7 Image Interpretation: Noninvasive Cancer


The focus of this chapter is to review the imaging characteristics of non-invasive cancer (ductal carcinoma in situ [DCIS]) and the MRI appearance of this lesion which often presents as non-mass enhancement. The increased sensitivity for MRI detection of DCIS in recent years, above and beyond the sensitivity of mammography, is likely due to improved spatial and temporal resolution made possible with use of modern higher field strength magnets and newer acquisition protocols. Reported MRI sensitivities for DCIS in the more recent literature are significantly higher than those of mammography and range from 79% to 97%. Ultrafast perfusion imaging is also able to detect non-mass enhancement (NME) reliably even at lower spatial resolution, with the advantage that absence of BPE in these 1-30 second images greatly improves lesion conspicuity. In this chapter we discuss not only the biology and the distinct molecular and genetic expression profiles of DCIS, but also the salient features of this diagnosis which can be challenging because NME is not generally seen on precontrast imaging and lacks a clear lesion interface and distinct margins. The focus on the imaging findings in this chapter is exemplified by 37 case examples of normal ducts, ductal pathology and DCIS. A discussion of MRI investigations of DCIS and the clinical management of patients with a DCIS diagnosis, is also included in this chapter.

7 Image Interpretation: Noninvasive Cancer

7.1 Background

Ductal carcinoma in situ (DCIS) has been known for many years as a “mammographic disease.” This diagnosis, rarely identified before the advent of mammographic screening, has increased dramatically over the years, with 63,410 new DCIS cases diagnosed in women in 2017 in the United States. The increasing rate of DCIS is strongly associated with a concurrent increase in rates of mammography screening and is similar to the increasing incidence of DCIS in other developed countries where breast screening programs are conducted. Early reports in the 1930s of a precursor lesion that could progress to invasion led to first use of the term carcinoma in situ. In the era before breast screening, most in situ lesions were detected clinically as a palpable mass, Paget’s disease, or nipple discharge. Incidence in the United States has increased sevenfold, from 1973 through the late 1990s, with the most rapid increase found among women older than 50 years. As of January 1, 2005, an estimated 500,000 women were living with a diagnosis of DCIS in the United States and this number is estimated to increase to more than one million women by 2020 assuming constant incidence and survival rates.

DCIS is defined as a preinvasive form of breast cancer whereby a clonal proliferation of malignant epithelial cells originating in the terminal ductal lobular unit (TDLU) remain confined to ducts and do not invade beyond the basement membrane into the surrounding breast tissue. Evidence suggests that approximately 30 to 50% of DCIS lesions will progress to invasion over time if left untreated. 1 , 2 The important question is, of course, whether advanced imaging can not only improve identification of DCIS but also select those lesions that are most likely to invade. DCIS is generally found as microcalcifications on mammography and nonmass enhancement (NME) on magnetic resonance imaging (MRI). Both methods exhibit morphologic and distribution characteristics, which reflect a spectrum of heterogeneous lesions with diverse histological, molecular, and genetic characteristics. MRI, although not as widely used clinically as mammography, is a functional imaging technique and has the highest sensitivity for DCIS of all imaging modalities. 3

7.2 Mammography

DCIS typically presents as a nonpalpable, 10- to 20-mm, calcified lesion detected at mammography, usually exhibiting calcifications in a grouped, linear, or segmental distribution. Calcifications with suspicious morphology on mammography include amorphous, course heterogeneous, fine pleomorphic, and fine linear or fine linear-branching subtypes. The typical fine linear malignant calcifications contained within lobules and ducts are probably caused by central necrosis occurring as a result of hypoxia, because blood supply by diffusion from extraductal vessels becomes inadequate due to rapid tumor growth. DCIS may involve multiple sites contained within the same ductal system separated by normal tissue (“skip lesions”), involving adjacent or even remote ductal systems which may occupy an entire breast lobe. 4 Although calcified necrotic tumor is a frequent mammographic presentation of DCIS, other findings such as mass, asymmetry (associated with fluid in the micropapillary subtype), or architectural distortion are seen in approximately 10 to 20% of cases.

7.3 Biology of Ductal Carcinoma In Situ

Noninvasive cancers comprise a heterogeneous group of lesions with variable histopathologic, biologic, and genetic features. Lesions that are heterogeneous in grade are assigned the highest grade; standard histologic assessment of DCIS typically involves assessment of both qualitative and quantitative features. Qualitative features include assessment of the architectural growth pattern, nuclear grade (high-, intermediate-, and low-grade cytologic features), and presence or absence of central necrosis. High-grade noninvasive lesions with high mitotic indices generally exhibit rapid growth rates and will almost invariably progress to invasion, whereas low-grade lesions may remain quiescent, never invade, and, if they do invade, will progress to low-grade invasive cancer. Tabar and colleagues have postulated that certain morphologic characteristics of calcifications represent a duct-forming invasive cancer rather than an in situ lesion and therefore patients with this type of presentation may require more aggressive treatment. Careful mammographic and pathologic evaluation with correlation of magnified mammographic imaging and large section histology specimens has informed this opinion. 5

Few studies have focused on risk factors for DCIS; however, it is generally agreed that the risk factors for in situ disease are the same as those for invasive breast cancer. These indicators include increasing age, family history of breast cancer, genetic predisposition, high mammographic density, late age at menopause, and nulliparity. The natural history of DCIS, and of breast cancer overall, is still poorly understood and it makes sense therefore to focus research efforts on this earliest stage of breast cancer in order to gain knowledge about its origins and the mechanisms responsible for progression from noninvasive to invasive disease. In order to achieve this goal, we must improve our understanding of the biology of DCIS and the key events responsible for its transition to invasion. Invasive tumors require a vascular supply for continued growth and depend on angiogenesis, which is the term describing the complex process leading to the formation of new blood vessels from a preexisting vascular network, and this is likely also true for DCIS lesions. 6 Neoangiogenesis in invasive cancer is mediated not only by vascular endothelial growth factor (VEGF), a potent angiogenic factor, but also by other angiogenic and antiangiogenic factors. Tumor angiogenesis is an independent prognostic factor in invasive cancer, and is correlated with VEGF, microvessel density (MVD), and contrast enhancement in breast MRI. It is reasonable therefore to expect that the kinetic behavior of DCIS enhancement would also reflect DCIS biology. Expression of VEGF has been found in approximately 85% of DCIS lesions. 7 Angiogenesis in preinvasive cancer may not necessarily be associated with the typical dense, leaky neovasculature seen with invasive cancers. Studies of the vascular distribution associated with DCIS have shown two patterns: (1) vascular cuffing forming a ring, wherein blood vessels pack densely around neoplastic ducts immediately underlying the basement membrane, 8 or (2) a more diffusely dispersed pattern with scattered permeating blood vessels located in the surrounding stroma. These patterns of microvasculature are reflected in the enhancement patterns at high-resolution MRI, presenting often as clustered ring or diffuse (heterogeneous/homogeneous) enhancement. The diffuse enhancement pattern is often associated with high histologic grade and necrosis.

7.3.1 Molecular Markers

Cancer is a genetic disease wherein malignant transformation is driven by changes in DNA. In the larger context of tumor biology, the molecular profiles of DCIS and invasive breast cancer are similar, supporting a common origin. The distinct molecular characteristics of DCIS mirror those of invasive breast cancer by tumor grade. 9 Molecular pathways are altered in DCIS, and characterization by DNA, RNA, and protein can not only elucidate the molecular pathways critical for cancer etiology but also identify disease subtypes that have the potential to correlate with prognosis and therapeutic prediction. Surprisingly, few differences on a genomic or gene-expression level exist between DCIS and invasive disease, and DCIS breast lesions are considered to be nonobligate precursors of invasive cancer. This general understanding has not resulted from tracking the natural history of this disease and following women with DCIS over time without treatment, but rather by acknowledgement of a large body of indirect evidence linking the precursor status of in situ disease to invasion. For example, considerable evidence points to the increased risk of invasive ductal carcinoma (IDC) recurrence at the resection site in women with prior DCIS diagnosis and treatment, and the frequent coexistence of invasive and noninvasive disease in the same lesion, sharing of many of the same molecular and genetic abnormalities in both. 10 , 11

Protein expression in DCIS is usually assessed via immunohistochemistry (IHC) obtained on tissue sections. Estrogen receptor (ER) status is a proven prognostic marker in breast cancer; its main clinical value is its ability to predict response to hormonal therapy. Most laboratories in the United States use IHC to determine ER and progesterone receptor (PR) results on primary breast carcinoma. Approximately 70 to 80% of DCIS lesions are ER-positive and are less likely to be associated with high nuclear grade, human epidermal growth factor (HER-2/neu) or p53 positivity, or a high proliferative rate (Ki-67). Only 20 to 30% of DCIS patients exhibit HER-2/neu overexpression 12 by measuring ErbB2 gene amplification, as assessed by IHC or fluorescence in situ hybridization (FISH). HER-2/neu-positive DCIS is more likely to be ER–, PR–, and have high nuclear grade. The proportion of HER-2/neu-positive DCIS is similar to IDC; however, the triple-negative phenotype (ER–, PR–, HER-2/neu-negative) is less common in DCIS. 13

7.3.2 Gene Expression Profiles

Microarray analysis, identifying specific gene expression profiles, yields prognostic and predictive information that may be useful for indicating the likelihood of response to therapy. In the past few years, there have been several commercially available prognostic gene expression profile assays developed for clinical breast cancer assessment, Oncotype DX and MammaPrint among them. These companies provide a commercial assay designed to assess tumor recurrence probability and have developed a prognostic indicator for DCIS, providing treatment decision support for patients with newly diagnosed breast cancer. The oncotype DX method utilizes quantitative reverse transcription-polymerase chain reaction to analyze the expression of 21 genes (16 cancer-related and 5 control genes) and to provide an estimated distant disease recurrence score ranging from 0 to 100. Further understanding of the genesis of aggressive forms of DCIS and how these lesions transform themselves and progress to invasion is needed before confident therapeutic management of women with this diagnosis can be determined.

7.4 MRI of Ductal Carcinoma In Situ

Reported MRI sensitivities for DCIS in the more recent literature are significantly higher than mammography and range from 79 to 97%. Optimal technique is a prerequisite for improved identification of NME, and when achieved, individual ducts are discernable and tumor is readily identified in both ducts and lobules. We know that DCIS exhibits heterogeneous findings on both mammography and MRI, with each modality exhibiting some features that are associated with lesion aggressiveness. The histologic classification of DCIS was initially based on metrics developed for IDC: invasive cancers classified as grade I, II, or III, and noninvasive cancers categorized as low, intermediate, or high grade based on nuclear features such as size and mitotic activity. Mixed histologic subtypes are found in more than one-half of DCIS cases. 14 DCIS, however, unlike IDC, exhibits singular architectural growth patterns that reflect cell distribution within the duct lumen; these patterns of tumor growth are often visualized on mammography as calcium distribution in ducts and lobules and on MRI as internal enhancement patterns of NME. The nuclear grading and histologic growth patterns of in situ lesions are classified as solid, papillary, micropapillary, cribriform, and presence or absence of necrosis. Studies have shown that imaging can reflect tumor biology, for example, fine linear/fine linear-branching patterns of calcifications at mammography show considerably worse survival outcome than amorphous or round calcifications, 15 and higher-grade in situ lesions at MRI exhibit increased contrast enhancement compared with low-grade DCIS. 3 , 8

Accurate diagnosis of DCIS may be challenging because NME is not generally seen on precontrast imaging and lacks a clear lesion interface and distinct margins. However, modern MRI methods obtained at higher spatial and temporal resolution show excellent visualization of involved ducts and lobules. 16 Typical signs include a distinctive nonmass morphology, clumped or clustered ring internal enhancement, in a segmental, linear, or regional distribution. Unlike mammography where the DCIS finding is often that of calcified necrotic tumor, MRI detects intermediate- and high-grade DCIS and associated foci of invasive cancer that is often occult at mammography and ultrasound.

7.4.1 Terminal Ductal Lobular Units and Ducts

Normal TDLUs measure about 1 mm in diameter, enhance in varying degrees, and represent normal background parenchymal enhancement (BPE) on MRI. The entire TDLU complex including surrounding fat and fibrous tissue measures about 5 mm. High-resolution MRI can visualize normal (nonenhancing) central ducts measuring 0.1 mm in diameter, seen best in fatty breasts (Fig. 7‑1). Abnormal enhancing ducts containing DCIS (Fig. 7‑2) may be visible not only in the subareolar region but also with variable distribution throughout the affected breast; these diseased ducts enlarge up to about 1.0 mm in diameter and are visible in any type of FGT.

Fig. 7.1 Normal subareolar ducts. Normal duct structures are visualized well in this fatty breast on the T2w non-fat-sat image (a) (short arrows); small cysts are also seen (long arrows). These findings are also visible on T1w fat-sat precontrast image (b), seen without enhancement on postcontrast T1w image (c), and subtraction image (d). Similar findings are seen on an adjacent slice showing normal ducts on T2w image (e, short arrows), cysts (e, long arrows), and T1w precontrast image (f). No enhancement is seen on postcontrast T1w image (g) or subtracted image (h). Nonenhancing ducts are benign.
Fig. 7.2 Enhancing duct containing high-grade DCIS. Subareolar ducts are seen bilaterally on T2w non-fat-sat image (a, arrows). T1w postcontrast image (b) and correlative subtraction image (c) show enhancement of an abnormal right subareolar duct, but no enhancement of a normal left duct. Extensive segmental right breast NME is shown with visible peripheral enhancing ducts. Histology: DCIS, high grade, solid with necrosis. ER (–), PR (+).

Benign, nonenhancing, dilated ducts are often identified in the subareolar region in women of all ages and may contain fluid or debris with signal intensities similar to water: hyperintense on T2-weighted (T2w) and hypointense on T1w series (Fig. 7‑3). Other ectatic ducts may contain proteinaceous or hemorrhagic intraductal material exhibiting variable signal on T2w and T1w series: the higher the protein content, the lower the signal intensity on T2w series and the higher the intensity on T1w series (Fig. 7‑4, Fig. 7‑5). Infrequently, benign ectatic ducts may become inflamed exhibiting duct wall and periductal enhancement separated by nonenhancing duct contents. These ducts can be differentiated from enhancing malignant ducts by their typical “tram-track” appearance on MRI (Fig. 7‑6 , Fig. 7‑7). Ducts with a linear enhancement distribution are clearly visible at high-resolution MRI and should be considered to be suspicious, whether visible centrally or elsewhere in the breast. This pattern of enhancement generally indicates a high-risk lesion, such as atypical duct hyperplasia (ADH) and lobular neoplasia, or DCIS. Examples of high-risk lesions are shown: pleomorphic LCIS (Fig. 7‑8), Fig. 7‑9, Fig. 7‑10), flat epithelial atypia (FEA) (Fig. 7‑11), and ADH (Fig. 7‑12). High-risk lesions exhibit MR findings which may be very similar in morphology and internal enhancement characteristics to DCIS lesions (Fig. 7‑13), with the exception that the enhancement is generally lower and detection is more difficult at lower field strength.

Fig. 7.3 Ectatic duct. Dilated subareolar duct is seen in the left breast on T2w non-fat-sat image (a), exhibits high signal on T1w precontrast image (b) and postcontrast image (c), and shows no abnormal enhancement on angiomap (d). The duct is not visible on subtraction image (e). The high duct signal represents intraductal fluid or proteinaceous material.
Fig. 7.4 Ectatic duct. A low-signal dilated subareolar duct is seen in the right breast on T2w non-fat-sat image (a), with several dilated ducts exhibiting high signal, visible on T1w precontrast image (b) and postcontrast source image (c). Sagittal reformatted source image (d) shows the largest duct to advantage. Absence of linear enhancement on subtracted image (e) confirms a benign diagnosis.
Fig. 7.5 Ectatic ducts. Precontrast T1w images (a, b) show bilateral ectatic high-signal subareolar ducts with dilated ducts extending into the central right breast. Postcontrast image (c) shows similar findings; however, no linear enhancement is seen on subtraction image (d).
Fig. 7.6 Inflamed ectatic duct. Patient presents with anterior left breast pain. MLO and CC cropped images of the anterior-central left breast (a, b) show a solitary dilated subareolar duct, also visible on ultrasound, exhibiting increased blood flow on color Doppler (c, d). MRI shows left subareolar enhancement on MIP image (e). A correlative dilated duct is visible on T2w non-fat-sat image (f) with a high duct signal seen on T1w precontrast image (g), likely representing intraductal fluid or proteinaceous material. Postcontrast source and subtracted images (h, i) exhibit duct wall enhancement with a classic “tram-track” appearance. The duct wall enhancement is seen to advantage on subtracted sagittal image (j). Clinical symptoms resolved within 2 months.
Fig. 7.7 Inflamed ectatic duct. T2w image does not show significant duct dilation (a), but postcontrast subtracted images at 1 minute and 2 minutes (b, c) exhibit duct wall enhancement with persistent enhancement pattern shown on the angiomap image (d).
Fig. 7.8 Pleomorphic and classic LCIS. Loosely scattered calcifications were found in the 12 o’clock position of the right breast at magnification mammography (a). MIP image (b) shows diffuse NME with heterogeneous enhancement, also seen on subtracted image. (c) Stereotactic biopsy of the mammographic calcifications yielded pleomorphic and classic LCIS and slab image (d).
Fig. 7.9 Pleomorphic LCIS. Screening MRI identified linear nonmass enhancement in the left breast (negative mammogram). Two adjacent slices, each showing a source and a correlative subtraction image, are shown (a–d). Linear enhancement is noted extending from the posterior breast toward the nipple. A central enhancing duct and more lateral enhancing ducts are visible. Two inferior subtraction images (e, f) exhibit multiple areas of linear enhancement likely representing additional enhancing ducts. It should be noted that the duct enhancement is low, below standard thresholds on CAD systems. MR-guided biopsy yielded pleomorphic LCIS with pagetoid extension. High spatial resolution is necessary for visualization of these subtle findings.
Fig. 7.10 Pleomorphic LCIS and ALH. Screening MRI identified a focus in the lateral left breast, with associated linear enhancement extending anteriorly toward the nipple. This lesion was only identified on T1w postcontrast subtraction imaging, in part because of low initial enhancement. MR-guided biopsy yielded pleomorphic LCIS and ALH.
Fig. 7.11 FEA, columnar cell change. Screening MRI identified linear distribution with a clustered ring internal enhancement pattern (arrows) on T1w postcontrast subtraction image. This lesion was seen well on one subtraction slice only. MR-guided biopsy yielded FEA and columnar cell change.
Fig. 7.12 ADH; spot magnification mammographic image (a) shows a faint, 5-mm, cluster of calcifications in the posterior 4 o’clock position of the right breast. Stereotactic biopsy yielded ADH. Biopsy clip (arrow) is seen on the T1w postcontrast source image (b) and subtracted image (c). NME is noted surrounding the clip-on images (b, c) and an anterior focus is also noted (long arrow). MRI-guided biopsy of the anterior focus yielded ADH.
Fig. 7.13 Low-grade DCIS. Patient presented with left breast intermittent clear discharge. Loosely scattered dense punctate and pleomorphic calcifications, within an area of asymmetry, were noted in the inferomedial left breast at mammography (a, b). Galactography identified a normal secreting duct leading to an area of mammographic asymmetry (c). Stereotaxic biopsy of the mammographic calcifications yielded low-grade DCIS. MRI shows mild BPE on MIP image (d) but no other findings. Postcontrast T1w source images (e) and subtracted image (f) exhibit clumped central enhancement measuring 11 mm with anterior, linear (ductal), and branching enhancement extending to the nipple. Sagittal reformatted image (g) is shown. Histology: low-grade DCIS, cribriform, and micropapillary, scattered within 7.0 cm of background ADH.

7.5 Morphology of Ductal Carcinoma In Situ

NME is described in the ACR Breast Imaging Reporting and Data System (BIRADS) MRI Lexicon 17 as enhancement that is not a mass or focus but is still discrete from normal, surrounding BPE. This definition includes enhancement patterns that may extend over small or large regions and may exhibit normal fibroglandular tissue or fat interspersed between the abnormally enhancing components. NME is characterized by its distribution and pattern of internal enhancement (Table 7‑1), and is the reported lesion type in the majority of DCIS cases. 18 , 19 Although any distribution pattern can be seen in DCIS lesions, segmental and linear enhancement is most commonly found. 10 , 19 , 20 The lexicon descriptors for NME are discussed below.

Table 7.1 Descriptors for nonmass enhancement


a. Focal

b. Linear

c. Segmental

d. Regional

e. Multiple regions

f. Diffuse

Internal enhancement patterns

a. Homogeneous

b. Heterogeneous

c. Clumped

d. Clustered ring

Source: American College of Radiology. 17

7.5.1 Distribution of Enhancement

Focal enhancement is defined as a small, confined area whose internal enhancement may be characterized as a nonmass internal enhancement pattern, occupying less than a breast quadrant volume and may exhibit fat or normal glandular tissue interspersed between the abnormally enhancing components (Fig. 7‑14). Linear enhancement is arrayed in a line (not necessarily a straight line) or a line that branches (Fig. 7‑15). This distribution may elevate suspicion for malignancy as it suggests enhancement within or around a duct. Segmental enhancement is defined as triangular or cone shaped with the apex at the nipple, suggesting enhancement within or around a duct or ducts and their branches, thus increasing the likelihood of malignancy (Fig. 7‑16, Fig. 7‑17, Fig. 7‑18, Fig. 7‑19). Regional enhancement encompasses more than a single duct system and is used for enhancement that occupies a large portion of breast tissue, at a minimum 25% of a quadrant. This distribution pattern can be seen in invasive cancers such as lobular or HER2-enriched lesions in addition to DCIS lesions, bearing in mind that lack of orientation toward the nipple might suggest an invasive process (Fig. 7‑20). Enhancement of multiple regions, by definition, does not conform to a segmental distribution and is seen in at least two large volumes of tissue (Fig. 7‑21). Diffuse categorization is defined as enhancement being distributed randomly throughout the breast (Fig. 7‑22).

Fig. 7.14 NME distribution: focal enhancement. Magnified image of the left breast LMCC shows a posterior saline implant and a cluster of punctate calcifications at 2 o’clock position mid-depth (a, arrow). Axial postcontrast T1w image shows bilateral saline implants and a correlative focal NME (b), seen also on slab image (thin MIP) (c) and subtraction image (d). Reformatted slab images, sagittal (e) and coronal (f), show the extent of this focal area of enhancement to advantage. Histology: 1-mm tubular carcinoma associated with 7-mm low-grade DCIS, ER/PR (+), HER-2/neu (–).
Fig. 7.15 NME distribution: linear enhancement. High-risk screening MRI shows enhancing masses in the central right breast and anteromedial left breast, both representing known fibroadenomata, seen on MIP image (a). Source postcontrast T1w image (b) shows possible linear enhancement (arrow), confirmed on subtraction images (c, d) (arrows), where multiple linear (ductal) areas of enhancement are identified. When multiple enhancing ducts are identified, segmental enhancement could also be described as linear, as shown on the sagittal reformatted image (e). MR-guided biopsy yielded high-grade DCIS, solid, ER (+), PR (–).
Fig. 7.16 NME distribution: segmental enhancement. Screening mammogram identified pleomorphic microcalcifications, segmentally distributed, in the upper outer quadrant of the left breast, with calcifications extending to the skin as shown in magnified CC image (a). MRI shows anterior left breast NME on the MIP image (b) with correlative T2w image (c) and slab postcontrast subtracted image (d). Postcontrast source subtraction images (d–f) show segmental enhancement from the anterior to the posterior breast, with individual ducts visible, and associated clumped enhancement. Sagittal reformatted image (g) is shown. Histology: DCIS, intermediate and high nuclear grade, associated with necrosis and microcalcifications, ER/PR (–).
Fig. 7.17 NME distribution: segmental enhancement. Screening mammogram identified pleomorphic linear calcifications in the anterolateral left breast on LMCC image (a). Stereotactic biopsy yielded carcinoma in situ, high-grade, solid type with central necrosis and associated microcalcifications. MRI shows a seroma at the site of stereotactic biopsy (short arrow) and linear (ductal) NME (long arrow) within a region of segmental enhancement extending from the central breast toward the nipple, on postcontrast thin MIP image (b). T1w postcontrast subtraction image (c) shows ducts enhancing below the CAD threshold, as seen on image (d). Sagittal slab reformatted source image (e) shows the distribution of NME (short arrows) and an anterior (postbiopsy) enhancing seroma (long arrow). (f, g) A correlation between NME in the central left breast on MRI and a region of asymmetry and distortion without calcification on the cropped CC mammogram. Histology: ductal carcinoma in situ, intermediate grade, solid type with associated central necrosis and microcalcifications.
Fig. 7.18 NME distribution: segmental enhancement. MRI screening of the left breast at time of a newly diagnosed right breast ILC is shown. Left breast mammogram was normal. A segmental NME occupying an entire breast lobe is seen on postcontrast T1w axial source image (a) and subtraction image (b). Extensive NME, extending from the posterior breast to the nipple, exhibits clumped and linear enhancement. The main lactiferous duct is shown to enhance to the nipple, seen well on sagittal reformatted image (c). Histology: ductal carcinoma in situ, high nuclear grade, solid type, with atypical lobular hyperplasia and DCIS focally extending into lactiferous duct of the nipple.
Fig. 7.19 NME distribution: segmental enhancement. Screening mammography identified a slight increase in the number of loosely scattered faint punctate and pleomorphic calcifications seen in the lateral left breast on cropped LMMLO view. (a) Biopsy of these calcifications revealed ADH and LCIS. MRI was requested for further assessment. Extensive segmental non-mass-like enhancement in the lateral left breast is noted on postcontrast MIP image (b) corresponding to the region of mammographic calcification. Several benign foci are also noted in the right breast. (c) Homogeneous enhancement and clumped NME, and (d) a seroma (arrow) from prior biopsy. Axial (e), sagittal (f), and coronal (g) slab reformatted images show the extent of enhancement. Histology: mammary carcinoma in situ, intermediate grade with mixed ductal and lobular features, associated with necrosis and calcification, ER/PR (+) with three foci of microinvasion.
Fig. 7.20 NME distribution: regional enhancement. Anterior and lateral regional enhancement and skin thickening is seen in the left breast on axial postcontrast thin MIP image (a). Axial T2w non-fat-sat image (b) shows skin thickening and fluid extending from distorted lateral breast tissue to the pectoral muscle (arrows). Precontrast T1w image (c), postcontrast source (d), and subtracted image (e) show skin thickening. (d, e) Nonmass enhancement. Reformatted images, sagittal (f) and coronal (g), show the extent of the regional enhancement. Left breast skin biopsy yielded invasive lobular carcinoma, infiltrating the dermis. Final histology: invasive lobular carcinoma, grade I/III, spanning an area of approximately 27.0 cm. ER/PR (+), Her2/neu (–). 13/18 positive axillary lymph nodes were identified with extracapsular extension present. Although the NME diagnosed in this case is similar to that seen in DCIS, the distribution is not segmental and therefore other etiologies should be considered. The presence of skin thickening and enhancement and posterior T2 fluid all indicate an aggressive invasive lesion.
Fig. 7.21 NME distribution: multiple regions enhancement. Mammography identifies two regions of developing asymmetry in the left breast (a, b, arrows). Correlative ultrasound of the medial asymmetry shows a hypoechoic irregular lesion (c) with increased blood flow on color Doppler (d). Postcontrast MIP image (e) exhibits nonmass enhancement in the central, lateral, and medial left breast. Diffuse distortion in the central left breast is seen on T2w non-fat-sat image (f, arrows) and precontrast T1w image (g, arrows). Postcontrast axial source image (h) and subtracted image (i) exhibit heterogeneous enhancement with predominantly persistent enhancement, seen on the angiomap image (j). Postcontrast axial source image (h) and subtracted image (i) exhibit heterogeneous enhancement with predominantly persistent enhancement, seen on the angiomap image (j). Thin MIP axial image (k) demonstrates the extent of nonmass enhancement, whereas sagittal and coronal reformatted images (l,m) additionally exhibit “ring-like” areas of tumor necrosis. Histology: triple-negative IDC grade 3 with associated DCIS. One positive sentinel node (1/3).
Fig. 7.22 NME distribution: diffuse enhancement. Diffuse pleomorphic calcifications were found in the left breast on mammography, with stereotactic biopsy yielding DCIS. MRI was requested for assessment of disease extent. Postcontrast MIP image (a) shows diffuse NME throughout the left breast with associated increased vascularity. Postcontrast source image (b) and subtraction image (c) show diffuse left breast enhancement. Slab reformatted images; axial (d), sagittal (e), and coronal (f) show the extent of disease with the sagittal image demonstrating orientation of enhancement toward the nipple. Histology: widespread high-grade solid DCIS with scattered foci of microinvasion.

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Feb 15, 2021 | Posted by in BREAST IMAGING | Comments Off on 7 Image Interpretation: Noninvasive Cancer
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