JSfD Abstracts 13. Dermatol. Sci. 8 (1994) 54-88
145
148
E-cadherin associated
expression in malignant with tumor progression
Himaki Eguchi and Takashi Medkal Unhwsiiy
Horlkoshi,
E-cadherln (E-CD), a Ca*‘-dspendent the maintenance
of in&cellular
immunohiiochemically monocbnal expressbn
adhesion
HECD-1.
In primary
67% of tumor
(11 .l%) or intracellularly
lesbn
pallem
analyzed
melanoma
using
a
70% of tumor (33%). The
to dermis. In me&static
for E-CD,
expressing
potency
ether
melanomas. the
In me&static
of E-CD expressbn
the loss of adhesion
decwassd
of tumor
by
~~118. The
cells of the nest of LN was mom than that of oiher or@ans and the
intmcelblar
pattern was dominant
of E-CD expmssbn nwastauc
Thesedata suggest that
in the nesl of LN.
m@ht be an initlll
ESTABLISHMENT AND CHAWCI7%IZATION OF HTLV-lPOSITIVE B-CELL LINES, MTB-1 AND TJA T. Nagatani, T. Nishiyama, M. Miyazawa, T. Mat&, N. Baba, H. Nakajima. Department of Dermatology, Yokohama City University School of Medicine, Yokohama 236, Japan
plays a ma@r role in
(37%) or intracellularfy
(55.4%).
is
Sapporo
of E-CD was
of melanomas,
cells w8re posltiie
of calls wllh the intercellular
poslilve
molecules,
celfa deeply invadiw
melanomas,
25%. su~@esting
of Denatobgy,
of malignant
E-CD either lntercalkdariy
of E-CD was wakeron
melanoma
The expressbn
secllons
intsroellularly number
Department
junctions.
on tissue
antbob/
cells expressed
about
loss
event in ihe invasion and proliferation
of
melanomas.
New cell lines, designated MTB-1 and TJA, were established from peripheral blood lymphocytes of patients with cutaneous B-ceII lymphoms and acute-type adult T-cell leukemIwlymphoma, respectively. MTB-1 cell Linewas positive for CD19, CD20, HLA-DR, surface IgG and surface K light chain and negative for CD3, CD4, CD10 and CD13. TJA cell line was positive for CD19, CD20 and HLA-DR, but negative for surface immunoglobulin, CD3, CD4, CD10 and CD13. MonockmaI integration of HTLV-1 p&ml DNA was detected in both MTB-1 and TJA cell lines by southern blot analysis. ClonaI marrangement of the immunogIobuIin heavy chain gcnc was also detected in both ceII lines by southern blot analysis. However, clonal rearrangement of the Tcell antigen receptor gene was not detected in both cell lines.
146
149
INDUCTION OF INTERCELLULAR ADHESION MOLECULE-1 EXPRESSION IN HUMAN MEIANOMA CELL LINES BY HYPERTHERMIA IN VITRO AND IN WV0
SCL-2
GENE
EXPRESSION
C. KIYOKAWA.
M. MORITA.
Three human melanoma rr&wle
(lCAM)-l
in dvo.
cell lirws were invesQated
expression
wheter intercellular
adhesion
ICAM-
immunoassay. antibody.
into the medium
was quantified
Also, the cells were stained
by a double
morwlOnal
into the nude mouse skins and heating the melamma nodUles by mlcrOwaVe hypeflhemia at 43’(: for 15 min. The results ware that all three cell lines increased shedding of ICAMwilh temperature dependent manner. The Cells treated with 41 C or 43C were clearly slained with the ardlbocly. The melanoma nests were sporadicalty
stained with the antibody after microwave
Thus, it was concluded
that hyperlhermia
lwman
melanoma
can induce ICAM-
hyperlhermia.
expression
in the
CUTANEOUS
of Dennatolc#.
0.
MORI.
Kurume
H. HACHISUKA
Un’k?ere@ school
and
Y.
SASAI.
of Me&iw,
Kucume,
Japan
cutaneous disease
lumors
indud@
sebonlwlc
by immunahemical
was irmwnohfstoche~ cellsof
SCCand
was detected
stained
SCE.
Using
in
SCE. SCC. hybm.
basal cells of normal
in situ hybridiution,
inhlbftiw
and Paget’s bd-2
mRNA
in basal cells of normal skin md tumor Mile.
showed that in situ hybrl&albn acts as ti
kemtoels,
staining and in sihr
of
bd-2
swtlng
is more sensitive tJ?an y.
of epidermal
cell apopbsll.
m
skin and tumor gene lntenefty bcl-2
The expression
of bcl-2
in
tumor calls ls related rrim the degree of malignancy.
150
VIDEO
WCROSCOPlC
MALlGluNT
DIFFERENTIAL
DIAOIOSIS
NELANOUA AND BENIGN YELANOCVTIC
‘DBpt.of
Dem..
*Division
of
Correct important
Shinrhu Univ. Sch. Dorm. Hokushin Gsnsral
diagnosis of early for improrwaent
cr~scop~.an
slectronic
ws analyzed compared
the
navy6 including roscopic faaturss patterns black
dots.
findings
random
oftan
al streaming. and on ingr ware preferentially vus usually exhibited gin faded out evsnly. of video macrw.cope in
of
with
dysplastic detected and
that
features
can
those
of
of with
P53
T. and Japan
GENE MUTATrCNS
y1
in
benign
brown
lesions. situ
mslanocytic video irregular
macpi-
globules
pseudopods
and
radi-
the
sole. the ridges of the skin aarkpigmmsnted. In contrast. benign neorderly pigment pattarns and ths mar-
These findings support the clinical diagnosis
of
KANEKURA
Kagoshlma
is highly video ma-
skin
of
Characteristic in situ mare
distribution
accompanied
magnify
6 lesions
news. in Nkl
EARLY
Y.ISHIHARA’, of Ysd., Yatrvmeto Hospital.Nakano.
malignant melanoma(kN) of the prognosis. Using
device
magnified
BETWEEN
IN HUMAN SKIN CANCERS
NEVUS
S.DGUCHI’.S.OHKUBO’,S.KAWACHI’.T.SAIDA’,snd
and
AND
cells both in vim and in viva.
147
gent
SKIN
We~edthebcl-2OeneexpressiMlinbjssuesectionsfrwnno~skinand
determinant
with an antl-ICAM-
in viw counier parl study was conducted by inoculating the cells
The
NORMAL
is induced by hyperlhelhenia both b virroand
Cells were lncuhated al 37C, 41 C. and 43C for 3 or 6 hr. and the
shedded
OF
TUMORS
Department
and
79
ths usefulness sarty YI.
and
University
T.
KANZAKI,
Faculty
Deparfment
of Hedlclne,
of
Dermatology,
Kagoshlma,
Japan
Mutations ,n ~53, a twn”r supressor gene, are one of the mosf common genet:c lesions ,n human cancers. In this study, mrmtatlons III exons 5 to 9 of the ~53 gene were screened I,, 4 squanous cell carcinomas (SCCs) of the skin 1 lesion which arose from xar due to burn, I from epldermodysplasla verruciformis, and 2 from actlnlc keratosls -and B basal cell carc~noinas (BCCs) --5 spontaneous lesions, 1 from organold nevus, ’ from xerodetma pignentosum, and I from basal cell nev~s -yndrome -by polymerase chain reactionsingle strand cor.formatlon polymorphism analysis. nutatlon of ~53 gene was detected in only I caseulth XC uhlch a~ose from actlnlc keratosls. The lncldence of the ~53 gene mutation ln this study is tower than those in previous literature. This flndlng lirplles that p53 mstaf,ons do not necessarily contrlbllte to the tumorlgenesis of skin cancers, especially those provoked by genoderaatosls.