 were identified. The 4 variants were located within or beside the
conserved binding sites of transcription factors TCF11, MZF1 and TAAC
box, indicating their potential effects on the regulation of CDC2L1
expression. No aberrant methylation of the CDC2L1 CpG island in the
promoter region was observed by sodium bisulfite genomic sequencing.
These results indicate that mutations are rare in the CDC2L1 gene in
these melanoma cell lines and melanoma families and that the aberrant
cytosine methylation of the CDC2L1 CpG island is not the mechanism of
CDC2L1 repression in melanoma. The contribution of 4 promoter
polymorphisms to the transcriptional regulation of the gene and its
association with melanoma warrants further investigation. Copyright 2002
Wiley-Liss, Inc.
4
UI - 12107107
AU - Straume O; Smeds J; Kumar R; Hemminki K; Akslen LA
TI -
Significant impact of promoter hypermethylation and the 540 C>T
polymorphism of CDKN2A in cutaneous melanoma of the vertical growth
phase.
SO - Am J Pathol 2002 Jul;161(1):229-37
AD - Department of Pathology, The Gade Institute, University of Bergen,
Bergen, Norway.
Promoter hypermethylation, mutations, and loss of heterozygosity in the
CDKN2A gene as well as polymorphisms at the 3'-untranslated region were
determined in vertical growth phase melanomas. Methylation-specific
polymerase chain reaction in soluti and in situ showed that 19% of the
cases were hypermethylated at the CDKN2A promoter region, and some of
these cases were heterogeneous with both methylated and unmethylated
tumor cells. Methylation was associated with increased tumor cell
proliferation by Ki-67 expression (P = 0.01) and decreased patient
survival (P = 0.025). Point mutations in CDKN2A were found in 4% of the
cases, whereas 90% had loss of heterozygosity at one or more of 4
markers studied. Furthermore, presence of the 540 C>T polymorphism at
the 3'-untranslated region of CDKN2A (23%) was associated with improved
survival in multivariate analysis (hazard ratio, 2.6; P = 0.02). Our
results suggest that promoter methylation of the CDKN2A gene is present
in a subgroup of the tumors and associated with increased tumor cell
proliferation and reduced survival. Further, the 540 C>T polymorphism
might define a distinct subgroup of low-grade vertical growth phase
melanomas. These findings support a significant role of the CDKN2A gene
in melanoma progression.
5
UI - 12034025
AU - Patel PS; Varney ML; Dave BJ; Singh RK
TI -
Regulation of constitutive and induced NF-kappaB activation in malignant
melanoma cells by capsaicin modulates interleukin-8 production and cell
proliferation.
SO - J Interferon Cytokine Res 2002 Apr;22(4):427-35
AD - Department of Pathology and Microbiology, The University of Nebraska
Medical Center, Omaha, NE 68198-7660, USA.
In the present study, we demonstrate that upregulation of
interleukin-1beta(IL-1beta)-mediated and tumor necrosis factor-alpha
(TNF-alpha)-mediated IL-8 expression in human malignant melanoma cells
is modulated by the activation of nuclear factor-kappaB (NF-kappaB).
Addition of capsaicin (8-methyl-N-vanillyl-6-nonenamide), a known
inhibitor of NF-kappaB, resulted in the inhibition of constitutive as
well as IL-1beta-induced and TNF-alpha-induced IL-8 expression in
melanoma cells. The inhibition of IL-8 expression was dependent on the
concentration of capsaicin and duration of treatment. Further,
electrophoretic mobility shift assay (EMSA) of nuclear extracts from
melanoma cells showed a constitutive activation of NF-kappaB and
activated protein 1 (AP-1), which was upregulated following treatment
with IL-1beta. Treatment of melanoma cells with capsaicin inhibited
activation of constitutive and IL-1beta-induced NF-kappaB, but not AP-1,
leading to inhibition of IL-8 expression. Further, downregulation of
IL-8 expression in capsaicin-treated melanoma cells resulted in
inhibition of in vitro cell proliferation. These results demonstrate
that constitutive and induced NF-kappaB activation regulates IL-8
expression in melanoma cells. Downregulation of constitutive and induced
NF-kappaB activation in malignant melanoma cells leads to inhibition of
IL-8 production and in vitro cell proliferation.
6
UI - 12120230
AU - Bartsch DK; Sina-Frey M; Ziegler A; Hahn SA; Przypadlo E; Kress R;
TI -
Gerdes B; Rieder H
Update of familial pancreatic cancer in Germany.
SO - Pancreatology 2001;1(5):510-6
AD - Department of Surgery, Philipps University of Marburg, Baldingerstrasse,
D-35033 Marburg, Germany. bartsch@mailer.uni-marburg.de
BACKGROUND/AIMS: The prevalence of familial pancreatic cancer (FPC) and
the characteristics of FPC have not yet been well investigated in the
German population. Therefore, a German case collection for FPC was
METHODS: The prevalence of pancreatic cancer (PC) as well as other
tumours and diseases was studied in families with at least 2
first-degree relatives with histologically confirmed PC, and in families
of patients with PC and a first-degree relative with malignant melanoma.
All participating family members were genetically counselled and
evaluated by a standardised questionnaire. RESULTS: In an 18-month
period, 73 independent kindreds with potential FPC contacted the
national case collection. So far, 20 kindreds have fulfilled the
criteria for FPC and have undergone complete workups. Most families
revealed an autosomal dominant pattern of inheritance. Twelve families
revealed an isolated accumulation of PC. Importantly, in 8 of 20 (35%)
families, additional tumour types such as melanoma, breast and prostate
cancer occurred. CONCLUSION: The observed phenotypic heterogeneity
indicates an association with predisposing tumour suppressor genes p16
and BRCA2 in up to 30% of FPC families. Mutation analysis of these
candidate genes might lead to the identification of the predisposing
gene defect in a proportion of FPC families.
7
UI - 12097256
AU - Wang E; Miller LD; Ohnmacht GA; Mocellin S; Perez-Diez A; Petersen D;
TI -
Zhao Y; Simon R; Powell JI; Asaki E; Alexander HR; Duray PH; Herlyn M;
Restifo NP; Liu ET; Rosenberg SA; Marincola FM
Prospective molecular profiling of melanoma metastases suggests
classifiers of immune responsiveness.
SO - Cancer Res 2002 Jul 1;62(13):3581-6
AD - Immunogenetics Section, Department of Transfusion Medicine, Clinical
Center, NIH, Bethesda, Maryland 20892, USA.
We amplified RNAs from 63 fine needle aspiration (FNA) samples from 37
s.c. melanoma metastases from 25 patients undergoing immunotherapy for
hybridization to a 6108-gene human cDNA chip. By prospectively following
the history of the lesions, we could correlate transcript patterns with
clinical outcome. Cluster analysis revealed a tight relationship among
autologous synchronously sampled tumors compared with unrelated lesions
(average Pearson's r = 0.83 and 0.7, respectively, P < 0.0003). As
reported previously, two subgroups of metastatic melanoma lesions were
identified that, however, had no predictive correlation with clinical
outcome. Ranking of gene expression data from pretreatment samples
identified approximately 30 genes predictive of clinical response (P <
0.001). Analysis of their annotations denoted that approximately half of
them were related to T-cell regulation, suggesting that immune
responsiveness might be predetermined by a tumor microenvironment
conducive to immune recognition.
8
UI - 10907962
AU - Palmieri G; Ascierto PA; Satriano SM; Strazzullo M; Apice G; Castello G
TI -
Circulating melanoma-associated markers detected by RT-PCR in patients
with classic Kaposi's sarcoma.
SO - Ann Oncol 2000 May;11(5):635-6
9
UI - 11843258
AU - Palmieri G; Cossu A; Lissia A; Leoncini L; Lazzi S; Ascierto PA;
TI -
Castello G; Tanda F
Detection of tyrosinase mRNA in tumor tissue microdissections from
classic Kaposi's sarcoma.
SO - Ann Oncol 2001 Dec;12(12):1765-6
10
UI - 12119345
AU - Dutoit V; Rubio-Godoy V; Pittet MJ; Zippelius A; Dietrich PY; Legal FA;
TI -
Guillaume P; Romero P; Cerottini JC; Houghten RA; Pinilla C; Valmori D
Degeneracy of antigen recognition as the molecular basis for the high
frequency of naive A2/Melan-a peptide multimer(+) CD8(+) T cells in
humans.
SO - J Exp Med 2002 Jul 15;196(2):207-16
AD - Division of Clinical Onco-Immunology, Ludwig Institute for Cancer
Research, University Hospital (CHUV), 1011 Lausanne, Switzerland.
In contrast with the low frequency of most single epitope reactive T
cells in the preimmune repertoire, up to 1 of 1,000 naive CD8(+) T cells
from A2(+) individuals specifically bind fluorescent A2/peptide
multimers incorporating the A27L analogue of the immunodominant 26-35
peptide from the melanocyte differentiation and melanoma associated
antigen Melan-A. This represents the only naive antigen-specific T cell
repertoire accessible to direct analysis in humans up to date. To get
insight into the molecular basis for the selection and maintenance of
such an abundant repertoire, we analyzed the functional diversity of T
cells composing this repertoire ex vivo at the clonal level.
Surprisingly, we found a significant proportion of multimer(+)
clonotypes that failed to recognize both Melan-A analogue and parental
peptides in a functional assay but efficiently recognized peptides from
proteins of self- or pathogen origin selected for their potential
functional cross-reactivity with Melan-A. Consistent with these data,
multimers incorporating some of the most frequently recognized peptides
specifically stained a proportion of naive CD8(+) T cells similar to
that observed with Melan-A multimers. Altogether these results indicate
that the high frequency of Melan-A multimer(+) T cells can be explained
by the existence of largely cross-reactive subsets of naive CD8(+) T
cells displaying multiple specificities.
11
13
14
15
16
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
UI - 12124804
AU - Reifenberger J; Knobbe CB; Wolter M; Blaschke B; Schulte KW; Pietsch T;
TI -
Ruzicka T; Reifenberger G
Molecular genetic analysis of malignant melanomas for aberrations of the
WNT signaling pathway genes CTNNB1, APC, ICAT and BTRC.
SO - Int J Cancer 2002 Aug 10;100(5):549-56
AD - Department of Dermatology, Heinrich-Heine-University, Dusseldorf,
Germany. reifenbergerj@med.uni-duesseldorf.de
Aberrant activation of the Wnt signaling pathway has been reported in
different human tumor types, including malignant melanomas. We
investigated 37 malignant melanomas (15 primary tumors and 22
metastases) for alterations of 4 genes encoding members of this pathway,
i.e., CTNNB1 (beta-catenin gene, 3p22.1), APC (adenomatous polyposis
coli gene, 5q22.2), BTRC (beta-transducin repeat-containing protein
gene, 10q24.3) and ICAT (inhibitor of beta-catenin and Tcf-4, 1p36.2).
Mutational analysis of CTNNB1 identified somatic mutations in 1 primary
melanoma and 1 melanoma metastasis from 2 different patients (5%). Both
mutations affected the N-terminal degradation box of beta-catenin, which
is important for the regulation of beta-catenin homeostasis. Another
primary melanoma carried a somatic APC missense mutation within the
known mutation cluster region in exon 15. Fourteen tumors (40%) showed
LOH at microsatellite markers on 1p36. None of the tumors had lost both
copies of the ICAT gene, but 1 melanoma metastasis carried a somatic
point mutation altering the translation start codon of ICAT. Real-time
RT-PCR showed markedly reduced ICAT transcript levels (
UI - 11930109
AU - Mulcahy KA; Alexander S; Platts KE; Wardle C; Sisley K; Rennie IG;
TI -
Murray AK
CD80-mediated induction of immunostimulation in two ocular melanoma cell
lines is augmented by interferon-gamma.
SO - Melanoma Res 2002 Apr;12(2):129-38
AD - Section of Oncology and Pathology (Cancer Studies), University of
Sheffield Medical School, Beech Hill Road, Sheffield, S10 2RX, UK.
Although the transfection of the T-cell costimulatory molecule CD80 cDNA
into human tumours can augment their immunogenicity in vitro, its
expression alone is ineffective in many tumour systems. We evaluated the
influence of CD80 expression on the immunostimulatory activity of ocular
melanoma cell lines and determined whether IFN-gamma could enhance the
effect. Two ocular melanoma cell lines were transfected with CD80 cDNA.
The immunostimulatory capacity of the CD80+ transfectants was determined
by their ability to stimulate the proliferation of allogeneic peripheral
blood mononuclear cells (PBMC). The influence of additional accessory
molecules on PBMC proliferation was assessed by pre-treating the CD80
transfectants with IFN-gamma. The CD80+ transfectants induced
proliferation of allogeneic PBMC. IFN-gamma treatment of the tumour
cells induced upregulated expression of MHC class I, de novo expression
of MHC class II and CD54, and enhanced the ability of the CD80+
transfectants to stimulate PBMC proliferation. CD4+ T cells were not
required for the proliferative response against untreated CD80+ tumour
cells but were necessary for the augmentation of proliferation observed
following IFN-gamma treatment. CD80+ ocular melanoma cells possess
immunostimulatory potential which is augmented by IFN-gamma induced
upregulation of cell surface molecules. Further studies on the role of
costimulatory molecules in inducing anti-tumour immunity in ocular
melanoma may help to define new strategies for application of
immunotherapeutic approaches to treat this aggressive disease.
UI - 11930111
AU - Boi S; Cristofolini P; Togni R; Girlando S; Camerani M; Donner D;
TI -
Cristofolini M; Dalla Palma P
Detection of nodal micrometastases using immunohistochemistry and PCR in
melanoma of the arm and trunk.
SO - Melanoma Res 2002 Apr;12(2):147-53
AD - Departments of Pathology, Santa Chiara Hospital, 38100 Trento, Italy.
boi@tn.aziendasanitaria.trentino.it.
Sentinel node (SN) mapping and biopsy seems at present the best way to
assess the nodal status in cutaneous melanoma without removing the
lymphatic chain. The procedure is minimally invasive, safe and low cost,
and allows selection of patients who can benefit from elective node
after lymphatic mapping from 95 patients (48 males and 47 females) with
stage I cutaneous melanoma affecting the trunk or limbs. Of these, 88
SNs from 74 patients were submitted to polymerase chain reaction (PCR)
in order to detect tyrosinase mRNA. A new antibody (anti-tyrosinase,
Clone T311, IgG2a type, Lab Vision Corporation) was used to detect nodal
micrometastases. The search for micrometastases was histologically
positive in 15 SNs and negative in 97. The 88 SNs examined using
molecular biology were positive in 40 cases and negative in 48. In 28
only the PCR was positive. The new antibody used to detect
micrometastases was shown to be very useful. Cases positive on both
conventional histology and PCR were Clark level II or more and were
thicker than 0.6 mm. No difference with regard to site or sex was
observed. Lymphoedema and hypersensitivity reactions, nor the inability
to work, did not occur. Only patients with histologically proven
micrometastases underwent elective node dissection. Cases positive only
on molecular biology were submitted to close follow-up.
UI - 11930117
AU - Pollock PM; Hayward N
TI -
Mutations in exon 3 of the beta-catenin gene are rare in melanoma cell
lines.
SO - Melanoma Res 2002 Apr;12(2):183-6
AD - Joint Experimental Oncology Program of the Queensland Institute of
Medical Research, The University of Queensland, and the Queensland
Cancer Fund, P.O. Royal Brisbane Hospital, Herston 4029, Australia.
Mutations in exon 3 of the CTNNB1 gene encoding beta-catenin have been
reported in colorectal cancer cell lines and tumours. Although one study
reported mutations or deletions affecting beta-catenin in 20% of
melanoma cell lines, subsequent reports detected a much lower frequency
of aberrations in uncultured melanomas. To determine whether this
difference in mutation frequency reflected an in vitro culturing
artefact, exon 3 of CTNNB1 was screened in a panel of 62 melanoma cell
lines. In addition, reverse transcription-polymerase chain reaction
(RT-PCR) was performed to detect intragenic deletions affecting exon 3.
One out of 62 (1.6%) cell lines was found to carry a mutation,
indicating that aberration of the Wnt-1/wingless pathway through
activation of beta-catenin is a rare event, even in melanoma cell lines.
UI - 11876522
AU - Dobrowolski R; Hein R; Buettner R; Bosserhoff AK
TI -
Loss of p14ARF expression in melanoma.
SO - Arch Dermatol Res 2002 Jan;293(11):545-51
AD - Institute of Pathology, University of RWTH Aachen, Germany.
Lack of p14ARF expression or its functional inactivation has been
observed in human and murine carcinomas. Although very few mutations of
p14ARF have been detected in some cancer types, changes in expression
seem to play an important role in the development of other human cancers
such as mesotheliomas. To examine the p14ARF gene and expression of
p14ARF protein in melanomas, we screened eight human melanoma cell lines
and primary human melanocytes by RT-PCR, sequencing and immunoblotting.
All melanoma cell lines analyzed expressed wild-type p14ARF mRNA as well
as protein. P14ARF expression was investigated by immunohistochemical
staining of 32 tissue samples of benign melanocytic nevi (n=14),
melanomas (n=12) and melanoma metastases (n=6). In contrast to the
results obtained from cell lines in vitro the immunohistochemical
stainings revealed a correlation between the progression of melanoma and
the lack of the p14ARF protein expression. Positive p14ARF protein
staining was observed in 11 of 14 benign nevi, in 3 of 12 melanomas and
in 0 of 6 melanoma metastases. In summary, we demonstrated a significant
inverse correlation between p14ARF protein expression and progression of
melanocytic tumors since the amount of p14ARF protein staining decreased
from benign melanocytic nevi to metastatic melanoma in situ. These
results suggest that p14ARF inactivation is important in the development
of melanomas.
UI - 11900878
AU - Bressac-de-Paillerets B; Avril MF; Chompret A; Demenais F
TI -
Genetic and environmental factors in cutaneous malignant melanoma.
SO - Biochimie 2002 Jan;84(1):67-74
AD - Service de genetique, Institut Gustave Roussy, Villejuif, France.
bressac@igr.fr
Cutaneous malignant melanoma (CMM) is an interesting example of
multifactorial disease, where both genetic and environmental factors are
involved and interact. Major risk factors include a personal and
familial history of melanoma, cutaneous and pigmentary characteristics,
sun exposure and reactions to sun exposure. Phenotypic risk factors are
likely to be genetically determined. Two high-risk melanoma
susceptibility genes-CDKN2A and CDK4-have been identified to date, with
a third gene p14(ARF) also being suspected of playing a role. Other
high-risk genes are anticipated by the existence of 9p21-unlinked
families. A low-risk melanoma-susceptibility gene-MC1R-has also been
identified. Current studies aim to identify other susceptibility genes
as well as to determine the respective contributions and interactions of
the various genetic and environmental factors of CMM and associated
phenotypes.
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