EURURO Vol. 72 No. 4

495 656

genomic profiling of BRCA2-mutant prostate cancers
demonstrated that IDC-P is associated with genomic
alterations portending poor prognosis . This may
contribute to the aggressive clinical progression of
BRCA2-mutant prostate cancers that contain IDC-P How-
ever, further studies are warranted to investigate the
functional significance of IDC-P.
While uncommon, the clinical significance of IDC-P in
the setting of low-grade disease should also be considered.
Identification of even low-volume IDC-P on prostate biopsy
may signal aggressiveness, even in the absence of high-
grade carcinoma Thus, the presence of IDC-P on prostate
biopsy has been suggested as an exclusion criterion for
active surveillance .
A limitation of this study was the variability in reporting
of IDC-P. First, the prevalence of IDC-P may be under-
reported in biopsy specimens because of incomplete
sampling. Second, different diagnostic criteria were used.
The criteria most commonly used were those proposed by
Guo and Epstein and McNeal et al however, many
studies used a combination of published criteria or listed
their own (Supplementary Table 1). Different criteria or
interpretations can influence IDC-P diagnosis and thus
may have affected the reporting of IDC-P. Furthermore, the
diagnostic criteria for IDC-P include a spectrum of
morphological features, as well as variants such as isolated
and ‘‘precursor’’ IDC-P. The significance of these variants
was not evaluated because of limited data on individual
IDC-P characteristics. Further work is required to standard-
ise IDC-P diagnostic criteria to ensure consistent diagnosis
and to consider the significance of distinct IDC-P features.
In conclusion, this study demonstrates a striking
association between IDC-P prevalence and aggressiveness
of prostate cancer. While IDC-P is rare in low-risk patient
cohorts, as the risk of poor outcome increases, so does the
prevalence of IDC-P. Greater awareness and reporting of
IDC-P may improve risk stratification and clinical manage-
ment of patients with prostate cancer.
Author contributions: Renea A. Taylor had full access to
all the data in the study and takes responsibility for the
integrity of the data and the accuracy of the data analysis.
Study concept and design: Porter, Lawrence, Clouston, Murphy, Pezaro,
Risbridger, Taylor.
Acquisition of data: Porter, Lawrence, Ilic, Pezaro, Risbridger, Taylor.
Analysis and interpretation of data: Porter, Lawrence, Ilic, Pezaro,
Risbridger, Taylor.
Drafting of the manuscript: Porter, Lawrence, Ilic, Pezaro, Risbridger,
Taylor.
Critical revision of the manuscript for important intellectual content: Porter,
Lawrence, Ilic, Clouston[3_TD$DIFF], Bolton, Frydenberg, Murphy, Pezaro, Risbridger,
Taylor.
Statistical analysis: Porter, Lawrence, Ilic.
Obtaining funding: Lawrence, Pezaro, Risbridger, Taylor.
Administrative, technical, or material support: Clouston[3_TD$DIFF], Bolton, Fryden-
berg, Murphy.
Supervision: Lawrence, Pezaro, Risbridger, Taylor.
Other: None.
Financial disclosures: Renea A. Taylor certifies that all conflicts of
interest, including specific financial interests and relationships and
affiliations relevant to the subject matter or materials discussed in the
manuscript (eg, employment/affiliation, grants or funding, consultan-
cies, honoraria, stock ownership or options, expert testimony, royalties,
or patents filed, received, or pending), are the following: None.
Funding/Support and role of the sponsor: This work was supported by
funding from the National Health and Medical Research Council of
Australia (fellowship 1035721 to M.G.L., fellowship 1102752 to G.P.R.,
project grant 1077799), the Victorian Cancer Agency (fellowship
MCRF15023 to R.A.T., CAPTIV programme)[4_TD$DIFF], the Peter and Lyndy White
Foundation, and the EJ Whitten Foundation. The sponsors played a role
in the design and conduct of the study.
Appendix A. Supplementary data
Supplementary data associated with this article can be
found, in the online version, at
.
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