Microscopic description:

In this case, proliferation of prostate carcinoma cells are expanding the prostatic ducts and acini and exhibiting irregular and branching contours. This expansion is forming cribriform to trabecular architecture. Some nuclei are pleomorphic with prominent nucleoli. Comedonecrosis is also present. P63 and HMWK highlight the preservation of the basal cells (brown), and AMACR highlights the inner carcinoma cells (pink).

Intraductal carcinoma of the prostate (IDC-P) can display trabecular, loose cribriform, dense cribriform, and solid architecture. This is due to progressive dedifferentiation with a reciprocal increase in proliferation. Neoplastic cells are usually pleomorphic with some 6 times larger than adjacent non-neoplastic nuclei. However, they sometimes have low grade morphology with small and regular glandular contour and uniform nuclei and, therefore, are difficult to distinguish from HGPIN glands. Between HGPIN and IDC-P, comedonecrosis is diagnostic of IDC-P, but it is not seen in all cases. IDC-P should be differentiated from HGPIN by its pronounced cytological atypia, nuclear pleomorphism, and cribriforming or solid architecture.

Table describing Intraductal carcinoma findings
Discussion:

Intraductal carcinoma of the prostate (IDC-P) is uncommon in prostate biopsies. In one study, the incidence was 10.6% (33/312 biopsies) of cancer-containing prostate biopsies. Studies have also shown that IDC-P is strongly associated with aggressive, high grade, typically Gleason grades 4/5, and high volume invasive prostate carcinoma as well as greater probability of extra-prostatic extension, seminal vesicle invasion, and pelvic lymph node metastasis.2,3 A diagnosis of IDC-P in a biopsy mandates an immediate repeat biopsy or definitive therapy even in the absence of documented invasive prostate carcinoma. Consequently, it is important to distinguish it from HGPIN.

Any lumen-spanning lesion comprising cytologically atypical cells that do not satisfy the diagnostic criteria for IDC-P but that exceed the criteria for HGPIN should be reported as ‘atypical intraductal proliferation’, with a recommendation for an immediate repeat biopsy because it may represent IDC-P and carries significantly elevated risk of finding cancer in repeat biopsies.2

Of note, Dawkins et al. studied the loss of heterozygosity (LOH) in prostate carcinoma and IDC-P and found that 60% of IDC-P showed genetic changes seen in prostate carcinoma with Gleason pattern 4/5.4

References:

Robinson B, Magi-Galluzzi C, Zhou M. Intraductal carcinoma of the prostate. Arch Pathol Lab Med 2012; 136: 418–25.

Zhou M. Intraductal carcinoma of the prostate: the whole story. Pathology. 2013 Oct;45(6):533-9. doi: 10.1097/PAT.0b013e3283653322. PMID: 24018805.

Rubin MA, de La Taille A, Bagiella E, Olsson CA, O'Toole KM. Cribriform carcinoma of the prostate and cribriform prostatic intraepithelial neoplasia: incidence and clinical implications. Am J Surg Pathol. 1998 Jul;22(7):840-8. doi: 10.1097/00000478-199807000-00006. PMID: 9669346.

Dawkins HJ, Sellner LN, Turbett GR, et al. Distinction between intraductal carcinoma of the prostate (IDC-P), high-grade dysplasia (PIN), and invasive prostatic adenocarcinoma, using molecular markers of cancer progression. Prostate 2000; 44: 265–70.

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