Tubular carcinomas are often nonpalpable and are usually detected mammographically as irregular mass lesions. The conclusion that screening mammography has resulted in an increase in the frequency of this type of carcinoma being diagnosed is supported by many studies. Tubular carcinomas constituted 8% of invasive carcinomas spanning 1.0 cm or less detected in the Breast Cancer Detection Demonstration Projects.¹⁵ In one U.S. screening program, tubular carcinomas were 7% of 138 breast cancers; all tubular carcinomas were detected by mammography, but only 30% of them were evident clinically.¹⁶ A study correlating breast carcinoma histology and method of detection found that 83% of 41 tubular carcinomas had been detected mammographically, 12% were self-detected by the patient, and only 5% were found at clinical examination.¹⁷ Louwman et al.¹⁰ reviewed data for Dutch women aged 50 to 64 years with breast carcinoma diagnosed between 1988 and 2004. They found that tubular carcinoma constituted 8% of 9,259 screen-detected carcinomas, 2% of 5,413 interval carcinomas, and 2.1% of 6,710 carcinomas in women who did not undergo screening mammography. Similar results were obtained in Great Britain, where Nagtegaal et al.¹⁸ found that tubular carcinomas were 8.4% of screen-detected carcinomas, 2% of interval carcinomas, and 2.1% of carcinomas in women not participating in a mammographic screening program, respectively.

Mammographic findings can be suggestive of tubular carcinoma, but are not specific. The radiologic differential diagnosis of tubular carcinoma includes benign sclerosing lesions such as radial scar or sclerosing adenosis (SA), as well as well-differentiated invasive duct carcinoma. In one study, the average radiographic size of nonpalpable tubular carcinomas was 0.8 cm and that of palpable lesions 1.2 cm.¹⁹ Most tubular carcinomas are spiculated (Fig. 13.1), and they often harbor calcifications.²⁰ Rounded lesions, densities with indistinct borders or calcifications in the absence of a mass rarely prove to be tubular carcinoma. Radiologically, tubular carcinoma and radial scar are nearly indistinguishable, as both lesions have similar growth patterns and tubular carcinoma can arise in a radial scar.^21,22 Ultrasonography is also helpful in detecting tubular carcinoma, especially small lesions that are inapparent mammographically.²³ No features specific for tubular carcinoma have been reported in magnetic resonance imaging studies.

Among women, the age at diagnosis of tubular carcinoma ranges from 24 to 92 years.^{7,8,10,13,14,24,25,26,27,28} In one series,²⁷ 75% of tumors were diagnosed in women between ages 50 and

79 years. A study based on Surveillance Epidemiology and End Results (SEER) data for breast carcinomas reported that 73.6% of 4,477 tubular carcinomas diagnosed in the United States from 1992 and 2007 occurred in women 50 to 79 years old, 17.5% in women 40 to 49 years old, 6.9% in women older than

80 years, and only 2% in women 30 to 39 years old.¹¹ Tubular carcinoma of the male breast has been reported,^24,25,29 but this tumor constitutes less than 1% of male breast carcinomas.^30,31

Tubular carcinoma was associated with a 40% frequency of positive family history of breast carcinoma among first-degree relatives in one study.³² This association may reflect selective factors related to the specific population studied, which included many women who had mammography performed because they had a positive family history. Others have not found a disproportionately high frequency of positive family history among relatives of women treated for tubular carcinoma.

In a multicenter population-based case-control study conducted in five metropolitan areas of the United States, 80.5% of tubular carcinomas occurred in Caucasian/White women,³³ and an epidemiologic study based on SEER data reported that 90% of patients with tubular carcinomas were non-Hispanic White women.¹¹ The remaining patients were almost equally distributed, respectively, among women of African American (3.6%), Asian/Pacific Islander (3.5%), Hispanic White (2.3%), and American Indian/Alaska Native (0.5%) race or ethnicity.¹¹

A family history of breast carcinoma in a first-degree relative tripled the risk of tubular carcinoma in premenopausal women, but was not significantly related to the occurrence of tubular carcinoma in postmenopausal patients.³³ At least two studies have reported a two- to threefold increase in the risk of having tubular carcinoma in postmenopausal women who used hormone replacement therapy.^33,34

Occasionally, a palpable lesion has reportedly been present for a substantial period before biopsy, or a relatively long duration can be established by retrospective review of mammograms, but the median duration prior to histologic diagnosis is about 2 months.^24,25,26

Rarely, superficial tumors may be fixed to the skin, producing retraction signs. Tubular carcinoma usually occurs in peripheral portions of the breast, and nipple discharge is an infrequent presenting symptom.⁷ However, tubular carcinoma can arise near the major lactiferous ducts in the nipple or slightly lower in the subareolar region and raise the differential diagnosis of florid papillomatosis of the nipple. In this setting, the finding of Paget disease supports the diagnosis of tubular carcinoma (Fig. 13.2). Paget disease is very rarely found in association with tubular carcinoma not involving the nipple, except when coexistent DCIS separately involves the latter.

A compilation of Netherlands registry data found that 70% of 3,456 patients with tubular carcinoma presented at stage I, 26% as stage II, 2% as stage III, and 1% as stage IV.¹⁰ According to SEER data, 90.5% of women diagnosed with tubular carcinoma presented at stage I, 8.9% at stage II, 0.4% at stage III, and 0.2% at stage IV.¹¹

The average frequency of axillary lymph node (ALN) metastases resulting from tubular carcinoma is about 10%,^{4,7,12,24,25,26,35,36,37,38,39,40} ranging from none^7,35 to 29%.²¹ A metaanalysis of 680 patients in published reports found axillary nodal metastases in 6.6% of those with pure tubular carcinoma and in 25% with “mixed” tubular carcinoma.⁴¹ Tubular carcinomas were only 1.5% of all carcinomas in a series of 142 patients with T1N1M0 disease.¹⁵

Affected lymph nodes are usually in the low axilla (level I), and only exceptionally are more than three lymph nodes involved.²⁴ Fedko et al.⁴² found lymph node metastases in 5 (5.4%) of 93 patients with pure tubular carcinoma and known lymph node status: 2 patients had macrometastases, and the other 3 had micrometastases. Two additional patients had lymph nodes occupied by isolated tumor cells (N0(i+)).⁴² The size of the primary tumor ranged from 0.9 to 1.5 cm. Bradford et al.⁴⁰ reported that 13.3% of patients with tubular carcinoma 1 cm or larger had axillary nodal metastases. On the other hand, Green et al.³⁷ reported that three tubular carcinomas with nodal metastases were smaller than 1 cm, including one 0.4-mm lesion. In a retrospective analysis of sentinel lymph node (SLN) biopsy in 234 patients with tubular carcinoma treated at nine different French institutions,⁴³ the procedure successfully identified one or more lymph nodes in 229/234 (98%) cases. Pathologic evaluation
of SLNs included routine stained sections and cytokeratin stains at three levels. Six of 234 (2.5%) patients had macrometastases, 15/234 (6.4%) had micrometastases, and 2/234 (0.8%) had isolated tumor cells (N0(i+)). The median size of the tubular carcinomas was 9.59 mm (range, 1 to 22). The median size of tumors with SLN metastases (either macroor micrometastases) was 12.17 versus 9.39 mm for tumors without lymph node metastases (p = 0.005). On multivariate analysis, pathologic tumor size greater than 10 mm was the only parameter significantly associated with lymph node metastases (p = 0.007). In this study, all patients with macrometastatic carcinoma had a tumor greater than 1 cm.

Most tubular carcinomas are 2 cm or less in diameter, but tumors as large as 4 cm have been described,^{4,6,7,24,25,26,44} and in one study the largest tumor spanned 12 cm.⁴⁵ In some instances, tumors reported to be larger than 5 cm may be examples of coalescent multifocal lesions. Some investigators have reported that 67%²⁷ to 87%²⁴ of tubular carcinomas were 1 cm or smaller. In the latter study,²⁴ the median size of 90 “pure” tubular carcinomas was 0.8 cm. Fifty-two percent of ductal carcinomas with tubular features were 1 cm or less. The median size of mixed duct and tubular lesions was 1.1 cm.

Ductal carcinoma in situ (DCIS) has been described in 21% to 84% of tubular carcinomas.^{6,24,25,38,50} The DCIS typically has papillary, micropapillary, or cribriform patterns or shows a mixed pattern²⁴ (Figs. 13.9 and 13.10). In a significant number of cases, the intraductal proliferation associated with tubular carcinoma, and from which carcinoma appears to have arisen, is histologically indistinguishable from atypical ductal hyperplasia (ADH). Tubular carcinoma may arise from or in association with a benign proliferative lesion with a radial scar configuration.^51,52

Tubular carcinoma frequently develops in breast tissue involved by a multifocal alteration of the terminal ductallobular units usually referred to as “columnar cell change (CCC)” (Figs. 13.9 and 13.10). This lesion was previously designated informally as “pretubular” hyperplasia.⁵³ The spectrum of columnar cell lesions ranges from CCC and columnar cell hyperplasia (CCH) without atypia through CCC and/or hyperplasia with atypia to DCIS. Atypical CCH is also referred to as “flat epithelial atypia” (FEA). Cystic dilatation of the involved acini is a characteristic feature of these lesions, and Goldstein and O’Malley⁴⁴ referred to carcinoma in this setting as “cancerization of small ectatic ducts of the breast by DCIS cells with apocrine snouts.” Cytomorphologic features common to all phases of CCC with atypia are nuclear hyperchromasia and a high nuclear-to-cytoplasmic ratio. Apical snouts are also frequently present at the luminal borders of ducts and ductules. The most subtle expression of this condition consists of a monostratified layer of cuboidal or low columnar cells, with the foregoing cytologic features. CCH is characterized by crowding of cells that become increasingly compressed and columnar, and display haphazard arrangement of the nuclei with respect to the basement membrane. Atypical CCH shows low-grade atypia with round to oval nuclei with smooth nuclear contour and finely dispersed homogeneous chromatin. Rare inconspicuous nucleoli are often seen abutting the nuclear membrane. The presence of blunt micropapillae or cribriform growth composed of the same proliferative cells with “streaming” or condensation of cells toward the lumen is often associated with atypical CCH, transitioning into ADH. The acini affected by CCCs may contain dense intraluminal flocculent secretions that often undergo calcification, forming small basophilic deposits. These laminated concretions are often detected mammographically as fine punctate clustered calcifications of indeterminate significance. DCIS with low nuclear grade and cribriform or micropapillary architecture often arises in the background of CCCs, whereas high-grade DCIS is extremely rare in this setting.^54,55

Columnar cell lesions are associated with classical lobular carcinoma in situ (LCIS) (Figs. 13.9 and 13.10), as well as with tubular carcinoma and tubulolobular carcinoma (described later).^53,56,57 This complex has been referred to as the “Rosen triad.”⁵⁸ In one study,⁵⁰ 8/14 (57%) tubular carcinomas had associated CCCs with atypia (FEA), 7/14 (50%) had micropapillary ADH, 3/14 (21%) had low nuclear grade DCIS

Stay updated, free articles. Join our Telegram channel

Join