Autocrine function for insulin-like growth factor I in human small cell lung cancer cell lines and fresh tumor cells

183

have the same risk of lung cancer the literature.

toms and abnormal

lung X-rays

non-smokers,

some

compared

and

cxsmokers.

should

are more

when

persons

with and without

chat the risk

of

cancer

co persons

constdered

the risk of lung

cancer.

with

smoking.

studies

may

conclusrons

have

can

evaluaccd.

risk

studies

are needed

Guscavsson

P, Plato

Occupar~onal

Mcdicme, Environ

Morcahcy garage

workers

workers but

Hogstedt

S-104

01 Stockholm.

was investigated

as mechanics,

among

servicemen,

cohort,

occupationally

six referents

between

selected

exposure

from

matched

exposure

show gous

deficrc

decermmed cation

a third

sion

established.

The

for at

1945 and

was estimated

by

with

a research

pathway

Tnzvarl Arch

Mal

Prof Med

The findmg exposed

CO dusts

professional fibrosis With

Macaulay

VM,

of

origm.

Sccur

hard

cumulative

exposure

asbestos exposure. Thescudy

the risk for lung

to

The relative

was2.4(95%CI

detectable

reference

chat might

indicates

in small

SCLC

cell Imes: HCl2, HC12

survey

in a cohort

higher

mortality

compounds

of workers

cxposcd

cpldemiological

mcreased

risk of bronchogcmc

ones,

about

du

Cedex.

a cause

of

authors.

we recall

and epidemiological

the

grounds,

role of cobalt

powder

or

mutagenous

effects.

A

has shown

carcinoma.

are necessary

growth

a relatively

Other

studies.

co asset or not

m subjects

cxposcd

was no response ‘“I-IGF-I

ancrbody.

?H]thymidine cultured

tumor

the

lion

was inhibited IGF-I,

stimulated ,208,

and cobalt.

SM1.25,

the findings

function

as an aucocrine

All

were

control

mamfesc

in

and growth

SCLC

of metastases with

cells,

studies factor

scrmula-

of recombmant basal

and IGF-I-

monoclonal

antibodies

control.

and suggest

in SCLC

in

IGF-

and specific

showed

m the presence by

SCLC.

cells,

seven samples

hut not the isocyplc

growth

(SM1.20B.

These results that IGF-I

in wro

can

and possibly

Decreased accumulation as a mechanism of resistance to cisdiamminedichloroplatinom(I1) in human non-small cell lung cancer cell lines: Relation to DNA damage and repair Bungo

M,

National

Fujiwara

Cancer 104 Cancer

The mechanism (CDDP)

in CDDP-resistant 7. l-fold

F. Dalphm

J-C, De Palmas

menu de

Medecine du Travail,

avenue

de C’erdun,

94010

J, Duchec J.-C, Brochard

Cenue

Crefeil

llospitolier

Cedex.

Arch

P. Deport-

Inrercommunal, Ma1 Prof

Med

40, Trav

1990;51:11-6. 1s the main etlological occupational

factor

of bronchopulmonary

and more particularly

genetic,

cancer intervene

Y,

Kasahara

K et al. Pharmacology

Division,

Center

Research

Instirule,

Chum-ku,

been proposed.

of resistance

human

([CL),

repair,

intracellular

non-small

one kind

several cell

frequency

of CDDP-induced and the amount

of DNA ICL

lung

damage

cancer

by

means

accumulacionofCDDPbymeansofacomicabsorpcion

cells

of DNA induced

of CDDP.

of intracellular

of processes

of CDDP

the formation

accumulation

technique

kinds

of the mechanism

we examined

cross-links and

Tsukiji,

co cis-diammmedlchloro-platioum(I1)

although

For elucidatron

resistant),

S-I-I

Res 1990;50:2549-53.

is still controversial,

Pill&e

hut ocher factors,

co IGF-I

also m viva.

Research ofageneticpredisposition toprimary bronchopulmonary cancer by the study of debrisoquine hydroxylation phenotype

Sot

and IGF-I-scmudaced

patients

Inhibited

of prewous

in cell

due co endogenous

conditions

As in cultured was

and aIR,

confirm

Tokyo

Tobacco

@ml.

synthesis

ICR-SC17

mcrease

asprration

on fresh

incorporation

100-500

DNA

n

was

We also tested fresh or newly

and four relapsed

I .2OB.

3 nM,

but not an isotypic

by fine needle

by SM

of [‘Hlthymidine

human SMI

untreated

(K(d)

@ml. by

effects

cultures.

greater

mcorporatron

amities

assays m serum-free

sites were demonstrable

binding

and basal

Anclprohferacrve liquid

but not ICR-

and lower

probably

aIR,

Immunoreac-

lOO-fold

100-1000

m HC12,

in tn 2

two classes of IGF-I

as measured

receptor

cells obtained

three prewously

with

[?H]thymidine

bindmg

incorporation

variant.

revealed

IGF-I,

syncbeus of IGF-I

by HC12

IGF-I

by monoclonal

.25) or the type J IGF

DNA

IS

and cell

co hard

Basic biology

Sew

human

I (IGF-I)

bropsles

on the role

n = 2,300)

enhancement

were inhibited

monoclonal

bound

lmes

factor

stimulates

condrcioned

0.1 nM,

of Medicine Re-

15, CotswoldRoad,

tumor

studies

analysis

In both cell

production.

I binding

of pulmonary

carcinoma,

co cobalt

carcmoma

IS

I l-7.

and ICR-SC17,

Scatchard

by recombmanc There

IGF-I

and ICR-SC17

enhanced

SMI

m workers

by numerous

have

race due CO bronchogenic

particularly metals

chmcal

better

hydrocarbons,

growth

(SCLC)

further

classic;

affinity.

numbers.

human

in medium

= 28,000)

showed

cancer

we report

was detected

Research.

Res 1990;50:25

lung

of serum-supplemented

in the pachogenesis

of bronchogenic

cobalt

Here

Both

IGF-I

Tours

carcmoma

us co drink

lead us COsuspect the carcinogenous

In VIUO, some

cell

cells.

that

de Medecine

37032

is now acknowledge

based on expenmencal,

has been

markers,

aromatic

chat insulin-like

lines and that recombinant

also

1990;51:323-5.

The role of cobalt

co a cast

Cancer

SCLC

1.3-

cancer.

B et al. Insrirut

led

expres-

cancer

JD et al. Section

of Cancer

previously

site of high (K(d)

Sot

no modifi-

phenotyprc

bronchtal

17

hasbeen

of chc tumor:

pharmacogenetlc

MJ, Teale

bmding

Increasing

de Medecine,

metals

Everard

search Loboralories.Inai~ute

for each of the 20 lung cancer cases.

cases of bronchogenrc

due Co hard metals

arguments, salts.

Trav

of isolated

versus

Autocrine function for insulin-like growth factor I in human small cell lung cancer cell lines and fresh tumor cells

than insulm.

lowcxposure.

Facui~e

K.B.P.

between

of polycychc

of

for the future.

affimty

study was performed

P, Rosmorduc

du Val-de&we,

of different

study

(W&I an homozy-

K.B.P.,P.H.D.B.

cxeresis and

occupa-

of this

of the phenotypes

among

with

No relaclon

the metabolism

the

men in Stockholm

Exposition to hard metal’s dusts and bronchogenic carcinoma G, Catclau

study

correlated

(B.P.C.O.),

results

mecaboliLers

hydroxylalion

within

mcrcascs

slow

time after surgical

of debrisoquine

The

hydroxylacion)

was found.

and 200 subjects

and caking intoaccount

For 14patlcncs

of P.H.D.B.

in a case-control

B.P.K.

in the reparcitlon

in debrtscquine

(8,5%)amongB.P.C.O.

cancer

debrisoquine

bronchopneumopathy

11(5.9%)

these two populations:

from

carcmogens,

difference

risk,

has been studied

smoking,

CO respiratory

no significant

of genetic

suffering

chronic

by age, sex, tobacco

mttogenesis

Lasfargues

obstructive

of bronchopulmonary

factor

(P.H.D.B.)

SC17.

with

with chose with exhaust

suffermg

this

188 subjects

were used

but not with cumulative

co dicscl

concerning

live IGF-I

rirkforlungcanccramongchchtghlycxposedmcn 4.5)ascompared

phenotype

survey,

tional

in the genesis

was found

active

The lung cancer risk mcreascd diesel exhaust,

and asbestos

A case-referent

being

hydroxylation

SM2 SNG Belmonr.

the 695 bus

or hostlers

in Stockholm

cxhausc

manner

So as co specify

We showed

A small excess of lungcancermorcalrCy

group.

of

C. Depar~mem

co diesel

as the reference

not

(K.B.P.).

cancer.

1970. The exposure when

wore

the mcerrelacionships

industrial

in the cohort

with

no defimce

relations

IIospital.

in five bus garages

hygreniscs.

of

in non negligible

1990;16:348-54.

mcrdencc

employed

least six months

E-B,

Karolinskn Health

and cancer

prevalence

cancer,

co evaluate

on

to diesel exhaust among bus garage

N, Lidstrom

Stand

I Work

lung

also

risk of lung cancer

higher

dose-response

and the risk of lung

Lung cancer and exposure workers

asbestosis exposure

chat asbestos

of

since

asbestosis

and asbestos

co their

suggested

a higher

with

show

but none of these studies

due

be drawn

Furchcr

of smoking,

have

the risk of lung

Some studies

chat the hrgher

IS only

or

oflungcancer.

persons

of smoking

It is unlikely

asbestosis

Some

asbescosls

&estosis,

effects

than

asbestosis

CObe smokers

evaluating

for

in

symp-

smokers

with

likeky

asbestosis.

is hlghcr

without

chc combined

CO persons

among

hasa large affccc on the risks

cancer among compared

addressed

that clinical

chat workers

are more

be consrdered

lung

indicate frequent

show

asbestow

Since smoking habits

workers

scudics

co those without

smoking

has not been adequately

Scudces of asbestos

(PC-9/0.5, interstrand

by CDDP,

its

measured

the

We

of the alkaline

platinum

have

resrstance

for

eluclon

intracellular

speccrophotome-