Tag Archives: breast

Breast Myofibroblastoma

Myofibroblastoma (MFB) of the breast is an uncommon but well described benign stromal neoplasm of the breast.  MFB can have many different morphologic patterns (see variants below), but important defining characteristics include:

  • Mesenchymal tumor without epimyoepithelial elements
  • No necrosis
  • Low proliferative activity (≤2 mitoses/10 hpf)
  • No atypical mitoses
  • Characteristic immunophenotype

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Special Subtypes of Breast Carcinoma

  • Lobular Carcinoma
  • Medullary Carcinoma
    • Pattern characteristic of BRCA1 associated carcinomas
      • 13% are medullary type
      • 60% have subset of medullary features
    • Well-circumscribed mass
      • Solid sheets of pleomorphic large cells containing prominent nucleoli In >75% of the mass
      • Frequent mitosis
      • Prominent lymphoplasmacytic inflammatory infiltrate surrounding and infiltrating the tumor
      • Pushing/non-infiltrating border
      • DCIS is minimal or absent
    • WHO recommends classifying tumor as “carcinomas with medullary features”
  • Micropapillary Carcinoma
  • Mucinous (colloid) carcinoma
  • Tubular Carcinoma
  • Papillary Carcinoma
  • Secretory Carcinoma
  • Inflammatory Carcinoma
    • Clinically present with breast erythema and thickening (peau d’orange)
    • Dermal lymphatics filled with tumor
    • 3-year survival rate 3-10%
  • Neuroendocrine Tumors
    • Well-differentiated Neuroendocrine Tumor
    • Small Cell Carcinoma

References

Kumar, Vinay, Abul K. Abbas, and Jon C. Aster. Robbins and Cotran Pathologic Basis of Disease. Ninth edition. Philadelphia, PA: Elsevier/Saunders, 2015.

Breast – Invasive Carcinoma

Invasive Breast Carcinoma
  • Invasive breast carcinomas not segregated out as a special subtype are classified as invasive ductal carcinoma, no special type (NST).  These tumors (and most of the special types) have prognosis and treatment plans based on the receptor status (and sometimes additional molecular profiling).
  • Receptor testing includes ER/PR/Her-2 and Ki-67 (proliferation marker)

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Breast Carcinoma – Risk Factors

  • Most common cancer in women (~225,000 cases/yr. with ~40,000 deaths/yr.)
  • Second most common cause of cancer death in women (lung #1)
  • Three major subtypes
    • ER+/Her-2 negative (50-65%)
    • Her-2 + (10-20%)
    • Triple negative – ER/PR/Her-2 negative (10-20%)
  • Breast cancers in African American women are more aggressive biologically, and are more likely to be ER-negative and high nuclear grade

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Breast – DCIS

Ductal Carcinoma In Situ (DCIS)
  • Neoplastic proliferation resembling small ducts with expanded duct and acinar structures
  • Myoepithelial cell layer is intact surrounding the neoplastic proliferation (non-invasive tumor)
  • Typically express E-Cadherin
  • Bilateral in 10-20% of cases
  • Detected by mammography (not clinically evident)
  • Represents 15-30% of neoplasms identified in screening populations
  • Typically identified by abnormal calcification, sometimes as abnormal densities
Comedo DCIS
  • High grade pleomorphic nuclei
  • Central necrosis
Non-comedo DCIS
  • Lacks either high grade nuclei or central necrosis
  • Subtypes/patterns
    • Solid DCIS
    • Micropapillary DCIS
    • Cribiform DCIS
  • DCIS grading
    • Low-grade DCIS
      • 1%/year risk of developing an invasive carcinoma
    • Intermediate-grade DCIS
    • High-grade DCIS
Paget Disease
  • Nipple manifestation of disease (1-4% of cases) – looks like eczema on the nipple
  • Tumor cells extend into the epidermis of the skin overlying the nipple from underlying DCIS within the ductal system of the breast.
  • 50-60% of women will have an underlying palpable mass
    • Vast majority will have an invasive carcinoma (often ER neg./Her-2 pos.)
    • Women without a palpable mass will usually only have DCIS
Photomicrographs
Breast - High Grade DCIS
High power view of high grade breast DCIS.
Breast - High Grade DCIS
High power view of breast high grade DCIS.
Smooth Muscle Myosin - High Grade DCIS
Smooth Muscle Myosin – High Grade DCIS
Smooth Muscle Myosin - High Grade DCIS
Smooth Muscle Myosin – High Grade DCIS
Smooth Muscle Myosin - High Grade DCIS
Smooth Muscle Myosin – High Grade DCIS
References

Kumar, Vinay, Abul K. Abbas, and Jon C. Aster. Robbins and Cotran Pathologic Basis of Disease. Ninth edition. Philadelphia, PA: Elsevier/Saunders, 2015. 

Breast – Atypical Lobular Hyperplasia (ALH)

Atypical lobular hyperplasia is a proliferation of epithelial cells in the terminal duct-lobular unit that lacks expression of E-cadherin and fills the lobular unit (but does not expand).  Some define ALH as filling or distending <50% of the acini within an affected lobule.  There is some variation between experts as the exact differentiating line between ALH and lobular carcinoma in situ (LCIS).  It is best to think of ALH and LCIS as representing a morphologic spectrum with filling and distention of lobular acini being the measured characteristic.
 
In some cases ALH/LCIS may appear similar to DCIS or merge with areas of DCIS.  E-cadherin is a helpful marker to differentiate between these lesions.  Clinically it is important to differentiate ALH/LCIS from DCIS because LCIS/ALH is an incidental finding on mammogram and represents a risk factor for bilateral breast carcinomas.  Management is not through local excision, but surveillance and hormonal therapy dependent upon the type of lesion.  DCIS is treated through local excision because these lesions tend to be localized/focal.
 
ALH carries an increased risk of developing an invasive breast carcinoma (4-5x relative risk, 13-17% lifetime risk), while LCIS carries an 8-10x increased relative risk, 25-30% lifetime risk).  These are the same risks as ALH and DCIS, respectively.  Although ALH/LCIS risk is bilateral, while ADH/DCIS tends to be more ipsilateral. 
Breast lesions and risk of developing an invasive carcinoma
Breast Cancer Risk Chart
Breast Cancer Risk Chart

References

Kumar, Vinay, Abul K. Abbas, and Jon C. Aster. Robbins and Cotran Pathologic Basis of Disease. Ninth edition. Philadelphia, PA: Elsevier/Saunders, 2015.  p. 1050-1051