EURURO Vol. 72 No. 4

Platinum Priority – Editorial

Referring to the article published on pp. 492–495 of this issue

Intraductal Carcinoma of the Prostate: Anonymous to Ominous

Melvin L.K. Chua

a , b ,

Theodorus H. van der Kwast

c ,

Robert G. Bristow

d , e , *

Division of Radiation Oncology, National Cancer Centre, Singapore;

Duke-NUS Graduate Medical School, Singapore;

Laboratory Medicine Program,

University Health Network, Toronto, Canada;

Radiation Medicine Program, Princess Margaret Cancer Center, University Health Network, Toronto, Canada;

Departments of Radiation Oncology and Medical Biophysics, University of Toronto, Toronto, Canada

Over the past decades, the term

intraductal carcinoma (IDC)

of the prostate gland

has transitioned from a period when it

described solely a distinct histomorphological entity

without significance, to the present era, in which the

occurrence of IDC in a prostate cancer independently

portends unfavorable prognosis. Historically, the first use of

IDC in the context of prostate cancer dates back to a

publication in 1973 describing the spread of carcinoma cells

of urothelial or prostate origin into antecedent benign

prostatic ducts

[1]

. The terminology was subsequently

refined in 1985 by Joseph Kovi and colleagues to specifically

annotate ductal spread of a prostatic adenocarcinoma

[2,3]

. The later adoption of high-grade prostatic intrae-

pithelial neoplasia (HG-PIN; as coined by Bostwick and

Brawer) led to the consideration of all intraglandular and

intraductal neoplastic proliferations as a single entity

[4] .

a result, IDC was dismissed into anonymity. Rightfully, IDC

is now acknowledged as being distinct from other

intraglandular lesions, and with the standardization of

histopathological diagnostic criteria for IDC, there is again

re-emergence of clinical evidence supporting the aggres-

sion of prostate cancers harboring this subpathology

[2,5]

It is therefore timely that this issue of

European Urology

includes a report by Porter et al

[6]

on the frequency of IDC

in a large database comprising several published series that

were screened and analyzed in a systemic review. Their

analysis revealed that IDC incidence is strongly associated

with increasing National Comprehensive Cancer Network

(NCCN) risk classes: 2.1% for low risk, 23.1% for intermedi-

ate risk, 36.7% for high risk, and 56.0% for metastatic disease.

Detection of IDC was also seemingly lower in biopsy than in

prostatectomy specimens (13.7% vs 31.1%); this is probably

because of undersampling bias. The limited material from a

biopsy would also preclude an accurate survey of the

subpathology extent within the tumor. Thus, future work

should be directed towards investigating the utility of

detecting IDC in diagnostic biopsies, and if prognostic

power is lower with this approach.

The analysis by Porter and colleagues is important as

alternative resources such as population-based National

Cancer Data Base and Surveillance, Epidemiology, and End

Results registries will not provide reliable estimates on the

prevalence of IDC given that it is currently under-reported

by pathologists. The reasons for this under-reporting

include: (1) difficulty in morphologically distinguishing

IDC from cribriform-type Gleason grade 4 prostate cancer

(exemplified by the presence of a rim of basal cells in IDC,

which often requires immunostaining for correct identifi-

cation;

Fig. 1

A); (2) confusion between IDC and another rare

variant, ductal adenocarcinoma; and (3) initial non-

requirement of pathologists to report on this subpathology,

which is now a requirement recommended in the 2017 Eu-

ropean Association for Urology (EAU) guidelines

[7]

. It is

possible that these caveats apply to the data analyzed by

Porter et al, given the wide ranges for IDC frequency (10–

40% in biopsies and 20–60% in prostatectomies in the

intermediate-risk subgroup) and the fact that accompa-

nying data on quality measures of pathology reporting such

as central review and immunostaining of basal cells for

consistency of IDC identification are lacking in this

systematic review.

While the association between IDC and higher NCCN risk

categories observed suggests that IDC may be a surrogate

for disease severity, this alone does not justify the separate

E U R O P E A N U R O L O G Y 7 2 ( 2 0 1 7 ) 4 9 6 – 4 9 8

available at

www.scienced irect.com

journal homepage:

www.europeanurology.com

DOI of original article:

http://dx.doi.org/10.1016/j.eururo.2017.03.013

* Corresponding author. Radiation Medicine Program, Princess Margaret Cancer Centre and Departments of Medical Biophysics and Radiation

Oncology, University of Toronto, 610 University Avenue, Toronto M5G 2M9, Canada. Tel. +1 416 9462936; Fax: +1 416 9464442.

E-mail address:

rob.bristow@rmp.uhn.on.ca

(R.G. Bristow).

http://dx.doi.org/10.1016/j.eururo.2017.04.004

0302-2838/