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NCI CANCERLIT® Search: Hereditary Melanoma - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
UI - 11721029
AU - Ferber D
TI -
Gene therapy. Safer and virus-free?
SO - Science 2001 Nov 23;294(5547):1638-42
2
UI - 11748642
AU - Meije CB; Hakvoort TB; Swart GW; Westerhof W; Lamers WH; Das PK
TI -
Gene expression patterns in melanocytic cells: candidate markers for
early stage and malignant transformation.
SO - J Pathol 2002 Jan;196(1):51-8
AD - Department of Pathology, Academic Medical Center, University of
Amsterdam, The Netherlands.
Different stages of differentiation of human melanocytic cells, such as
normal melanocytes, naevus and melanoma cells, reflect distinct gene
expression patterns. A PCR-based subtractive hybridization and display
method was applied to identify genes that are differentially expressed
in melanocytic cells in relation to early stage and malignant
transformation. This resulted in the identification of a number of
candidate cDNAs differentially expressed among melanocytes, naevus
cells, and (non)-metastatic melanoma cells. Out of this collection of
cDNAs, 16 clones were screened that comprised 12 novel genes, one
previously identified expressed sequence tag related to vesicular
trafficking (Ras-related protein Rab5b). The other three were also known
genes that were either related to cell motility (beta-tubulin), pre-mRNA
splicing (small nuclear protein U1A), or of unknown function (the human
TI227-H gene). The differential expression patterns of Rab5b and two
novel gene fragments (pCMa1, pCMn2) were further assessed in melanocytic
cells. pCMa1 was expressed more in metastatic melanoma than in primary
melanoma cells. In contrast, pCMn2 was expressed in both non-metastatic
and metastatic melanoma cells, but was not detectable in either normal
melanocytes or naevus cells. The Ras-related protein Rab5b showed lower
levels of expression in highly metastatic than in other melanoma cells.
These three cDNAs may therefore be involved in the early stage and
malignant transformation of melanocytes. Copyright 2001 John Wiley &
Sons, Ltd.
3
UI - 11815963
AU - Lynch HT; Brand RE; Hogg D; Deters CA; Fusaro RM; Lynch JF; Liu L;
TI -
Knezetic J; Lassam NJ; Goggins M; Kern S
Phenotypic variation in eight extended CDKN2A germline mutation familial
atypical multiple mole melanoma-pancreatic carcinoma-prone families: the
familial atypical mole melanoma-pancreatic carcinoma syndrome.
SO - Cancer 2002 Jan 1;94(1):84-96
AD - Department of Preventive Medicine, Creighton University School of
Medicine, Omaha, Nebraska 68178, USA. trlynch@creighton.edu
BACKGROUND: Hereditary pancreatic carcinoma shows extant phenotypic and
genotypic heterogeneity as evidenced by its integral association with a
variety of hereditary cancer syndromes inclusive of the familial
atypical multiple mole melanoma (FAMMM) syndrome in concert with CDKN2A
(p16) germline mutations. METHODS: Creighton University's familial
pancreatic carcinoma resource comprises 159 families of which 19 (12%)
show the FAMMM cutaneous phenotypes. The authors describe eight families
with the FAMMM-pancreatic carcinoma (FAMMM-PC) association in concert
with a CDKN2A germline mutation. Each family was thoroughly educated
about all facets of the study, including the molecular genetics, reduced
penetrance of CDKN2A mutations, and their variable expressivity. Genetic
counseling was provided to each patient. RESULTS: Diversity in cancer
presentation within and among the families was noteworthy, wherein
melanoma predominated in certain of the families whereas pancreatic
carcinoma predominated in others. Early-onset pancreatic carcinoma (at
ages 35, 45, 46, and 49 years) appeared in some of the families whereas
markedly later-onset pancreatic carcinoma occurred in others. There were
four incidences of melanoma and pancreatic carcinoma as double primaries
in the same individuals. One patient with melanoma and pancreatic
carcinoma had a third primary of breast carcinoma. Another patient had
sarcoma, esophageal carcinoma, and two melanoma primaries, whereas his
daughter had sarcoma and was a carrier of a CDKN2A mutation.
CONCLUSIONS: The authors suggest that these tumors may collectively, in
concert with CDKN2A mutations, constitute a "new" putative hereditary
carcinoma syndrome referred to as FAMMM-PC. More clinical and molecular
genetic research on additional families with pancreatic carcinoma in
concert with the FAMMM will be required. Copyright 2002 American Cancer
Society.
4
UI - 11506326
AU - Chana JS; Grover R; Wilson GD; Hudson DA; Forders M; Sanders R;
TI -
Grobbelaar AO
The prognostic importance of c-myc oncogene expression in head and neck
melanoma.
SO - Ann Plast Surg 2001 Aug;47(2):172-7
AD - RAFT Institute of Plastic Surgery, Mt Vernon Hospital, Northwood,
Middlesex, UK.
Melanomas of the head and neck have a poorer prognosis than melanomas
arising at other cutaneous sites. To study the biology of this disease,
the expression of the c-myc oncogene was studied in tumors from 97
patients with head and neck melanoma using the technique of flow
cytometry. Survival analysis revealed that stratification of patients
according to oncogene expression provided a prognostic marker with
shorter overall survival in tumors with high nuclear c-myc oncoprotein
positivity (log-rank test, chi2 = 8.77, p < 0.005). Multifactorial
analysis using Cox's proportional hazards model revealed nuclear c-myc
oncoprotein to be an independent prognostic marker (log-rank test, chi2
= 8.82, p = 0.005). These results support the authors' previous studies
of the prognostic value of c-myc expression in melanoma and suggest that
estimation of c-myc oncoprotein may be of clinical importance in
identifying high-risk patients.
5
UI - 11807902
AU - Mantelli M; Barile M; Ciotti P; Ghiorzo P; Lantieri F; Pastorino L;
TI -
Catricala C; Torre GD; Folco U; Grammatico P; Padovani L; Pasini B;
Rovini D; Queirolo P; Rainero ML; Santi PL; Sertoli RM; Goldstein AM;
Bianchi-Scarra G; Societa Italiana Dermatologia; Gruppo Italiano Studi
Epidemiologici in Dermatologia
High prevalence of the G101W germline mutation in the CDKN2A
(P16(ink4a)) gene in 62 Italian malignant melanoma families.
SO - Am J Med Genet 2002 Jan 22;107(3):214-21
AD - Dipartimento di Oncologia, Biologia e Genetica, Universita degli Studi
di Genova, Genova, Italy.
CDKN2A germline mutation frequency estimates are commonly based on
families with several melanoma cases. When we started counseling in a
research setting on gene susceptibility analysis in northern and central
Italy, however, we mostly found small families with few cases. Here we
briefly characterize those kindred, estimate CDKN2A/CDK4 mutation test
yields, and provide indications on the possibility of implementing
formal DNA testing for melanoma-prone families in Italy. In September
1995 we started genetic counseling in a research setting at our Medical
Genetics Center. Screening for CDKN2A/CDK4 mutations was performed on
families with two melanoma patients, one of whom was younger than 50
years at onset, the other complying with one of the following: 1) being
a first-degree relative, 2) having an additional relative with
pancreatic cancer, or 3) having multiple primary melanomas. Sixty-two of
67 (80%) melanoma cases met our criteria. Four previously described
CDKN2A mutations (G101W, R24P, V126D, and N71S) were found in 21 of the
62 families (34%) with a high prevalence of G101W (18/21). The
percentage of families with two melanoma cases/family harboring a
mutation was low (7%, 2/27), but rose to 45% (9/20) if one of the
melanoma patients carried multiple melanomas or if pancreatic cancer was
present in that family. In the 15 families with three melanoma cases the
presence of a mutation was higher (67%, 10/15) and reached 100% in the 4
families with four or more melanoma cases. Our results suggest that
CDKN2A/CDK4 counseling-based mutational analysis may be reasonably
efficient also for families with two melanoma cases, if one patient
carries multiple melanomas or if pancreatic cancer is present in the
family. Copyright 2002 Wiley-Liss, Inc.
6
UI - 11782382
AU - Sturm RA; Satyamoorthy K; Meier F; Gardiner BB; Smit DJ; Vaidya B;
TI -
Herlyn M
Osteonectin/SPARC induction by ectopic beta(3) integrin in human radial
growth phase primary melanoma cells.
SO - Cancer Res 2002 Jan 1;62(1):226-32
AD - The Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
R.Sturm@imb.uq.edu.au
Expression of the beta(3) integrin subunit in melanoma in situ has been
found to correlate with tumor thickness, the ability to invade and
metastasize, and poor prognosis. Transition from the radial growth phase
(RGP) to the vertical growth phase (VGP) is a critical step in melanoma
progression and survival and is distinguished by the expression of
beta(3) integrin. The molecular pathways that operate in melanoma cells
associated with invasion and metastasis were examined by ectopic
induction of the beta(3) integrin subunit in RGP SBcl2 and WM1552C
melanoma cells, which converts these cells to a VGP phenotype. We used
cDNA representational difference analysis subtractive hybridization
between beta(3)-positive and -negative melanoma cells to assess gene
expression profile changes accompanying RGP to VGP transition. Fourteen
fragments from known genes including osteonectin (also known as SPARC
and BM-40) were identified after three rounds of representational
difference analysis. Induction of osteonectin was confirmed by Northern
and Western blot analysis and immunohistochemistry and correlated in
organotypic cultures with the beta(3)-induced progression from RGP to
VGP melanoma. Expression of osteonectin was also associated with reduced
adhesion to vitronectin, but not to fibronectin. Osteonectin expression
was not blocked when melanoma cells were cultured with
anti-alpha(v)beta(3) LM609 mAb, mitogen-activated protein kinase, or
protein kinase C inhibitors, indicating that other signaling pathway(s)
operate through alpha(v)beta(3) integrin during conversion from RGP to
VGP.
7
UI - 11781663
AU - Narita M; Bahar R; Hatano M; Kang MM; Tokuhisa T; Goto S; Saisho H;
TI -
Sakiyama S; Tagawa M
Tissue-specific expression of a suicide gene for selective killing of
neuroblastoma cells using a promoter region of the NCX gene.
SO - Cancer Gene Ther 2001 Dec;8(12):997-1002
AD - Division of Pathology, Chiba Cancer Center Research Institute, Chiba,
Japan.
The human NCX gene, a homologue of the murine neural crest homeobox
(Ncx/Hox11L.1) gene whose expression is restricted to a subset of neural
crest-derived tissues, was expressed in human neuroblastoma cells but
not in other tumors or fibroblasts. A 4.5-kb genomic fragment in the
5'-flanking region of the NCX gene efficiently transcribed the fused
luciferase reporter gene in human neuroblastoma cells but not in
non-neuroblastoma cells. Sequential deletion of this regulatory region
from the 5' side demonstrated that a 1.7-kb fragment upstream from the
start codon retained the preferential promoter activity in neuroblastoma
cells. The transcriptional activation by the NCX promoter was stronger
than that by the SV40 T antigen promoter in human neuroblastoma cells.
Transfection of neuroblastoma cells with the NCX promoter-linked herpes
simplex virus-thymidine kinase (HSV-TK) gene increased their sensitivity
to ganciclovir. The regulatory region of the NCX gene is thus useful for
neuroblastoma-specific suicide gene therapy.
8
UI - 11809177
AU - Walker GJ; Hayward NK
TI -
p16INK4A and p14ARF tumour suppressors in melanoma: lessons from the
mouse.
SO - Lancet 2002 Jan 5;359(9300):7-8
AD - Human Genetics Laboratory, Queensland Institute of Medical Research,
Royal Brisbane Hospital, Queensland, 4029, Brisbane, Australia.
9
UI - 11809676
AU - Deng J; Kloosterbooer F; Xia W; Hung MC
TI -
The NH(2)-terminal and conserved region 2 domains of adenovirus E1A
mediate two distinct mechanisms of tumor suppression.
SO - Cancer Res 2002 Jan 15;62(2):346-50
AD - Department of Molecular and Cellular Oncology, The University of Texas,
M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Adenovirus E1A has been shown to suppress tumor growth and induce
apoptosis in response to stress. To determine the mechanisms and regions
of E1A that mediate these functions, we characterized stable
transfectants of various E1A mutants in murine melanoma cells both in
vitro and in vivo. Three E1A-mutant constructs were used in this study,
those having a single deletion at either the NH(2)-terminal (dl1101) or
conserved region 2 (CR2) domain (dl1108), or double deletions at both
domains (dl0108). The in vitro study showed that the CR2 domain is
required for E1A-mediated apoptosis, whereas the NH(2)-terminal domain
is dispensable. The in vivo study showed that dl1101 and dl1108 were
still able to suppress tumor growth, whereas dl0108 lost
tumor-suppressive activity. By in situ immunohistostaining, we found
that factor VIII, a marker for angiogenesis, was greatly suppressed in
dl1108 transfectants that are resistant to apoptosis. Thus, inhibition
of angiogenesis is involved in the NH(2)-terminal domain of E1A. In
conclusion, we suggest that the NH(2)-terminal and CR2 domain of E1A
mediate two distinct mechanisms of tumor suppression.
10
UI - 10606060
AU - Pasquini P
TI -
Does assessment of family history of melanoma provide valid information?
SO - Arch Dermatol 1999 Dec;135(12):1527-8
11
UI - 11295943
AU - Fusaro RM
TI -
The validation of medical histories in kindreds.
SO - Arch Dermatol 2001 Apr;137(4):506-7
12
UI - 11556532
AU - Llewellyn K; Barnhill RL
TI -
Distinguishing Spitz tumors from malignant melanoma: potential role of
comparative genomic hybridization and fluorescence in situ hybridization
in diagnosis and prognosis.
SO - Adv Anat Pathol 2001 Sep;8(5):249-54
AD - Department of Dermatology, George Washington University, Washington, DC,
USA.
13
UI - 11742542
AU - Jean D; Guillaume N; Frade R
TI -
Characterization of human cathepsin L promoter and identification of
binding sites for NF-Y, Sp1 and Sp3 that are essential for its activity.
SO - Biochem J 2002 Jan 1;361(Pt 1):173-84
AD - Immunochimie des Regulations Cellulaires et des Interactions Virales,
INSERM U.354, Centre INSERM, Hopital Saint-Antoine, 184 rue du Faubourg
Saint-Antoine, 75012 Paris, France.
Cathepsin L is a cysteine protease whose overexpression in human
melanoma cells increases their tumorigenicity and switches their
phenotype from non-metastatic to highly metastatic. Regulation of the
transcription of the gene encoding human cathepsin L has not been yet
studied and only preliminary data exist on the promoter regulation of
the gene encoding rodent cathepsin L. In the present study we identified
molecular elements involved in the transcriptional regulation of human
cathepsin L in melanoma cells. The sequence of the 5'-flanking region of
the gene encoding human cathepsin L was determined up to 3263 bp
upstream of the translation start site. The major transcription
intiation site was located. Three mRNA splice variants, differing in
their 5' untranslated ends, were identified. Regulatory regions crucial
for cathepsin L promoter activity were characterized between -1489 and
-1646 bp. In this region, two GC boxes (-1590/-1595 and -1545/-1550) and
a CCAAT motif (-1571/-1575) were involved in specific DNA-protein
interactions. An electrophoretic mobility-shift assay demonstrated that
Sp1 and Sp3 transcription factors bound to these GC boxes, and only the
transcription factor nuclear factor Y (NF-Y) bound to the CCAAT motif.
Mutagenesis studies demonstrated that these binding sites contributed at
least 85% of cathepsin L promoter activity. Thus structural and
functional analysis demonstrated that binding sites for NF-Y, Sp1 and
Sp3 are essential for transcription of the gene encoding human cathepsin
L in melanoma cells.
14
UI - 11821057
AU - Slominski A; Semak I; Pisarchik A; Sweatman T; Szczesniewski A; Wortsman
TI -
J
Conversion of L-tryptophan to serotonin and melatonin in human melanoma
cells.
SO - FEBS Lett 2002 Jan 30;511(1-3):102-6
AD - Department of Pathology, University of Tennessee Health Science Center,
Memphis, TN 38163, USA. aslominski@utmem.edu
We showed in human melanoma cells tryptophan hydroxylase (TPH) and
hydroxyindole methyltransferase genes expression with the sequential
enzymatic activities of TPH, serotonin (Ser) N-acetyltransferase and
hydroxyindole methyltransferase. The presence of the products Ser,
5OH-tryptophan, N-acetylserotonin, melatonin (Mel), 5-methoxytryptamine
and 5-methoxytryptophol was documented by liquid chromatography-mass
spectrometry. Thus, human melanoma cells can synthesize and metabolize
Ser and Mel.
15
UI - 11550811
AU - Waldmann V; Wacker J; Deichmann M
TI -
Mutations of the activation-associated phosphorylation sites at codons
308 and 473 of protein kinase B are absent in human melanoma.
SO - Arch Dermatol Res 2001 Jul;293(7):368-72
AD - Department of Dermatology, University of Heidelberg, Germany.
16
UI - 11472999
AU - von Heydebreck A; Huber W; Poustka A; Vingron M
TI -
Identifying splits with clear separation: a new class discovery method
for gene expression data.
SO - Bioinformatics 2001;17 Suppl 1():S107-14
AD - Division of Computational Molecular Biology, Max-Planck-Institute for
Molecular Genetics, Ihnestr. 73, D-14195 Berlin, Germany.
heydebre@molgen.mpg.de
We present a new class discovery method for microarray gene expression
data. Based on a collection of gene expression profiles from different
tissue samples, the method searches for binary class distinctions in the
set of samples that show clear separation in the expression levels of
specific subsets of genes. Several mutually independent class
distinctions may be found, which is difficult to obtain from most
commonly used clustering algorithms. Each class distinction can be
biologically interpreted in terms of its supporting genes. The
mathematical characterization of the favored class distinctions is based
on statistical concepts. By analyzing three data sets from cancer gene
expression studies, we demonstrate that our method is able to detect
biologically relevant structures, for example cancer subtypes, in an
unsupervised fashion.
17
UI - 10922411
AU - Borg A; Sandberg T; Nilsson K; Johannsson O; Klinker M; Masback A;
TI -
Westerdahl J; Olsson H; Ingvar C
High frequency of multiple melanomas and breast and pancreas carcinomas
in CDKN2A mutation-positive melanoma families.
SO - J Natl Cancer Inst 2000 Aug 2;92(15):1260-6
AD - Department of Oncology, University Hospital, Lund, Sweden.
BACKGROUND:: Inherited mutations in the CDKN2A tumor suppressor gene,
which encodes the p16(INK4a) protein, and in the cyclin-dependent kinase
4 (CDK4) gene confer susceptibility to cutaneous malignant melanoma. We
analyzed families with two or more cases of melanoma for germline
mutations in CDKN2A and CDK4 to elucidate the contribution of these gene
defects to familial malignant melanoma and to the occurrence of other
cancer types. METHODS:: The entire CDKN2A coding region and exon 2 of
the CDK4 gene of an affected member of each of 52 families from southern
Sweden with at least two cases of melanoma in first- or second-degree
relatives were screened for mutations by use of polymerase chain
reaction-single-strand conformation polymorphism analysis. Statistical
tests were two-sided. RESULTS:: CDKN2A mutations were found in 10 (19%)
of the 52 families. Nine families carried an identical alteration
consisting of the insertion of arginine at position 113 of p16(INK4a),
and one carried a missense mutation, in which the valine at position 115
was replaced with a glycine. The 113insArg mutant p16(INK4a) was unable
to bind cdk4 and cdk6 in an in vitro binding assay. Six of the 113insArg
families had at least one member with multiple primary melanomas; the
113insArg families also had a high frequency of other malignancies-in
particular, breast cancer (a total of eight cases compared with the
expected 2.1; P =.0014) and pancreatic cancer (a total of six cases
compared with the expected 0.16; P<.0001). Families with breast cancer
also had a propensity for multiple melanomas in females, suggesting that
a sex-dependent factor may modify the phenotypic expression of CDKN2A
alterations. CONCLUSIONS:: Our findings confirm that the majority of
CDKN2A-associated melanoma families in Sweden are due to a single
founder mutation. They also show that families with the CDKN2A 113insArg
mutation have an increased risk not only of multiple melanomas and
pancreatic carcinoma but also of breast cancer.
18
UI - 11181786
AU - Plna K; Hemminki K
TI -
Re: High frequency of multiple melanomas and breast and pancreas
carcinomas in CDKN2A mutation-positive melanoma families.
SO - J Natl Cancer Inst 2001 Feb 21;93(4):323-5
19
UI - 11844511
AU - Shahbazi M; Pravica V; Nasreen N; Fakhoury H; Fryer AA; Strange RC;
TI -
Hutchinson PE; Osborne JE; Lear JT; Smith AG; Hutchinson IV
Association between functional polymorphism in EGF gene and malignant
melanoma.
SO - Lancet 2002 Feb 2;359(9304):397-401
AD - Immunology Research Group, School of Biological Sciences, Stopford
Building, University of Manchester, Manchester M13 9PT, UK.
BACKGROUND: Malignant melanoma, the most serious cutaneous malignancy,
has attracted substantial attention because of its rapidly increasing
incidence and the poor prognosis of some tumours. Little is known of the
genetic factors that mediate susceptibility to, and outcome of, sporadic
malignant melanoma. Because of its role in mitogenesis, which is
especially relevant to wound healing, tumorigenesis, and proliferation
of epidermal tissues, epidermal growth factor (EGF) is an attractive
candidate in which to look for genetic polymorphisms. METHODS: We
enrolled 135 white European patients with malignant melanoma and 99
healthy white European controls, and screened a selection of DNA samples
for polymorphisms in the promoter and 5' untranslated region of the EGF
gene by analysis. We then screened DNA samples from all participants for
the identified polymorphism by restriction-fragment-length polymorphism
(RFLP) analysis. In-vitro EGF production was measured in
peripheral-blood mononuclear cells from 34 controls, and the results
were compared with the individuals' EGF genotypes. FINDINGS: We
identified a single nucleotide substitution (G to A) at position 61 of
the EGF gene. Allele frequencies in the controls were 56% EGF 61*A and
44% EGF 61*G. Cells from individuals homozygous for the 61*A allele
produced significantly less EGF than cells from 61*G homozygotes
(p=0.0004) or heterozygous A/G individuals (p=0.001). Compared with the
A/A genotype, G/G was significantly associated with Breslow thickness
(p=0.045) and with risk of malignant melanoma (odds ratio 4.9 [95% CI
2.3-10.2], p<0.0001). INTERPRETATION: This study suggests that high EGF
production might be important in the development of malignant melanoma.
20
UI - 11850817
AU - Recio JA; Merlino G
TI -
Hepatocyte growth factor/scatter factor activates proliferation in
melanoma cells through p38 MAPK, ATF-2 and cyclin D1.
SO - Oncogene 2002 Feb 7;21(7):1000-8
AD - Laboratory of Molecular Biology, National Cancer Institute, National
Institutes of Health, Bethesda, MD 20892-4264, USA.
Members of the mitogen-activated protein kinase (MAPK) superfamily,
including p38 kinase and SAPK/JNK, play a central role in mediating
cellular response to environmental stress, growth factors and cytokines.
Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional
cytokine capable of eliciting mitogenic, motogenic and morphogenetic
activities in responsive cells, and has been implicated in tumor
development and metastasis. Binding of HGF/SF to its tyrosine kinase
receptor c-Met stimulates multiple signal transduction pathways, leading
to the activation of numerous transcription factors. We here report that
HGF/SF can induce cyclin D1 expression in mouse melanoma cells, and that
this up-regulation is mediated in part by the activating transcription
factor-2 (ATF-2). HGF/SF-mediated phosphorylation of ATF-2 was reduced
in the presence of either the p38 kinase-specific inhibitor SB203580, a
dominant negative p38 mutant, the SAPK/JNK inhibitor JNK-interacting
protein-1 (JIP-1), or the phosphatidylinositol 3-kinase (PI3K)-specific
inhibitor LY294002. Activation of p38 kinase by HGF/SF was partially
blocked by the PI3K-specific inhibitor as well. The upstream kinases for
p38, MKK3/6, did not become activated following HGF/SF exposure, and
ATF-2 activation was undiminished by transient transfection of a
dominant negative MKK6 mutant. However, transcriptional up-regulation of
cyclin D1 by HGF/SF was partially inhibited by the p38 kinase-specific
inhibitor, and cyclin D1 protein induction was partially blocked by a
dominant negative ATF-2 mutant. Notably, the p38 kinase-specific
inhibitor was able to block melanoma cell proliferation but not
motility. We conclude that the ATF-2 transcription factor becomes
activated by HGF/SF through p38 MAPK and SAPK/JNK. Moreover, the
p38-ATF-2 pathway can help mediate proliferation signals in tumor cells
through transcriptional activation of key cell cycle regulators.
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