Surgical Pathology Review: easing the transitions

February 2021—New from CAP Publications is Surgical Pathology Review, by Daniel D. Mais, MD, associate professor of pathology, Department of Pathology, University of Texas Long School of Medicine, San Antonio. He and 14 other contributors wrote this book to ease the transition through board exams and into practice, Dr. Mais writes in the preface. Here is what he told CAP TODAY about the book. (The section on epithelial proliferative lesions in the chapter on breast begins below.)

You write in your preface that this book is intended to fill a gap. Can you explain what that gap is?
The available textbooks are of two main types. First, there are some whose purpose is to teach basic concepts in pathology to medical students. The second type is intended to be used by practicing pathologists engaged in diagnostic work. But these two are like circles in a Venn diagram that do not overlap. There is a knowledge set that is beyond the scope of the first type of book and perhaps considered of insufficient practical import for the second. It is this set of knowledge that we thought deserved a textbook.

You also write that some web-based resources are excellent but that in your view a book with a beginning and end is better for the learner in pathology. How so?
The unstated premise is that it is important to have a finite set of facts about which one is certain, to serve as anchors in contextualizing the universe of other facts and conjecture. The bottomlessness of the internet can at times prove very useful in accessing the latter. One of our tasks as educators is to delimit a set of what we consider essential knowledge, as prerequisites for the acquisition of additional knowledge.

How is your book organized and who is your intended audience?
The book is intended for pathologists, at any level of experience but particularly those near the end of training, who seek a once-over review. It is organized in the traditional way, organ by organ. The only exception is the final chapter, titled “Special Topics,” which includes a variety of things applicable throughout. We broke each entity considered into subsections, including its context, clinical findings, prototypical morphologic findings, special studies, and treatment and prognosis.

What can you tell us about the other 14 contributors?
Essential to a project like this is a group of people who share a vision and remain committed until realizing it. In this regard I was grateful to have the help of several colleagues, each having unique subspecialty expertise. Most of them are UT faculty, who provided either original contributions or expert review in ENT pathology (Gab­riela Gonzalez), GI pathology (Gonzalez), pancreatic pathology (Gonzalez), liver (Adam Booth), breast (Alia Nazarullah), gynecologic (Philip Valente, Abby Richmond), genitourinary (Richmond), medical renal (Yanli Ding), lung (Sarah Hackman), mediastinum (Hackman, Douglas Warden), skin (Olaoluwa Bode-Omoleye), bone and soft tissue (Josefine Heim-Hall), CNS (Andrea Gilbert), and lymph nodes and spleen (Nazarullah).

Here, from the newly released Surgical Pathology Review, is the section on epithelial proliferative lesions in the chapter on breast. Other sections in that chapter are fibrocystic lesions, benign tumors, papillary lesions, invasive carcinoma, biphasic tumors and stromal tumors, and infectious and inflammatory disorders.

To order (PUB130), call 800-323-4040 option 1 or go to www.cap.org (Shop tab) ($100 for members, $125 for others). For the ebook ($95), go to ebooks.cap.org. If you are interested in writing a book, contact Caryn Tursky at ctursky@cap.org.

Breast: Epithelial proliferative lesions
Usual ductal hyperplasia (UDH)

Context

• UDH is a benign intraductal proliferation of hyperplastic, nonneoplastic, ductal epithelial cells.
• A distinction is often made between mild UDH, which has the risk profile of nonproliferative breast lesions, and moderate to florid UDH, which are associated with a slightly (1.5–2×) increased risk of breast carcinoma.

Clinical findings

• Usually occurs as an incidental finding within fibrocystic changes or other benign lesions.

Prototypical morphology

• UDH is identified when the ductal epithelium exceeds the normal one- to two-cell thickness, after accounting for tangential sectioning and other artifacts.
• Mild UDH is present when the ductal epithelium is up to four cells thick; on the other end of the spectrum, florid UDH fills duct lumens, while moderate UDH is between these extremes.
• The essential features of UDH, in contrast to DCIS and ADH, include cellular heterogeneity and architectural disorganization.
• The hyperplastic cellular population is cytologically heterogeneous and haphazardly arranged, with irregular cell spacing; the effect of this unevenness is luminal structures with rough, wavy borders and elongated, slit-like spaces (Figure 5-7).
• These slit-like spaces are typically found at the periphery of the duct lumen, with intervening epithelial “bridges” that are tapered rather than stout.
• Micropapillary UDH usually has broad-based elongated micropapillae with tapering ends (unlike ADH, which has narrow-based, short, bulbous micropapillae).
• The epithelium may appear spindled and “streaming,” particularly in “bridges” between adjacent spaces where the cells are generally aligned parallel to the lumen and may lay flat against it.
• Individual ductal epithelial cell nuclei are oval and frequently grooved. They have pale dispersed chromatin and small indistinct nucleoli.

Special studies

• CK5 (or other basal keratins) and CK8/18 (luminal keratins) show a mosaic pattern of expression—a reflection of cellular heterogeneity—in contrast to low-grade DCIS and ADH, which are uniformly negative.
• Similarly, ER shows patchy and variable positivity in UDH, in contrast to strong and diffuse expression in ADH and low-grade DCIS.

Treatment and prognosis

• These are benign lesions.
• Aside from mild UDH, there is a 1.5–2× risk for subsequent breast cancer (similar to other proliferative lesions without atypia).

Flat epithelial atypia (FEA)

Context

• Nonobligate precursor lesion, clonally related to low-grade DCIS and tubular carcinoma, a relationship manifested in Rosen’s triad (association of flat epithelial atypia, lobular neoplasia, and tubular carcinoma).

Clinical findings

• FEA often presents as an incidental finding or as mammographic microcalcifications.

Prototypical morphology

• There are expanded terminal duct-lobular units in a pattern similar to blunt duct adenosis/columnar cell alteration; however, the luminal spaces tend to be more rigid and round.
• As in blunt duct adenosis/columnar cell alteration, the cells may be columnar or cuboidal, and apical cytoplasmic snouts and luminal calcifications are often present.
• The luminal cells (Figure 5-8) are monomorphic, contain small nucleoli, and have nuclei that are enlarged, rounded, and without polarity; these are the main features that distinguish FEA from blunt duct adenosis/columnar cell alteration, and these are the features that it has in common with ADH/DCIS.
• The epithelial proliferation is flat (it may be pseudostratified but is not stratified), with no architectural complexity or bridging, in contrast to ADH/DCIS.
• Careful evaluation of adjacent foci for atypical lobular hyperplasia, ADH, and DCIS is recommended.
  Special studies
• The luminal cells are strongly positive for ER and Bcl-2.

Treatment and prognosis

• Excision is not recommended where there is good radiologic/pathologic correlation.