Breast cancer classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mirdula Sharma, MBBS [2] Soroush Seifirad, M.D.[3]

Overview[edit | edit source]

Breast cancer may be classified according to anatomy into 4 subtypes: ductal, lobular, sarcoma, and lymphoma. There are also other methods of classification such as classification based on gene expression, and classification based on hormone receptors present. In practice, a combination of all above mentioned classification is combined with the surgical characteristics of tumors and radiologic findings is being applied for patient management, treatment planning, and prognosis determination.

Classification based on histopathology[edit | edit source]

Malignant Tumors[edit | edit source]

Benign Tumors[edit | edit source]

• Phyllodes tumor^[1]
• Mammary fibromatosis: 0.2% of all breast tumors 5
• Benign papillary lesions of the breast

• Papilloma

• Intraductal papilloma
• Solitary papilloma of breast
• Central solitary papilloma of breast
• Peripheral solitary papilloma of breast
• Multiple papillomata of breast

• Juvenile papillomatosis of breast

• Granular cell tumor of the breast

Classification based on hormone receptors present[edit | edit source]

• Hormone receptor positive: either estrogen or progesterone receptors are present
• Hormone receptor negative: breast cancer cells do not have either estrogen or progesterone receptors
• HER2 positive: If excess copies of HER2 gene
• HER2 negative: If excess copies of HER2 gene are not present
• Triple positive: cancers that are ER-positive, PR-positive, and have too much HER2
• Triple negative: If the breast cancer cells don not have estrogen or progesterone receptors and don’t have too much HER2

Classification based on gene expression[edit | edit source]

• Luminal type: are estrogen receptor (ER)–positive

• Luminal A:

• Expression of luminal (low molecular weight) cytokeratins, high expression of hormone receptors and related genes
• 50% of invasive bresat cancer, ER/PR positive, HER2/neu negative
• Tubular carcinoma, Cribriform carcinoma, Low grade invasive ductal carcinoma, NOS, Classic lobularcarcinoma
• Response to endocrine therapy
• Variable response to chemotherapy
• Low grade,
• Grows slowly,
• Good prognosis (the best prognosis)

• Luminal B :

• Expression of luminal (low molecular weight) cytokeratins, moderate-low expression of hormone receptors and related genes
• 20% of invasive breast cancer, ER/PR positive, HER2/neu expression variable, higher proliferation than Luminal A, higher histologic grade than Luminal A
• Invasive ductal carcinoma, NOS Micropapillary carcinoma
• Response to endocrine therapy (tamoxifene and aromatase inhibitors) not as good as Luminal A
• Variable response to chemotherapy (better than Luminal A)
• Prognosis not as good as Luminal A
• Grows faster

• HER2/neu

• High expression of HER2/neu, low expression of ER and related genes
• 15% of invasive breast cancer, ER/PR negative, HER2/neu positive, high proliferation, diffuse TP53 mutation, high histologic grade and nodal positivity
• High grade invasive ductal carcinoma, NOS
• Response to trastuzumab (Herceptin)
• Response to chemotherapy with antracyclins
• Usually unfavorable prognosis

• Basal like

• High expression of basal epithelial genes and basal cytokeratins, low expression of ER and related genes, low expression of HER2/neu
• ~15% of invasive breast cancer, most ER/PR, HER2/neu negative (triple negative), high proliferation, diffuse TP53 mutation, BRCA1 dysfunction (germline, sporadi
• High grade invasive ductal carcinoma, NOS Metaplastic carcinoma, Medullary carcinoma
• No response to endocrine therapy or trastuzumab
• Sensitive to platinum group chemotherapy and PARP inhibitors
• Not all, but usually worse prognosis^[2]

References[edit | edit source]

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