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I

believe

the

future

of

screening

strategy

is

hidden

in

DNA. Cancer

is

a multifactorial disease

that

arises

from

the

complex

interplay

between

genetic

and

environmental

factors. Genetic polymorphism

is defined as

the presence of

different

allele

sequences

for

a

single

gene;

it

is

sometimes

linked

to

variations

in

the

expression of

constitutive DNA.

Susceptibility means an

increased

risk

conferred by one or

more polymorphisms (allele

types) of a given gene or genes

that

expose

the

individual,

family,

or

group

of

persons

(ethnic or geographic variations)

to

the genotoxic effects of

environmental

carcinogens.

Differences

in

the

ability

to

activate

carcinogens may

contribute

to host

susceptibility

and may

be

associated with

the

risk

of

BCa

and

RCC.

The

environmental

risk

factors

for

developing

BCa

and

RCC,

such

as

smoking,

are

common,

although

only

a

fraction

of

people

exposed

to

these

risks

eventually

develop

these

diseases.

Genomewide

association

studies

(GWASs) were

recently

performed

for

RCC

and

BCa

[11–15] .

The

GWAS

approach

allows

a

search

for

novel

susceptibility

loci

throughout

the

genome

in a hypothesis-freemanner.

In recent years, GWASs

have

emerged

as

a

powerful

approach

in

the

discovery

of

genetics underlying

complex

traits

such

as

cancer.

Diagnostic

tools

based

on DNA

alterations

and

that

can

provide high

specificity

and

sensitivity would

clearly

be

of

enormous benefit

to patients.

Screening

for RCC

and BCa

in

smokers

appears

to

be

too broad

of

a

strategy

in 2014,

and

the appropriate method

is not

to screen only highly exposed

patients

(tobacco)

but

to

screen

only

those

patients

(with

DNA

susceptibility) who are

likely

subsequently

to develop

the

disease.

Until

these

tests

are

available,

smoking

avoidance

and

smoking

cessation

are

the

two most

critical

and

realistic

policies

to

promote

in

2014.

Preventing

BCa

and

RCC

is

certainly

the

most

important

approach

to

reduce

their

incidences

and

patient

mortality.

Therefore,

the

World

Urologic

Oncology

Federation

has

initiated

the

Global

Bladder

Cancer

Prevention

Program

with

the

goal

of

integrating

smoking

cessation

into

urologic

practices

as

a

primary

prevention.

Conflicts

of

interest:

The

author

has

nothing

to

disclose.

References

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[2]

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[3]

Ljungberg B, Cowan NC, Hanbury DC, et al. EAU guidelines on renal cell carcinoma: the 2010 update. Eur Urol 2010;58:398–406

.

[4]

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[5]

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[6]

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[9]

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[10]

Krabbe LM, Svatek RS, Shariat SF, Messing E, Lotan Y. Bladder cancer risk: use of the PLCO and NLST to identify a suitable screening cohort. Urol Oncol 2015;33:65.e19–e25

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[11]

Audenet F, Cancel-Tassin G, Bigot P, et al. Germline genetic varia- tions at 11q13 and 12p11 locus modulate age at onset for renal cell carcinoma. J Urol 2014;191:487–92

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[12]

Fu YP, Kohaar I, Moore LE, et al. The 19q12 bladder cancer GWAS signal: association with cyclin E function and aggressive disease. Cancer Res 2014;74:5808–18.

[13]

Purdue MP, Johansson M, Zelenika D, et al. Genome-wide associa- tion study of renal cell carcinoma identifies two susceptibility loci on 2p21 and 11q13.3. Nat Genet 2011;43:60–5.

[14]

Rothman N, Garcia-Closas M, Chatterjee N, et al. A multi-stage genome-wide association study of bladder cancer identifies multi- ple susceptibility loci. Nat Genet 2010;42:978–84.

[15]

Wu X, Scelo G, Purdue MP, et al. A genome-wide association study identifies a novel susceptibility locus for renal cell carcinoma on 12p11.23. Hum Mol Genet 2012;21:456–62.

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