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DERS (reproductive) > L33- Breast Pathology II > Flashcards

L33- Breast Pathology II Flashcards

1
Q

Breast CA:

  • (1) age group
  • (2) cancer type
  • (sporadic/hereditary)
A

1- >40y/o, 25% postmenopausal

2- adenocarcinoma

3- both

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2
Q

list the many risk factors for sporadic breast CA

A
  • peaks 75-80 y/o
  • early menarche, late menopause, later age at first live birth
  • FHx, race/ethnicity, US > Japan, Taiwan
  • atypical hyperplasia
  • high estrogen (replacement therapy or obesity / high fat diet)

-radiation exposure

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3
Q

list the many risk factors for hereditary breast CA

A

BRCA1/2

Li Fraumeni syndrome (p53) or variant (CHEK2)

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4
Q

BRCA1:

  • (more/less) common than 2
  • 20-40% risk of (2)
  • chr(3)
A

1- more

2- ovarian CA, prostatic / pancreatic cancer

3- 17q21

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5
Q

BRCA2:

  • (more/less) common than 1
  • 10-20% risk of (2)
  • chr(3)
A

1- less

2- ovarian CA, (inc risk male breast CA), prostatic / pancreatic CA

3- 13q12

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6
Q

Li Fraumeni:
-syndrome = (1) mutation and (2) cancers

-variant = (3) mutation and (4) cancers

A

1- p53
2- breast, sarcoma, leukemia, brain tumor, adrenal cortex

3- CHEK2
4- prostate, thyroid, kidney, colon

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7
Q

list the types of Breast carcinomas

A

Non-infiltrating = Carcinoma in situ:

  • DCIS (ductal carcinoma in situ): comedo/high grade, non-comedo, Paget’s disease
  • LCIS (lobular carcinoma in situ)

Infiltrating carcinoma:

  • ductal, 80%
  • lobular, 10%
  • tubular / cribiform, 6%
  • mucinous, medullary, papillary, metaplastic (4-5%)
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8
Q

All brease CAs arise from (1) cells.

DCIS / LCIS classification is based on (2)

A

1- cells in the terminal duct lobular unit

2- resemblance to normal involved spaces (ductal or lobular)

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9
Q

DCIS:

  • usually (uni-/bi-lateral)
  • (2)% chance of malignancy, (3)% chance of death
  • (4) Tx
A

1- unilateral, 80-90%

2- untreated low-grade DCIS chance of malignancy is 1% per year

3- 2%

4- mastectomy (95% curative), breast conservation surgery

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10
Q

Comedo DCIS = (1):

  • (2)% chance of invasion with (high/low) recurrence rate
  • (3) are related genes
A

1- high grade DCIS, intraductal tumor
2- 60%
3- high
4- ER, PR, HER2Neu positive

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11
Q

Comedo DCIS histological appearance

A
  • ducts filled with tumor cells

- large central necrosis and calcification (inspissated material- able to be squeezed out like toothpaste)

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12
Q

non-comedo DCIS = (1)

-(2) histological appearance

A

1- cribiform DCIS

2- rounded / cookie cutter like spaces

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13
Q

LCIS:

  • (older/younger) women mostly
  • usually (uni-/bi-lateral)
  • (3)% chance of malignancy
  • (4) genetic association
A

1- younger (incidental finding usually)

2- unilateral, 60-80%

3- untreated low-grade LCIS chance of malignancy is 1% per year

4- loss of E-cadherin

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14
Q

LCIS histological appearance

A
  • lobuar distension
  • oval, noncohesive cells
  • no pleomorphism or mitoses
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15
Q

LCIS:

  • (1) clinical appearance
  • (2) Tx
A

-incidental biopsy finding, no calcifications or densities on mammography

Tx- close f/u and mammographic screening OR bilateral prophylactic mastectomy

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16
Q

LCIS:

  • (1) clinical appearance
  • (2) Tx
A

-incidental biopsy finding, no calcifications or densities on mammography

Tx- close f/u and mammographic screening OR bilateral prophylactic mastectomy

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17
Q

Paget Disease, breast:

  • breast CA in (1)% cases
  • describe carcinoma location: (2) generally via (3) process
A

1- 1-4%

2- intraductal carcinoma in large duct –> spread to skin, areola, nipple

3- extend from a DCIS via ductal system via latiferous sinuses into nipple skin

18
Q

Paget disease, breast:

  • (1) clinical presentation
  • (2) examination notes
A

1- unilateral pruritic erythematous eruption with a scale crust — may be mistaken for eczema

2- palpable mass may not be present — may have underlying DCIS in same breast

19
Q

Paget disease, breast:

  • (1) biopsy results
  • related to (2) expression
  • (3) is present in 99.99% of cases
A

1- large hyperchromatic nucleus with halo

2- (poorly differentiated cells via) HER2/neu overexpression — ER negative

3- underlying intraductal or invasive carcinoma

20
Q

Infiltrating ductal carcinoma, NST

-size and description

A

(no special type)

  • Scirrhous- hard, dense desmoplasia
  • 3-4 cm, infiltrative edge
  • cords / nests of cells depend on level of differentiation
  • necrosis, calcification

-molecular classification correlated to prognosis / response to therapy

21
Q

Ductal carcinoma, NOS molecular classifications distribution

A

Luminal A, 40-55%
Luminal B, 15-20%
Basal like, 13-25%
HER2 positive, 7-12%

22
Q

Ductal Carcinoma, NOS, luminal A:

  • (1) genetic associations
  • (2) onset / growth pattern
  • (3) aggressiveness
A

1- ER+, HER2/neu-

2- postmenpausal, slow growing

3- well or moderate differentiation –> responds well to hormonal Tx and small number to chemotherapy

23
Q

Ductal Carcinoma, NOS, luminal B:

  • (1) genetic associations
  • (2) aggressiveness
A

1- ER+, PR+, HER2/neu+

2- LN metastasis — may respond to chemotherapy

24
Q

Ductal Carcinoma, NOS, basal like:

  • (1) genetic associations
  • (2) aggressiveness
A

1- ER-, PR-, HER2/neu-, BRCA1+, younger females

2- high grade, metastasis to brain, few complete chemotherapy

25
Q

Ductal Carcinoma, NOS, HER2+:

  • (1) genetic associations
  • (2) aggressiveness
A

1- ER+, HER2+

2- poorly differentiated — high frequency brain metastasis

26
Q

Medullary Carcinoma:

  • (1) physical exam appearance
  • (2) histological appearance
  • (3) prognosis
A

1- fleshy, soft, well-circumscribed (can be confused with benign lesion)

2- large syncytial sheets of large oval cells, little stroma, lymphoplasmacytic immune response, well circumscribed

3- good

27
Q

Lobular carcinoma:

  • (1) genetic association
  • (2) are an added difficulty to Dx
  • (3) frequent metastatic sites
  • (4) general apperance
A

1- loss of E-cadherin

2- 25% cases have subtle mammographic / palpable abnormalities

3- leptomeninges, GIT, ovaries, uterus, peritoneum

4- poorly outline, indurated, non-distinct mass + minimal dysplasia

28
Q

Lobular carcinoma histological appearance

A

-discohesive infiltrating tumor cells: signet ring cells

Single file: (foot-prints of Indians on the sand in linear fashion) - single file tumor cells, round and uniform

Bull’s eye pattern: tumor cells around normal acini / ducts +/- ductal carcinoma (= mixed pattern)

29
Q

Inflammatory breast carcinoma:

  • (1) age and race affected most
  • (2) clinical appearance
  • (3) aggressiveness
A

1- young black women

2- swollen erythematous breast via dermal lymphatic obstruction by tumor (mimics non-neoplastic inflammatory lesions)

3- underlying carcinoma is diffusely invasive — poor prognosis

30
Q

Pair the breast tumors with the following:

  • non-metastasizing
  • uncommonly metastasizing
  • metastasizing
A

NON: DCIS, LCIS

UNcommon: colloid, medullary, papillary

Metastasizing: all others

31
Q

list parameters evaluated from resection specimen

A
  • size, type, grade, distance to margin
  • lymphatic space invasion
  • LN status if pos.: <0.2mm, 0.2-2mm, >2mm
  • hormonal receptor status: ER, PR (estrogen, progesterone)
32
Q

what is the purpose and subsequent actions of ER/PR testing

A

-estrogen or progesterone receptor positive tumor –> predicts likelihood of benefit of endocrine Tx

Positive: >1% tumor in sample is positive => endocrine Tx

Negative: <1% tumor in sample is positive — Oncologist decision for endocrine therapy

33
Q

describe ER/PR status and endocrine therapy response rate

A

(estrogen/ER- 60% of cancers, progesterone/PR // Tx w/ Tamoxifen)
-ER+/PR+ –> 60-70% response rate, less chemo
-ER-/PR+ –> 50%
-ER+/PR- –> 40%
ER-/PR- –> <10%

34
Q

HER2 = (1- include family)

  • chr(2)
  • (3) function
  • (4) purpose in testing
A

1- human epidermal GFR2, EGF familt

2- chr17q21

3- regulates cell proliferation, survival, motility, invasion

4- prognostic / predictive marker —– 25% have overexpression –> worse prognosis (brain metastasis)

35
Q

describe role of HER2 status in Tx

A

-lack of response to chemotherapy and hormonal therapy

Tx: Herceptin / Trastuzumab therapy

  • humanized monoclonal Ig against HER2
  • can’t cross BBB, not for metastatic disease
  • ~20% Her2+ Pts respond
36
Q

Major prognostic factors for breast CA

A
  • distant metastasis
  • absence of distant metastasis: axillary LN status, then size

Others: invasive v In situ, locall advanced CA, inflammatory CA

37
Q

Minor prognostic factors for breast CA

A

Histological: subtype, grade,

  • ER/PR receptors, HER2, lymphovascular invasion
  • proliferative rate, DNA content, gene expression profiling

-response to neoadjuvant Tx

38
Q

Mammography:

  • can catch up (1)% of cancers
  • mainly (2) cancers
A

1- 60-80%

2- Intraductal carcinoma; FCC- proliferative, sclerosin adenosis, radial scar

39
Q

Breast CA Tx

A
  • lumpectomy
  • simple mastectomy +/- LN
  • postoperative irradiation
  • chemotherapy
  • immunotherapy (herceptin)
  • hormone therapy (tamoxifen)
40
Q

Gynecomastia = (1) analog in men:

  • (2) risk factors
  • (3) microscopic changes
A

1- FCC analog

2- inc estrogens (endo-/exo-genous), reduced androgens + cirrhosis, Klinefelter’s (XXY), alcohol / marijuana / heroin, antiretroviral therapy, anabolic steroids, testicular neoplasms

3- intraductal hyperplasia with dense collagenous CT

41
Q

Male breast carcinoma:

  • (1) risk factors
  • (2) character / aggressiveness
  • (3) IHC results usually
A

1- reduced testicular function, XXY, FHx, exogenous ER, age, infertility, obesity, breast disease hx, ionizing radiation

2- rapid infiltration (less breast substance) — similar staging / Tx as females

3- ER+ tumors

DERS (reproductive) (14 decks)

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