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EndoRepro 2 Exam 1 > Path Pt 1: Breast > Flashcards

Path Pt 1: Breast Flashcards

1
Q

supernumerary nipples or breasts

A

persistence of epidermal thickenings along the milk line

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2
Q

normal ductal system may extend into the SQ tissue of the chest wall or axillary fossa (axillary tail of Spence)

  • areas not clinically identified as breast tissue
  • prophylactic mastectomies reduce, but do NOT eliminate the risk of breast cancer
  • most breast tissue drains to axillary lymph nodes
A

accessory axillary breast tissue

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3
Q

congenitally inverted nipples are usually of little significance
- correct spontaneously during pregnancy or with simple traction

A

congenital nipple inversion

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4
Q

what is more of a concern than congenital nipple inversion?

A

acquired nipple inversion

- may indicate invasive cancer or inflammatory nipple disease

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5
Q

mastalgia, mastodynia

A

breast pain

  • diffuse: usually due to premenstrual edema
  • localized: often due to ruptured cysts, physical injury, infection
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6
Q

almost all painless masses are what?

A

benign

- only 10% of breast cancers present with pain

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7
Q

most commonly, masses are what?

A

cysts, fibroadenomas, or invasive carcinomas

- usually benign in premenopausal women

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8
Q

what are the likelihoods of malignancy with age?

A
  • 10% < 40 years
  • 60% > 50 years

NOTE: risk of malignancy in a woman with nipple discharge also increases with age

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9
Q

how are 1/3 of carcinomas detected?

A

palpable masses

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10
Q

why does screening have little effect on mortality?

A

because most palpable cancers have metastasized

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11
Q

what is considered the most worrisome for carcinoma if spontaneous, unilateral and the patient is >60?

A

nipple discharge

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12
Q

what is milky galactorrhea associated with?

A

increase in prolactin, hypothyroidism, endocrine anovulatory syndromes, methyldopa, phenothiazines

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13
Q

when is bloody or serous nipple discharge usually seen?

A

with a papilloma or cyst

- blood also seen during pregnancy due to rapid tissue remodeling

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14
Q

what should you think of in a patient >60 years old that presents with spontaneous unilateral discharge?

A

cancer

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15
Q

what is the most common site for breast carcinoma in females?

A

upper outer: 50%
20% central or sub-areolar (most common in males)
10% in remaining quadrants

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16
Q

what are the most common palpable masses in the breast?

A

cysts, fibroadenomas, and invasive carcinomas

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17
Q

benign lesions are more common with who?

A

premenopausal women

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18
Q

what are the principal signs of breast carcinoma?

A

densities and calcifications

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19
Q

what is the most common way to detect breast cancer?

A

mammogram

- increase sensitivity and specificity as patient ages: fibrous, radiodense tissue -> fatty radiolucent tissue

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20
Q

lesions that replease adipose tissue with radiodense tissue

  • rounded = benign fibroadenoma or cyst
  • irregular = invasive carcinoma
A

densities

- mammography identifies lesions 1cm in size vs 2-3cm by palpation

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21
Q

these form on sevretions, necrotic debris or hyalinized stroma
- usually benign lesion: clusters of apocrine glands, hyalinized fibroadenomas, sclerosing adenosis

A

calcifications

- if associated with malignancy: small, irregular, numerous and clustered -> ductal carcinoma in situ

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22
Q

rare, outside of lactational period

- caused by infections, autoimmune disease, or foreign body-type reactions to extravasated keratin secretions

A

inflammatory disorders of the breast

  • “inflammatory breast cancer” mimics inflammation by obstruction dermal vasculature with tumor emboli
  • ALWAYS consider in females with erythematous, swollen breast
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23
Q
  • acute mastitis
  • squamous metaplasia of lactiferous ducts
  • duct ectasia
  • fat necrosis
  • lymphocytic mastopathy (diabetic mastopathy)
  • granulomatous mastitis
A

types of inflammatory breast disorders

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24
Q

cracks and fissures of the nipple cause the breast to be vulnerable to bacteria during the first month of breast feeding
- erythematous and painful

A

acute bacterial mastitis

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25
Q

what organisms cause acute bacterial mastitis?

A

staphylococcus aureus (step less commonly) invade the tissue involving a single duct system or sector

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26
Q

what can happen if mastitis is left untreated?

A

can spread to the entire breast

  • staph -> single or multiple abscesses
  • strep -> cellulitis
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27
Q

what is the tx for mastitis?

A

abx, continue expression of breast milk, rarely requires surgery

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28
Q

subareolar abscesses, periductal mastitis, Zuska disease

  • painful, erythematous subareolar mass that appears to be a bacterial abscess
  • recurrent: fistula tunnels under smooth muscle of the nipple, opening to the skin at the edge of the areola
  • inverted nipple
A

squamous metaplasia of lactiferous ducts

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29
Q

what are the risk factors for squamous metaplasia of lactiferous ducts?

A

90% of patients are smokers

- may be due to relative vitamin A deficiency, or toxic substance in tobacco smoke

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30
Q

keratinizing squamous metaplasia of the nipple ducts

  • ductal system is plugged by shed cells -> dilation and eventually rupture of the duct
  • acute inflammation may occur secondary to anaerobic bacterial infection
A

squamous metaplasia of lactiferous ducts

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31
Q

what happens when keratin spills into the surrounding periductal tissue?

A

intense chronic granulomatous response

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32
Q

what is the tx for squamous metaplasia of lactiferous ducts?

A

they commonly recur following drainage due to remaining keratinizing epithelium
- curative if the duct and fistula tract are surgically removed

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33
Q

palpable areolar mass

  • associated with thick, white nipple secretions, +/- skin retraction
  • pain and erythema are RARE
  • IRREGULAR PALPABLE MASS MIMICS INVASIVE CARCINOMA CLINICALLY AND ON IMAGING
A

duct ectasia

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34
Q

what are the risk factors for duct ectasia?

A

susceptible females are multiparous and in their 5-6th decade
- NOT associated with smoking

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35
Q

ectatic dilated ducts with inspissated (thickened) secretions and lipid laden macrophages

  • rupture -> periductal and interstitial inflammatory reaction with lymphocytes and plasma cells also joining the party
  • formation of granulomas around cholesterol deposits and secretions -> irregular mass with skin and nipple retraction
A

duct ectasia

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36
Q

painless, palpable mass with skin thickening or retraction and/or mammographic densities or calcifications
- 50% of females have history of prior surgery or breast trauma

A

fat necrosis in the breast

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37
Q

what does acute fat necrosis look like on a histo slide?

A

neutrophils and macrophages

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38
Q

what does chronic fat necrosis look like on a histo slide?

A

fibroblasts and inflammatory cells lead to giant cells, calcifications and deposition of hemosiderin -> scar tissue (ill-defined, firm, grey white nodules containing small chalky white foci

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39
Q

single or multiple hard, palpable masses or mammographic densities

  • dense collagenized stroma = difficult to need biopsy
  • thick BM of atrophic ducts and lobules
  • surrounded by prominent lymphocytic infiltrate
A

lymphocytic mastopathy (sclerosing lymphocytic lobulitis)

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40
Q

what patients is lymphocytic mastopathy most common in?

A
  • *T1DM** or autoimmune

- thought to be autoimmune problem

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41
Q

may be due to systemic or localized granulomatous disease (TB, sarcoidosis)

  • uncommon
  • occurs in parous females, associated with lobules
  • possibly a hypersensitivity reaction to antigens expressed by lactation
A

granulomatous mastitis

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42
Q

what is the tx for granulomatous mastitis?

A

steroids

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43
Q

what is caused by corynebacteria?
- causes a localized infection of TB or fungi due to the immunocompromise or adjacent to foreign objects (piercing or prosthesis)

A

cystic neutrophilic granulomatous mastitis

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44
Q

these lesions are detected by mammography or as incidental findings in surgical specimens
- three groups: nonproliferative, proliferative, atypical hyperplasia

A

benign epithelial lesions

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45
Q

these benign lesions are NOT associated with an increased risk of breast cancer

A

non-proliferative breast changes

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46
Q

small increase in the risk of subsequent carcinoma in either breast
- predictors of risk but unlikely to be true precursors of carcinoma

A

proliferative breast disease (without atypia)

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47
Q

has some but not all histological features required for diagnosis of carcinoma in situ
- moderately increased risk of carcinoma

A

atypical hyperplasia

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48
Q

group of morphological fibrocystic changes

  • not associated with risk of breast cancer (non-proliferative)
  • cystic change, often with apocrine metaplasia
  • fibrosis
  • adenosis
A

non-proliferative (fibrocystic) breast changes

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49
Q

what causes cysts in non-proliferative breast changes?

A

due to lobule dilation

  • may coalesce into larger cysts
  • unopened cysts contain turbid, semi-translucent brown-blue fluid (blue domed cyst)
  • lined with flattened, atrophic epithelium or metaplastic apocrine cells
  • calcifications commonly seen on mammography (concerning if they are solitary or firm to palpation)
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50
Q

what is the dx of cysts?

A

confirmed after disappearance of the cysts due to fine needle aspiration of contents

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51
Q

occurs due to release of secretory material into the stroma from (often) ruptured cysts
- contributes to palpable nodularity of the breast

A

fibrosis

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52
Q

increase in the number of acini/lobule

  • normal in pregnancy or focal change in nonpregnant females
  • lined with columnar cells
  • chromosome 16 deletion = FLAT EPITHELIAL ATYPIA
  • mass and/or calcifications seen in the lumen
A

adenosis

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53
Q

what is the earliest recognizable precursor lesion of low-grade breast cancer?

A

chromosome 16 deletion -> flat epithelial atypia

- no increased risk of breast cancer

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54
Q

palpable masses in pregnancy or lactating women

- normal appearing breast tissue with exaggerated lactational changes

A

lactational adenoma

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55
Q

proliferations of epithelial cells without atypia

  • small increase in risk of subsequent carcinoma of either breast
  • **predictors of risk but unlikely to be true precursors of carcinoma
  • no clonal lesions or genetic changes
A

proliferative breast disease without atypia

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56
Q

increase in number of luminal (ductal) and myoepithelial cells fill and distend ducts and lobules

  • normal: ducts and lobules are lined with a double layer of myoepithelial cells and luminal cells
  • irregular lumens found in the periphery (usually incidental finding)
A

epithelial hyperplasia

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57
Q

increase is number of ACINI are compressed and distored in the central portion of the lesion
- lumen compression due to stromal fibrosis (sclerosing part) -> histological pattern that closely mimics invasive carcinoma

A

sclerosing adenosis

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58
Q

sclerosing adenosis, papilloma, and epithelial hyperplasia

  • radical scar irregularly shaped, mimics invasive carcinoma
  • central nidus of entrapped glands in hyalinized stroma surrounded by long, radiating projections into stroma
  • not associated with prior trauma or surgery
A

complex sclerosing lesion

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59
Q

growth within a dilated duct

  • composed of intraductal lesions with fibrovascular cores lined by myoepithelial and luminal cells (both)
  • 80% produce nipple discharge
  • usually solitary and seen in the lactiferous sinuses of the nipple
  • small duct = multiple and located deeper in the ductal system
  • often seen with epithelial hyperplasia and apocrine metaplasia
A

papilloma

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60
Q

what causes bloody discharge in a papilloma?

A

infarct of stalk due to torsion

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61
Q

what causes serous discharge in a papilloma?

A

intermittent blockage and release of secretins

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62
Q

what is NOT a pre-cursor to cancer, unlike most other forms of metaplasia?

A

apocrine metaplasia

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63
Q

enlargement of the male breast, only BENIGN lesion of the male breast

  • unilateral or bilateral button-like subareolar enlargement
  • small increase risk of breast cancer
  • increase in dense, collagenous connective tissue and epithelial hyperplasia of the duct lining with tapering micro-papillae
  • no lobule formation
A

gynecomastia

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64
Q

imbalance between estrogens and androgens due to

  • puberty
  • aging
  • decreased testicular androgen production
  • hyperestrinism
  • liver cirrhosis
  • drugs (alcohol, marijuana, heroin, antiretroviral, steroids)
  • klinefelter or functional testicular neoplasms
A

causes of gynecomastia

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65
Q

clonal proliferation with some, but not all, histological features of ductal carcinoma in situ (DCIS)

  • moderate increase in the risk of carcinoma of the breast
  • chromosome 16q loss or 17p gain (also seen in CIS)
  • pagetoid spread
A

proliferative breast disease with atypia

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66
Q

partially fills duct - ductal carcinoma in situ fills the duct)

  • may have cribiform spaces
  • monomorphic epithelial proliferation
A

atypical ductal hyperplasia

67
Q

cells identical to lobular carcinoma is situ (LCIS)

  • atypical lobular cells that do not fill/distend > 50% lobule acini
  • the atypical lobular cells may lie between the ductal basement membrane that the normal luminal cells
  • LOSS OF E-CADHERIN (same as lobular carcinoma in situ)
A

atypical lobular hyperplasia

68
Q
  • 1.5-2x increased risk of cancer in proliferative disease
  • 4-5x increased risk of cancer in proliferative disease with atypia
  • <20% develop breast cancer and may choose surveillance over radical treatment options
  • risk is increased in BOTH breasts, though ipsilateral may have higher risk
  • tx may involve bilateral prophylactic mastectomy or estrogen antagonists (tamoxifen)
A

risk of carcinoma from BENIGN epithelial lesions

69
Q

what is the most common non-skin malignancy in females?

A

carcinoma of the breast

- 2nd most common cause of cancer death in women after lung cancer

70
Q

what are the three biological groups of adenocarcinoma of the breast?

A
  1. estrogen receptor positive, HER2-negative = 50-65%
  2. estrogen receptor positive/negative, HER2-positive = 10-20%
  3. estrogen receptor negative, HER2-negative = 10-20%
71
Q

rare in females < 25, rapid increase in incidence after 30

  • increased risk due to western lifestyle: delayed pregnancy, fewer pregnancies, and decreased breastfeeding
  • African American females have highest mortality rate as they have less access to screening and they have more aggressive cancers
  • non-Hispanic women have the greatest risk, Ashkenazi jews are more likely to have BRCA1/2 mutations
A

risk factors for adenocarcinoma of the breast

72
Q

earlier menarche or later menopause

  • later pregnancy, or no pregnancy
  • atypical hyperplasia or proliferative disease
  • menopausal hormone therapy with estrogen and progestin over multiple years
A

risk factors for adenocarcinoma of the breast

73
Q

what are most breast cancers?

A

estrogen receptor positive cacinoma

  • no associated risk with oral contraceptive therapy
  • oopherectomy (decreasing estrogen) causes 75% decrease in chance of breast cancer
  • antiestrogenic drugs (tamoxifen or aromatase inhibitors) decrease risk of estrogen receptor positive breast cancer
74
Q

4-6x increase risk of estrogen receptor positive or negative

  • clusters in families
  • related to other factors (late age at first birth, fewer children, hormone replacement therapy)
  • may be due to failure or normal involution in older females
A

dense breast risk factors

75
Q

Hodgkin patients in their teens and early 20’s have what?

A

20-30% increase risk over 10-30 years with radiation exposure

76
Q
  • moderate or heavy alcohol intake
  • obese postmenopausal females due to increase risk of estrogen synthesis in fat deposits
  • obese females > 40 have DECREASED risk due to anovulatory cycles and low progesterone levels
  • probable small protective effect for physically active females
  • no associated risk with intake of any foods
A

metabolism risk factors for breast carcinoma

77
Q

why is it that the longer women breastfeed, the lower their risk of carcinoma?

A

lactation suppresses ovulation and may trigger terminal differentiation of luminal cells
- may explain lower rates in developing countries

78
Q

12% of breast carcinomas occur due to what?

A

inheritance of susceptibility genes

  • may be AD
  • BRCA1/2, TP53, CHEK2 (all tumor supressors) 8% of familial breast carcinomas
79
Q

what is Li-Fraumeni syndrome?

A

germline mutation in TP53, associated with HNPCC -> most commonly HER2-positive

80
Q

what does a mutation in PTEN cause?

A

Cowden syndrome

81
Q

what does a mutation in STK11 cause?

A

Peutz-Jeghers syndrome

82
Q

what does a mutation in ATM cause?

A

ataxia telangiectasia

83
Q

what is responsible for 80-90% of “single gene” occurrences?

A

BRCA 1/2 in breast carcinoma

  • 3% of all breast cancers
  • 30-90% penetrance depending on specific mutation
  • also increased risk of other epithelial cancers (prostate or pancreatic)
84
Q

located on chromosome 17q21

  • marked increase in risk of ovarian carcinoma
  • often poorly differentiated
  • have medullary features (syncytial growth pattern with pushing margins and lymphocytic response)
  • biologically similar to ER-neg, HER2-neg breast cancers identified as “basal-like” by gene expression profiling
A

BRCA1

85
Q

located on chromosome 13.12.3

  • more frequently associated with MALE breast cancer
  • relatively poorly differentiated, more likely to be ER-positive
A

BRCA2

86
Q

arise via the dominant pathway of breast cancer development in 50-60% of cases

  • most common subtype of breast cancer in individuals who inherit germline mutations of BRCA2
  • most common form of invasive breast cancer
  • associated with chromosome 1q gains, chromosome 16q loss, and PIK3CA activating mutations
A

Er(+), HER2(+)

87
Q

what are thought to be precursor lesions for ER(+), HER2(+) breast cancer?

A

same mutations as seen in flat epithelial atypia and atypical ductal hyperplasia

88
Q

what type of breast cancers are termed “luminal”?

A

ER(+)

  • most closely resemble normal breast luminal cells regarding mRNA expression
  • dominated by genes regulated by estrogen
89
Q

these represent 20% of all breast cancers, can be ER(+) or (-)

  • associated with HER2 gene amplification on chromosome 17q
  • can be over-expressed if there is ERBB2 mutation
A

HER2(+)

90
Q

what is the most common cancer in patients with TP53 mutations (Li-Fraumeni syndrome)?

A

HER2(+) breast cancer

91
Q

what is the precursor lesion of HER(+) cancer?

A

atypical apocrine adenosis

92
Q

how do you look for HEr(+)?

A

HER2 staining or FISH amplification

93
Q

this cancer arises through a distinct pathway, independent of estrogen receptor mediated changed or HER2 amplifications

  • 15% of all breast cancers
  • MOST COMMON IN PATIENTS WITH GERMLINE BRCA1
A

ER(-), HER2(-)

94
Q

sporadic forms of ER(-), HER2(-) often have loss of what, instead of BRCA1?

A

TP53

- BRCA1 can be methylated/silenced later via epigenetics

95
Q

increased frequency in African American females

- basal-like pattern of mRNA expression that includes many genes that are expressed in normal myoepithelial cells

A

ER(-), HER2(-)

96
Q

PIK3CA, HER2, MYC, CCND1, TP53, BRCA1/2

A

driver mutations of breast cancer

  • subclonal heterogeneity contributes to tumor progression and resistance to treatment
  • the neoplastic cells require the stroma for development (high density regions)
  • fibrous stroma is a marker for risk
97
Q

52% of all single gene hereditary cancers

  • risk of breast cancer by age 70: 40-90%
  • mutations are rare, inactivated in 50%
  • tumor suppressor, transcription regulation, repair of dsDNA breaks
  • poorly differetiated
  • OFTEN TRIPLE NEGATIVE: ER(-), HER2(-), one other
  • associated with other cancers: ovarian, male breast, prostate, pancreas, fallopian tubes
A

BRCA1

98
Q

32% of all single gene hereditary cancers

  • risk of breast cancer by age 70: 30-90%
  • mutations and loss of expression are rare
  • tumor suppressor, transcription regulation, repair of dsDNA breaks
  • Biallelic germline mutations cause a rare form of Fanconi anemia
  • associated with other cancers: ovarian, male breast, prostate, pancreas, stomach, melanoma, gallbladder, bile duct, pharynx
A

BRCA2

99
Q

3% of all single gene hereditary cancers

  • risk of breast cancer by age 70 >90%
  • mutations in 20%
  • LOH (loss of heterozygosity): 30-42%
  • MOST FREQUENT IN TRIPLE (-) CANCERS
  • tumor supressor
  • most commonly mutation gene in sporadic breast cancers
  • 53% are ER(-), HER2(-)
  • associated cancers: sarcoma, leukemia, brain, adenocortical carcinoma
A

TP53

100
Q

95% of all breast malignancies

  • first arise in the duct/lobular system as CIS
  • at presentation, 70% have breached the basement membrane and invaded the stroma (malignant)
A

adenomcarcinoma

101
Q

neoplastic proliferation of epithelial cells confined to ducts and lobules by the basement membrane

  • may be classified as ductal or lobular (LCIS or DCIS)
  • actually arise from cells in the terminal duct lobular unit
A

CIS

102
Q

malignant clonal proliferation of epithelial cells limited to ducts and lobules by basement membrane

  • myoepithelial cells are preserved in involved ducts/lobules, though may be diminished
  • can spread through the ductal system -> extensive lesions of an entire breast sector
  • comedo or non-comedo
  • most have multiple growth patterns
A

DCIS (ductal)

103
Q

what is the dx of DCIS?

A

almost ALWAYS detected by mammography

  • identified as calcifications with secretory material, necrosis
  • less commonly identified as density due to periductal fibrosis
  • rarely produces nipple discharge
  • bilateral in 10-20% of cases
104
Q

what are the risk factors for DCIS?

A

nuclear grade and necrosis predict local recurrence and progression to invasion better than architecture

105
Q

these are usually detected as clustered or linear and branching areas of calcification on mammography
- may occasionally produce nodularity

A

comedo DCIS

106
Q

what are the two defining features of comedo DCIS?

A
  1. tumors with pleomorphic, high grade nuclei

2. areas of central necrosis

107
Q

lacks high grade nuclei or central necrosis

  • cribiform pattern: rounded spaces within ducts (cookie cutter) or solid pattern
  • micropapillary pattern: bulbous protrusions with fibrovascular core in complex intraductal patterns
  • true papillae pattern: fibrovascular core without myoepithalial cell layer
A

Non-comedo DCIS

108
Q

what is the tx for DCIS?

A

surgical excision and radiation/tamoxifen

- mastectomy 95% curative

109
Q

rare, unilateral erythematous eruption and scale crust (map-like)

  • pruritis is common, may be confused with eczema
  • malignant cells extend via the lactiferous sinuses into nipple skin, without crossing the basement membrane -> disruption of the epithelial barrier -> extracellular fluid leakage only nipple surface
A

Paget Disease of the Nipple

  • paget cells are larger than surrounding keratinocytes and are seen singly or in small clusters within the epidermis
  • the cells have pale cytoplasm containing mucopolysaccharide with stains PAS positive
110
Q

what is the dx of Paget disease of the nipple?

A

nipple biopsy or cytology of exudate

  • 50-60% have palpable mass that indicates there is also invasive carcinoma
  • carcinomas are poorly differentiated, Er(-), HER2(+)
  • IF NO PALPABLE MASS, TYPICALLY ONLY DCIS
111
Q

clonal proliferation of cells within ducts and lobules growing in a discohesive fashion due to acquired loss-of function mutation of E-cadherin

  • cells identical to hyperplasia or invasive carcinoma
  • cells expand, but do not distort spaces, preserving the underlying lobular architecture
  • 2x chance of being bilateral than DCIS, must check the other breast after being found
A

LCIS

112
Q

what is the dx of LCIS?

A
  • *ALWAYS AN INCIDENTAL BIOPSY FINDING**
  • not associated with calcifications of stromal reactions that produce mammographic densities
  • incidence did NOT decrease after introduction of mammogram screening
  • E-cadhern (-)
  • ER(+), PR(+), HER2(-)
  • LCIS is bilateral in 20-40% of cases
113
Q

uniform population of cells with oval/round nuclei and small nucleioli

  • mucin (+) signet ring cells
  • lack of E-cadherin = rounded cells not attached to adjacent cells (discohesive)
  • does not form cribiform spaces or papillae (like DCIS)
  • no involvement with nipple skin
  • no necrosis or secretions = no calcifications
A

LCIS

114
Q

what is LCIS a risk factor for?

A

invasive carcinoma

  • develops in 25-35% of women over 20-30 years
  • risk is almost as high in the contralateral breast (unlike DCIS)
  • 3x more likely to get invasive lobular carcinoma from LCIS than DCIS
115
Q

what is the tx for LCIS?

A

close follow up with mammographic screening since the risk of progression is similar to DCIS
- bilateral prophylactic mastectomy, tamoxifen can also be done

116
Q

ER(+), HER2(-), low proliferation

  • most common subtype of cancer in older females and males
  • most commonly detected via mammography
  • most common in females on hormone replacement therapy
  • often found at an early stage and cured by surgery
A

invasive carcinoma

117
Q

what is the tx for invasive carcinoma?

A 
hormone therapy (gene expression is regulated by estrogen receptors)
- chemotherapy not helpful
118
Q

estrogen receptor levels may be low and progesterone receptor may be low or absent

  • MOST COMMON CARCINOMAS ASSOC WITH BRCA2 GERMLINE MUTATION
  • mRNA expression similar to other ER(+) cancers
  • 10% show a complete response to chemo, better prognosis than patients who don’t respond
A

ER(+), HER2(-), high proliferation

119
Q

second most common molecular subtype of invasive breast cancer

  • 50% are ER(+), but there is low expression and absent progesterone receptor
  • more common in young, non-white females
  • half of patients with TP53 mutations (Li-Fraumeni syndrome) are ER(+)/HER2(+)
  • mRNA: increased HER2 expression and increase expression of proliferating genes
A

HER2(+)

120
Q

what is the dx of HER2(+)?

A

subtype is identified via protein over-expression or gene amplification
- detect HER2 with antibody or FISH

121
Q

what is the tx of HER2(+)?

A

1/3 respond completely to targeted monoconal Ab therapy (trastuzumab) that binds and blocks HER2 receptor activity = excellent prognosis
- many pts have resistance to trastuzumab due to truncated HER2

122
Q

most common in young, premenopausal females (especially African American or Hispanic)

  • palpable mass between mammographies due to high proliferation and rapid growth
  • share genetic similarities with serous ovarian carcinomas
A

ER(-), HER2(-) = Basal-like triple negative carcinoma

123
Q

majority of carcinomas arising in women with BRCA1 mutations are of this type
- must do assay for protein or gene amplification to determine if targeting ER or HER2 is indicated

A

ER(-), HER2(-)

- metastasize when small -> viscera + brain

124
Q

what is the tx of ER(-), HER2(-)?

A

30% respond well to chemotherapy

  • local recurrence is common, even with mastectomy
  • prolonged survival after distant metastasis is rare
125
Q

calcifications on mammography without densities

- hard, irregular radiodense masses with a desmoplastic stromal reaction

A

ER(-), HER2(-)

126
Q

grating sound when scraped due to small, central pinpoint foci or streaks of chalky white desmoplastic stroma with occasional calcification
- sometime present with well-circumscribed masses with sheets of tumor cells with little stromal reaction

A

ER(-), HER2(-)

127
Q

variable differentiation, with most of well differentiated tumors in this group

  • may present with mucinous, papillary, cribiform or lobular patterns
  • high proliferation type expresses Ki67
A

ER(+), HER2(-)

128
Q

almost all are poorly differentiated

  • many have circumscribed pushing borders with central fibrotic or necrotic center
  • prominent lymphocytic infiltrate (carcinoma with medullary features)
  • spindle cell, squamous and matrix producing patterns may be seen
  • DCIS is very limited or ot present
  • express basal keratins
A

ER(-), HER2(-)

129
Q

well or moderately differentiated lobular, tubular, and mucinous

A

ER(+), HER2(-) LOW proliferation

130
Q

poorly differentiated, lobular

A

ER(+), HER2(-) HIGH proliferation

131
Q

some apocrine

A

HER2(+), ER(+/-)

132
Q

medullary, adenoid cystic, secretory, metaplastic

A

ER(-), HER2(-)

133
Q

biallelic loss of CDH1 which encodes E-cadherin

- tumors are discohesive and may not incite a desmoplastic response

A

lobular carcinoma

- histo: discohesive infiltrating tumor cells, signet ring cells containing intracytoplasmic mucin droplets

134
Q

many features of BRCA1 associated carcinomas

  • most not associated with BRCA1 mutations, 2/3 are downregulated
  • presence of lymphocytic infiltrates within the tumors associated with higher survival rates and great response to chemo
A

medullary carcinoma

135
Q

characteristic pattern of anchorage independent growth

- the cells still express E-cadherin and are adherent to each other, but DO NOT RETAIN THE STROMA

A

micropapillary carcinoma

136
Q

hard, irregular mass

  • diffuse infiltrative pattern with minimal desmoplasia
  • difficult to palpate or detect with imaging
  • presence of discohesive, infiltrating tumor cells (E-cadherin negative)
  • signet ring cells with intracytoplasmic mucin droplets
  • indian filing: single cells lined up like box cards
  • no tubule formation
A

lobular carcinoma morphology

137
Q

soft or rubery and has a pale gray-blue gelatin appearance

- cells clustered in small islands with large mucin lakes

A

mucinous (colloid) carcinoma

138
Q
  • consists of well-formed tubules
  • may be mistaken for a benign sclerosing lesion
  • cribiform pattern may be present
  • apocrine snouts are typical
  • calcifications may be seen in lumens
  • associated with flat epithelial atypia, atypical hyperplasia, LCIS or low grade DCIS
A

tubular carcinoma

139
Q

produces true papilla: fronts of fibrovascular tissue lined by tumor cells
- two special histologic types frequently overexpress HER2

A

papillary carcinoma

140
Q

HER2(+)

  • cells resemble those that line sweat glands
  • enlarged round nuclei with prominent nucleioli and abundant eosinophilic or granular cytoplasm
A

apocrine carcinoma

141
Q

forms hollow balls of cells that float within intercellular fluid creating structures that mimic the appearance of true papillae

A

micropapillary carcinoma

142
Q

most common subtype of ER(-), HER2(-)

  • soft due to minimal desmoplasia
  • presents as a well circumscribed mass
  • solid, syncytium sheets of large cells with large, pleomorphic nuclei, prominent nucleioli
  • frequent mitotic figures
  • lymphocytoplasmic infiltrate surrounding and within the border
  • **pushing (non-infiltrative) border
  • DCIS is minimal or absent
A

medullary carcinoma

143
Q

ER(-), HER2(-)

- mimics lactating breasts by forming dilated spaces filled with eosinophilic material

A

secretory carcinoma

144
Q

extensive invasion and proliferation within lymphatic channels

  • causes swelling that mimics non-neoplastic inflammatory lesions
  • typically high grade with very poor prognosis
  • do not belong to any specific molecular subtype
A

inflammatory carcinoma

145
Q

4-14% associated with BRCA2 mutations

  • much more likely for tumors to be ER(+)
  • present as 2-3cm palpable, subareolar mass, +/- discharge
  • close to the skin and underlying thoracic wall
  • can invade structures -> ulcerations
  • 50% have metastasized at presentation (lungs, brain, bone, liver)
A

male breast cancer

- tx: mastectomy + axillary LN dissection

146
Q

what is the most important factor in absence of distant metastasis of breast cancer?

A

axillary metastasis

  • no nodal involvement = 70-80%
  • 1-3 lymph nodes = 35-40%
  • 10+ lymph nodes = 10-15%
147
Q

what does it mean if sentinel LN’s are negative?

A

it is unlikely that the cancer has spread any further

- pt can be spared complete axillary dissection

148
Q

when is tumor size less important?

A

HER2(+) and ER(-), may metastasize when small

  • proliferative rate is related and important in this subtype
  • may respond better to chemotherapy
149
Q
  • *coopers ligaments tethered to edematous skin = peau d’orange**
  • dermal lymphatics are filled with metastatic carcinoma that blocks lymphatic drainage

present with breast erythema and skin thickening = very poor prognosis (pt often have distance metastasis)
- may be confused with mastitis

A

inflammatory carcinoma

- 60% are ER(-), while 40-50% are HER2(+)

150
Q

tumor cells are present within vascular spaces in about half of all invasive carcinomas

  • strongly associated with the presence of lymph node metastasis
  • poor prognostic factor for local recurrence
A

lymphovascular invasion

151
Q

what are the most and least favorable subtypes of lymphovascular invasion?

A

most favorable: well differentiated ER+, HER2-, low proliferation
least favorable: poor differentiation ER+, HER2+

152
Q

what does a high proliferative rate usually mean?

A

poor prognosis, but potentially better response to chemotherapy

153
Q

dreaded complication of breast cancer, common in women in areas with limited resources
- patients that don’t receive treatment and get extensive local disease with ulceration of the skin

A

carcinoma en curiasse (carcinoma of the breastplate)

154
Q

what are the two types of stroma in the breast?

A
  1. intralobular: fibroadenoma, phyllodes tumors

2. interlobular: tumors are similar to others found in CT throughout the body (lipoma, angiosarcoma)

155
Q

most common benign tumor of the female breast

  • polyclonal hyperplasia of the lobular stroma
  • most commonly in 20-30 year olds
  • present with palpable mass
  • epithelium is hormonally responsive
  • increase in size due to lactational changes in pregnancy
A

fibroadenoma

  • can be very small to large
  • well-circumscribed, rubbery, grey-white nodules that bulge above the surroinding tissue and contain slit-like spaces
  • delicate and myxoid stroma resembles normal intra-lobular stroma
156
Q

what causes a fibroadenoma?

A

almost half of women receiving cyclosporin A after renal transplantation develop multiple and bilateral fibroadenomas that regress after cessation of treatment

  • may be associated with clonal cytogenic aberrations confined to the stromal component
  • considered a proliferative change without atypia
157
Q

tumors that arise from intralovular stroma, but are much less common than fibroadenomas

  • most common in 6th decade
  • detected as palpable mass or seen on mammography
  • most are cystic and behave in a benign mannor
  • chromosome 1q gains
  • HOXB13 overexpression
A

phyllodes tumor

158
Q
  • can be small to large, LEAF-LIKE
  • larger lesions have bulbous protrusions due to nodules of proliferating stroma covered by epithelium
  • higher cellularity, mitotic rate, nuclear pleomorphism, stromal overgrowth, infiltrative borders (vs. fibroadenomas)
  • high grade = difficult to distinguish from malignant sarcomas as they can have a foci of mesenchymal differentiation
A

phyllodes tumor

159
Q

why is lymph node dissection contraindicated in phyllodes tumors?

A

BECAUSE LYMPH NODE SPREAD IS RARE

160
Q

what is the only breast tumor equally common in both males and females?

A

myofibroblastoma

161
Q

fat containing lesions, benign, only importance is to distinguish them from malignancies

A

lipoma

162
Q

clonal proliferation of fibroblasts and myofibroblasts that present as irregular infiltrating mass that can involve both skin and muscle

A

fibromatosis

- locally aggressive, does not metastasize

163
Q

the only sarcoma that occurs with any frequency in the breast (still less than 0.5% of malignancies)

  • occur in the breast parenchyma of young females (35 year olds)
  • high grade poor prognosis
  • sporadis, or complication of therapy (edema, or 5-10 years after radiation)
A

angiosarcoma

EndoRepro 2 Exam 1 (25 decks)

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