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Atypical Apocrine Adenosis: Diagnostic Challenges and Pitfalls.

Apocrine features are found in a high percentage of breast specimens, both in biopsies and resections, involving benign, innocuous lesions and invasive breast cancer. Epithelial cells with apocrine features can look atypical and, because there are no reliable biomarkers of malignancy, definite categorization of these lesions is often challenging. Diagnosis is made on hematoxylin-eosin stains alone, based on morphology. The objective of the present article is to review the spectrum of atypical apocrine lesions and their differential diagnoses, to highlight helpful diagnostic clues.

Furthermore, we will present the current knowledge on molecular markers of atypical apocrine lesions, which may become valuable diagnostic and therapeutic tools in the near future.

COMMENT

Normal Apocrine Cells, Apocrine Metaplasia, and Apocrine Adenosis

Apocrine cells are enlarged epithelial cells, usually with abundant granular, eosinophilic cytoplasm (type A cells), which sometimes show apical luminal blebbing or snouting and distinctive cell membranes (Figure 1). A less-common type, type B cells, contain foamy cytoplasm with small vacuoles that may coalesce. (1,2) The nuclei in both types of apocrine cells are round; they vary in size and have vesicular chromatin with conspicuous nucleoli. These cells are usually present in the apocrine sweat glands of the axilla and in the periareolar apocrine glands. They stain with periodic acid-Schiff after diastase digestion and are positive for epithelial membrane antigen and cytokeratins 8 and 18. Phenotypically, they are negative for estrogen and progesterone receptor but positive for androgen receptor and gross cystic disease fluid protein. Staining of basal cytokeratins, such as CK5/6, is variable and may be negative. (1) The loss of myoepithelial cells around benign and neoplastic apocrine lesions is well documented (Figure 2). (3)

Apocrine cells can be found in several different histologic lesions and are often regarded as apocrine change. Among benign lesions with apocrine cells are apocrine metaplasia, apocrine adenosis, papillomas, fibroadenomas, and apocrine adenoma. Among atypical and malignant lesions with apocrine features are atypical apocrine adenosis (AAA), apocrine ductal carcinoma in situ (DCIS), and invasive carcinoma with apocrine features.

Apocrine metaplasia is the most-common type of metaplastic change in the breast. It is frequently seen in women older than 30 years, increases with age, (4) and is associated with fibrocystic change. The apocrine cells can be arranged in a single layer or in multiple layers and may even form papillae. Apocrine cells may form the lining of macroscopic and microscopic cysts. Although presenting most commonly as apocrine cysts, apocrine metaplasia is frequently seen in fibroadenomas, papillomas, and sclerosing adenosis. The cytologic features of apocrine cells can be worrisome and, if associated with a reduction or loss in the myoepithelial cell layer, may prompt an erroneous diagnosis of malignancy. (3) Data regarding the relationship between apocrine metaplasia and invasive breast cancer are controversial; some authors have found an increase risk when associated with proliferative lesions, whereas others have found no such association. (5,6) It has been hypothesized that the same stimuli that cause breast cancer could also cause apocrine metaplasia. (7) The current consensus is that apocrine metaplasia is not preneoplastic. Although few molecular studies have been carried out, it has been reported that at least some portions of apocrine cysts with papillary hyperplasia may be clonal neoplasms, (8) but the significance of this finding remains uncertain.

Apocrine adenosis refers to apocrine change in sclerosing adenosis (Figure 3). In the past, some authors used the term apocrine adenosis to describe several different benign entities, such as apocrine metaplasia in a lobule and apocrine change in radial scars. However, in recent years the diagnosis of apocrine adenosis has been restricted to apocrine metaplasia superimposed on sclerosing adenosis. (9,10) On low power, the nuclear and nucleolar prominence that are characteristic of apocrine metaplasia can raise the question of atypia. In other cases, characteristic apocrine features may be absent; the cytoplasm can look gray or amphophilic. (11) The stroma associated with apocrine adenosis is fibrotic and compresses the glands and tubules. The enlarged apocrine cells, coupled with stromal distortion, may be misinterpreted as malignancy. To avoid these pitfalls, it is important to recognize the presence of apocrine features and myoepithelial cells around the lobulocentric proliferations of small acini.

Apocrine change in papillomas and fibroadenomas may be extensive. In some cases, florid apocrine change can be difficult to distinguish from low-grade DCIS. Features supportive of a malignant process include the presence of definite architectural patterns of DCIS (cribriform, micropapillary) with involvement of lobules outside the fibroadenoma/papilloma involvement of more than one terminal duct lobular unit, mitoses, and necrosis. Rare benign entities, such as apocrine adenomas, have been described and may be misdiagnosed as malignant if the entity is not readily recognized. (9) These are usually composed of papillary and tubular structures lined by apocrine cells, forming a distinct mass. These lesions are benign and do not recur. (9)

Apocrine Atypia and AAA

Apocrine proliferations may look atypical because of architecture or cytology. However, when the term apocrine atypia is used, it usually refers to cytologic atypia. It has been reported that significant cytologic atypia in apocrine cells is characterized by a 3-fold nuclear enlargement, prominent/ multiple pleomorphic nucleoli, and hyperchromasia.12 The term atypical apocrine adenosis refers to apocrine atypia within sclerosing adenosis (Figure 4).

Apocrine cells are almost always larger than regular ductal cells. When nuclear size is assessed in apocrine proliferations, benign apocrine nuclei are used for comparison (ideally from adjacent apocrine cysts). It is important to consider that some degree of variation in nuclear size and an occasional enlarged nucleus are acceptable in completely benign apocrine lesions. Although in daily diagnostic practice, it may be difficult to assess, Seidman et al (10(p2351)) point out that "a nucleus that has a diameter of 1.73 times a neighboring nucleus has an area 3 times this nucleus." In addition, they highlight that the most striking atypical feature is the nucleolar enlargement, not the nucleolar prominence per se, because distinct nucleoli are almost invariably present in apocrine change, and markedly pleomorphic enlarged nuclei are usually present in apocrine carcinomas. (10) Nuclear hyperchromasia and irregularities of the nuclear membrane may be affected by fixation artifacts, stain intensity, and section thickness; hence, they are not always reliable features. Additionally, cytoplasmic vacuoles may be a feature of apocrine atypia. Although small cytoplasmic vacuoles can be seen in type B apocrine cells, in one study of AAA, foci with nuclear atypia were found to have abundant clear to foamy cytoplasm. (10) Mitotic figures may or may not be present.

Atypical apocrine adenosis is a rare entity. AAA comprised 0.4% of 9340 cases in a series from the Mayo Clinic. (13) Because of its rarity, long-term studies looking at clinical outcome and risk for invasive carcinomas are lacking. Sclerosing adenosis has a relative risk of 1.7 for invasive carcinoma, (14) and it is unclear how atypical apocrine change modifies this risk. The few available long-term follow-up studies of excision biopsies suggest that AAA occurring in isolation is not associated with increased breast cancer risk (Table). In a series of 37 patients from the Mayo Clinic, 3 (8%) developed invasive carcinoma comparable to their benign breast disease cohort (7.8% of 9340 patients), suggesting that AAA may not be a precursor of breast carcinoma. (13) Although Seidman et al (10) reported an increased risk of carcinoma in older women, the Mayo Clinic study did not find an increased risk association with age. Nevertheless, AAA was more commonly seen in older women in the Mayo cohort as well. In the only study looking at outcomes on core biopsy, there were no upgrades to carcinoma in 7 cases of isolated AAA. (14)

Differential Diagnosis of AAA

The main differential diagnoses of AAA includes: apocrine DCIS involving sclerosing adenosis, pleomorphic lobular carcinoma involving sclerosing adenosis, and invasive carcinoma.

AAA Versus Apocrine DCIS.--Apocrine DCIS has been recognized since 1997. (15) Although there have been no unified diagnostic criteria, the most accepted one is the presence of ducts filled with neoplastic apocrine cells (Figure 5). As with other types of DCIS, apocrine DCIS can exhibit solid, cribriform, or micropapillary architecture. Necrosis and microcalcifications are frequent but are not necessary for the diagnosis. The nuclear grade of apocrine DCIS can be low, intermediate, or high. Grading should be performed on the foci showing the greatest degree of pleomorphism. The diagnosis of high-grade DCIS is usually straightforward, consisting of cells with marked nuclear atypia, prominent nucleoli, and comedo-type necrosis.

In a core biopsy, AAA needs to be distinguished from apocrine DCIS extending into sclerosing adenosis. In the absence of definite patterns of DCIS (eg, cribriform, micropapillary, and comedonecrosis), the presence of glands with solid expansion by atypical apocrine cells favors the diagnosis of apocrine DCIS (Figure 6). (11) This diagnosis is further supported by finding necrosis or mitosis. (11) On the other hand, the presence of atypical apocrine cells in a single layer suggests AAA (Figure 7). Tavassoli and Norris (16) use the term atypical apocrine metaplasia when the normal breast epithelium is replaced by a single layer of markedly pleomorphic apocrine cells with a 3-fold variation in nuclear size. They use the term atypical apocrine hyperplasia when (1) these atypical cells are stratified or form tufts without epithelial bridges, or (2) epithelial bridges or a complete cribriform pattern involves the entire duct space in a lesion of less than 2 mm. Lesions greater than 2 mm were considered apocrine DCIS, but not all experts agree. In some cases, the stroma may be very sclerotic, and DCIS may not produce a characteristic expansile pattern.

In cases in which there is no definite expansion, mitosis, or necrosis, lesion size may be taken into consideration. O'Malley et al (17) set out to classify 54 unusual apocrine lesions into useful diagnostic groups using nuclear features and size/extent. The authors selected challenging cases, including those originally diagnosed as atypical ductal hyperplasia (ADH) with apocrine features, apocrine DCIS, or lesions with unusual apocrine cytology. They defined 4 possible diagnoses based on a cutoff of 4 mm and nuclear atypia: DCIS, limited DCIS, borderline DCIS, and atypia. Although this classification may be useful, the study had no follow-up, and the clinical relevance of this classification remains unknown.

The diagnosis of low nuclear grade apocrine DCIS should be made with caution. Leal et al (18) classified apocrine DCIS into low, intermediate, and high grade based on nuclear criteria and the presence of comedonecrosis. Of their 35 cases, 10 were classified as low-grade apocrine DCIS, but only one of these cases had nuclear grade 1 features: small (X1-2) to intermediate (X3-4) sized nuclei, single nucleoli, and low pleomorphism. Most low-grade apocrine DCIS had moderate nuclear pleomorphism and multiple nucleoli with occasional large multinucleate cells. Tavassoli and Norris (19) classified 37 cases of apocrine DCIS into 3 categories (noncomedo, papillary, and comedo). Most cases of apocrine DCIS (n = 32) were high nuclear grade, and the remaining (n = 5) were intermediate grade. There were no cases of low-grade apocrine DCIS. Thus, we recommend a conservative approach to the diagnosis of low-grade apocrine DCIS.

AAA Versus Pleomorphic Lobular Carcinoma In Situ.--The differential diagnosis of AAA includes, in some cases, pleomorphic lobular carcinoma in situ involving sclerosing adenosis (Figure 8, A through C). Pleomorphic lobular carcinoma in situ cells exhibit a greater degree of nuclear pleomorphism compared with classic lobular carcinoma in-situ with prominent nucleoli. Pleomorphic lobular carcinoma in situ cells may have abundant eosinophilic cytoplasm positive for gross cystic disease fluid protein (GCDFP-15), a marker of apocrine differentiation. (20) When confronted with this differential diagnosis, an E-cadherin is helpful because this stain is negative in pleomorphic lobular carcinoma in situ and positive in apocrine DCIS and AAA. (20-22)

AAA Versus Invasive Carcinoma.--Apocrine change in sclerosing adenosis, with or without atypia, may be misinterpreted as invasive carcinoma because of the combination of enlarged cells and stromal distortion (Figure 9). In one study, 25% (4 of 12) of the pathologists diagnosed apocrine adenosis as invasive carcinoma. (23) Myoepithelial stains, when positive, are helpful in these situations (Figure 10, A through F). However, the myoepithelial cell layer may be attenuated or lost in benign and neoplastic apocrine proliferations. Thus, several myoepithelial markers targeting both nuclei (p63) and cytoplasm (smooth muscle myosin, muscle-specific actin) may be necessary to distinguish AAA or DCIS in sclerosing adenosis from invasive carcinoma. A diagnosis of invasion should not be based on the lack of myoepithelial cells alone. Collagen stains may serve to highlight the basement membrane. The lobulocentric arrangement of sclerosing adenosis may be another helpful morphologic clue.

Architectural Atypia in Apocrine Lesions

Architectural atypia can also be been seen in apocrine proliferations. This is typically seen when apocrine changes are superimposed on underlying patterns diagnostic of ADH (Figure 11). These include rigid arches, cribriform spaces, and bulbous papillae involving the acinus entirely or focally. Some prefer to use the term ADH with apocrine features, whereas other may refer to it as atypical apocrine hyperplasia. (16) In some cases of apocrine adenosis, the cytoplasm may be gray or amphophilic. The rounded nuclei, increased cytoplasmic volume, and distinct cell membranes may contribute to a "monotonous" look in some acini (Figure 12). This may raise concern for ADH, when the apocrine nature of the lesion is not suspected. To further confuse the matter, stains to differentiate between usual ductal hyperplasia and ADH are not helpful because CK5/6 is usually lost in apocrine change and may be interpreted erroneously. Estrogen receptor tends to be negative in apocrine change, in contrast to usual ductal hyperplasia, in which it is variably positive.

Our Approach to the Diagnosis of Atypical Apocrine Lesions in Core Biopsies

At our institution, we apply cytologic criteria to diagnose apocrine atypia, requiring a minimum 3-fold variation in nuclear size. (12) Although we use a size cutoff for DCIS, the extent of the lesion is taken into consideration, along with architectural features and background breast morphology. In our experience, markers that highlight the presence of myoepithelial cells (eg, p63, smooth muscle myosin, and muscle-specific actin) have been most helpful in differentiating AAA from invasive carcinoma. In some cases with mild architectural atypia suspicious for DCIS, deeper sections reveal diagnostic features of DCIS. Most patients with a diagnosis of AAA without a higher risk lesion on core biopsy will undergo an excision. As with all core biopsies, radiopathologic concordance is necessary to ensure that the target lesion has been adequately sampled.

Molecular Features of AAA

Several authors have studied the molecular alterations with a role in apocrine lesions. It is striking that apocrine metaplasia has been found to lose expression of Bcl2, an inhibitor of apoptosis, (24,25) but this is not seen in apocrine DCIS or invasive carcinoma with apocrine features. GCDFP-15 is often used as a marker for carcinoma with apocrine features because it is related to androgen receptors; this association was proved by Naderi and Meyer. (26) A recent study (27) proposes and presents evidence suggesting that carcinomas with apocrine features arise from atypical and benign precursors. Gromol et al (27) compared several immunohistochemical markers in ductal carcinoma, carcinomas with apocrine features and apocrine DCIS. Their results show how malignant lesions acquire mutations as they become more aggressive. However, no phenotypical markers have been found to help distinguish atypical from malignant lesions. The molecular alterations, if any, in AAA have not been characterized.

CONCLUSIONS

Apocrine change is an everyday finding in breast specimens. Careful assessment of these specimens is vital because differential diagnosis of "atypical" lesions often includes both benign and malignant entities, with completely different therapeutic and prognostic implications. Unfortunately, there are no helpful molecular biomarkers, and the histologic criteria on hematoxylin-eosin slides remain the gold standard of diagnosis. We believe it is necessary to understand the complex spectrum of apocrine atypia to accurately diagnose these lesions, avoiding unnecessary procedures.

References

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(2.) Wells CA, El-Ayat, GA. Non-operative breast pathology: apocrine lesions. J Clin Pathol. 2007; 60(12):1313-1320.

(3.) Tramm T, Kim JY, Tavassoli FA. Diminished number or complete loss of myoepithelialcellassociatedwith metaplastic andneoplastic apocrine lesions of the breast. Am J Sur Pathol. 2011; 35(2):202-211.

(4.) Eusebi V, Damiani S, Losi L, Millis RR. Apocrine differentiation in breast epithelium. Adv Anat Pathol. 1997; 4(3):139-155.

(5.) Wellings SR, Alpers CE. Apocrine cystic metaplasia: subgross pathology and prevalence in cancer-associated versus random autopsy breast. Hum Pathol. 1987; 18(4):381-386.

(6.) Ahmed A. Apocrine metaplasia in cystic hyperplastic mastopathy: histochemical and ultra-structural observations. J Pathol. 1975; 115(4):211-214.

(7.) Viacava P, Naccarato AG, Bevilacqua G. Apocrine epithelium of the breast: does it result from metaplasia? Virchows Arch. 1997; 431(3):205-209.

(8.) Jones C, Damiani S, Wells D, Chaggar R, Lakhami SR, Eusebi V. Molecular cytogenetic comparison of apocrine hyperplasia and apocrine carcinoma of the breast. Am J Pathol. 2001; 158(1):207-214.

(9.) Masood S, Rosa M. The challenge of apocrine proliferation of the breast: a morphologic approach. Pathol Res Pract. 2009; 205(3):155-164.

(10.) Seidman Jd, Ashton M, Lefkowitz M. Atypical apocrine adenosis of the breast; a clinicopathological study of 37 patients with 8.7 year follow up. Cancer. 1996; 77(12):2529-2537.

(11.) Hoda SA, Brogi E, Koerner FC, Rosen PP. Rosen's Breast Pathology. 4th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2014: 104.

(12.) Visscher DW. Apocrine ductal carcinoma in situ involving a sclerosing lesion with adenosis: report of a case. Arch Pathol Lab Med. 2009; 133(11):1817-1821.

(13.) Fuehrer N, Hartmann L, Degnim A. Atypical apocrine adenosis of the breast: long term follow-up in 37 patients. Arch Pathol Lab Med. 2012; 136(2): 179-182.

(14.) Calhoun BC, Booth NC. Atypical apocrine adenosis diagnosed on core biopsy: implications for management. Hum Pathol. 2014; 45(10):2130-2135.

(15.) Consensus Conference Committee, American Cancer Society. Consensus conference on the classification of ductal carcinoma in situ. Cancer. 1997; 80(9): 1798-1802.

(16.) Tavassoli FA, Norris HJ. A comparison of the results of long-term follow up for atypical intraductal carcinoma of the breast. Cancer. 1990; 65(3):518-529.

(17.) O'Malley FP, Page DL, Nelson EH, Dupont WD. Ductal carcinoma in situ of the breast with apocrine cytology: definition of a borderline category. Hum Pathol. 1994; 25(2):164-168.

(18.) Leal C, Henrique R, Monterio P. Apocrine ductal carcinoma in situ of the breast: histologic classification and expression of biologic markers. Hum Pathol. 2001; 32(5):487-493.

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(20.) Eubesi V, Magalhaes F, Azzopardi JG. Pleomorphic lobular carcinoma of the breast: an aggressive tumor showing apocrine differentiation. Hum Pathol. 1992; 23:655-662.

(21.) Kaya H, Aribal E, Yegen C. Apocrine differentiation in invasive pleomorphic lobular carcinoma with in situ ductal and lobular apocrine carcinoma: a case report. Pathol Oncol Res. 2002; 8(6):151-152.

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Jaya Ruth Asirvatham, MD; Maria Monica Garcia Falcone, MD; Celina G. Kleer, MD

Accepted for publication May 19, 2016.

From the Departments of Pathology and Laboratory Medicine (Drs Asirvatham and Kleer) and the Comprehensive Cancer Center (Dr Kleer), University of Michigan Hospital and Health Systems, Ann Arbor; and Department of Pathology, CEMIC University Hospital, Buenos Aires, Argentina (Dr Falcone).

The authors have no relevant financial interest in the products or companies described in this article.

Presented in part at the New Frontiers in Pathology; October 2224, 2015; Ann Arbor, Michigan.

Corresponding author: Celina G. Kleer, MD, Department of Pathology and Laboratory Medicine, University of Michigan Hospital and Health Systems, 1500 E Medical Center Dr, Ann Arbor, MI 48109 (email: kleer@umich.edu).

Please Note: Illustration(s) are not available due to copyright restrictions.

Caption: Figure 1. Benign apocrine cysts composed of apocrine cells with granular eosinophilic cytoplasm (hematoxylin-eosin, original magnification X20).

Caption: Figure 2. p63 for myoepithelial cells is largely negative except in the lower right-hand corner (hematoxylin-eosin, original magnification X20).

Caption: Figure 3. Sclerosing adenosis with apocrine features (hematoxylineosin, original magnification X10).

Caption: Figure 4. Atypical apocrine cells with enlarged nuclei, prominent nucleoli in comparison to adjacent apocrine cells (hematoxylin-eosin, original magnification X40).

Caption: Figure 5. Intermediate-grade apocrine ductal carcinoma in situ with central necrosis and cancerization of lobules (hematoxylin-eosin, original magnification X20).

Caption: Figure 6. Acini are expanded by cells with vacuolated cytoplasm and marked nuclear pleomorphism, features of apocrine ductal carcinoma in situ (hematoxylin-eosin, original magnification X40).

Caption: Figure 7. Single layer of atypical apocrine cells within sclerosing adenosis mimicking invasive carcinoma (hematoxylin-eosin, original magnification X60).

Caption: Figure 8. Case of pleomorphic lobular carcinoma in situ involving sclerosing adenosis. A, Sclerosing lesion with central pale area. B, Cells with apocrine features containing abundant eosinophilic cytoplasm and enlarged nuclei. C, The cells are negative for E-cadherin, confirming lobular phenotype (hematoxylin-eosin, original magnifications X4 [A] and X40 [B]; original magnification X40 [C]).

Caption: Figure 9. Low- to intermediate-grade apocrine ductal carcinoma in situ involving sclerosing adenosis and mimicking invasive carcinoma (hematoxylin-eosin, original magnification X10).

Caption: Figure 10. A case of apocrine ductal carcinoma in situ involving a sclerosing adenosis on core biopsy. A and B, Sclerosing papillary lesion with focal, irregular, hyperchromatic areas with stromal distortion, suspicious for invasion. C and D, Higher power shows atypical apocrine cells with areas of expansion. E and F, Smooth muscle myosin stains highlight myoepithelial cells. Cribriform pattern of ductal carcinoma in situ is evident (hematoxylin-eosin, original magnifications X4 [A and B], X10 [C], X40 [D]; original magnifications X20 [E] and X10 [F]).

Caption: Figure 11. Rigid arches and punched-out space involving a single acinus in keeping with atypical ductal hyperplasia (hematoxylin-eosin, original magnification X40).

Caption: Figure 12. Apocrine adenosis with florid hyperplasia. Monotonous appearing areas raise concern for atypical ductal hyperplasia. Variation in nuclear size and abundant cytoplasm in other areas attest to the apocrine nature of the lesion (hematoxylin-eosin, original magnification X20).
Clinical Outcomes of Atypical Apocrine Adenosis

Source, y                  Cases,     Follow-up,   Carcinoma,
                           No./Type   Mean         n of N

Carter et al, (28) 1991    51/EB      35 mo        0 of 47
Seidman et al, (10) 1996   37/EB       8.7 y       4 of 37 (a)

Fuehrer et al, (13) 2012   37/EB      14 y         3 of 37 (b)
Calhoun et al, (14) 2014   12/CNB     --           0 of 7 (c)

Source, y                  Mean Age,   Conclusion
                               y

Carter et al, (28) 1991       58       Recommended clinical follow-up
Seidman et al, (10) 1996      60       Increased risk in women older
                                         than 60 y
Fuehrer et al, (13) 2012      59       No increased risk
Calhoun et al, (14) 2014      60       May not require surgical
                                         excision

Abbreviations: CNB, core needle biopsy; EB, excision biopsy.

(a) All 4 were invasive ductal carcinoma after a mean follow-up of
5.6 years; 1 of 4 patients had conventional atypical ductal
hyperplasia elsewhere in the biopsy.

(b) One invasive ductal carcinoma after 4 years of follow-up, 1
invasive mixed ductal and lobular carcinoma after 18 years of follow
up, and 1 case of contralateral ductal carcinoma in situ after 12
years of follow-up.

(c) Five cases had a more-advanced lesion in the same core or a
concurrent ipsilateral biopsy.
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Author:Asirvatham, Jaya Ruth; Falcone, Maria Monica Garcia; Kleer, Celina G.
Publication:Archives of Pathology & Laboratory Medicine
Date:Oct 1, 2016
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