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ENRP II > Breast Pathology Robbins/Lecture Part 2 > Flashcards

Breast Pathology Robbins/Lecture Part 2 Flashcards

1
Q

DCIS is treated _ as subsequent invasive carcinomas usually occur at the same site where as LCIS confers _ risk

A

locally

bilateral risk

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2
Q

white women are typically diagnosed with breast cancer around the age of? while black people and hispanic people are diagnosed with breast cancer when?

A

WW: 63
AW: 59
Hispanic: 56

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3
Q

why has the percentage of deaths from breast cancer decreased

A

mammography and other more effective treatment modalities

death rate mortality has not decreased in african american women (those who have the most risk of death)- this is due to unequal acess to care and that more aggresive breast cancers have a predilection for african americans

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4
Q

beyond female sex the major factors associated with an increase risk of breast cancer is?

A

hereditary factors, lifetime exposure to estrogen (early menses, late menopause), environmental factors, high breast density, radiation (high dose), obesity

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5
Q

what are the major factors that decrease the risk of breast cancer?

A

pregnancy prior to 20 years of age and prolonged breast feeding

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6
Q

the major risk factor for sporadic breast cancer are related to?

sporadic breast cancer is genetic/environmental factors/epigenetics

A

hormone exposure: gender, age at menarche and menopause, reproductive history, breast feeing, and exogenous estrogwns

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7
Q

familial breast cancer is?

25% of breast cancers

A

family history is present but negative for BRCA

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8
Q

hereditary breast cancer is?

10% of all breast cancers

A

BRCA1 or BRCA2 positive or TP53

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9
Q

the most important high penetrance susceptability genes for hereditary breast cancer are

A

tumor suppressor genes that typically regulate genomic stability and are involved in pro-growth signaling

BRCA1 and BRCA2

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10
Q

BRCA1 and BRCA2 are human genes that produce?

A

tumor suppresor proteins

tumor suppresor proteins help repair damaged DNA

  • in a mutation DNA damage cannot be repaired properly and are more liekly to develop into cancer
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11
Q

mutations in BRCA1 and BRAC2 are responsible for _ percent of single gene familial breast cancers and about _ percent of all breast cancers

A

90%

3%

penetrance varies: the percentage of carriers who develop breast cancer varies)

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12
Q

it is believed that one quarter to one third of breast cancers occur due to inheritance of?

A

a susceptability gene

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13
Q

breast cancer is rare in women younger than _ and increases in incidence rapidly after age _

A

25

age 30

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14
Q

all breast cancers can be sperated into 3 major groups: what are they, and when does their incidence peak?

A

ER/luminal- peaks later in live around 65
HER2/ERBB2- plataeus later in life
TNBC-plateaus later in life

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15
Q

Describe the ER aka luminal positive pathway for breast cancer

A
  1. normal breast
  2. BRCA2 mutation
  3. 1q gain, 16q loss
  4. Flat epithelal atypia- precursor
  5. PIK3CA (signaling molecule) mutation
  6. atypical ductal hyperplasia- precursor
  7. DCIS- precursor
  8. invasive luminal cancer

dominant pathway of breast cancers 50-60% of all breast cancers

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16
Q

luminal cancers are high in ER and are also high in by negative feedback

A

PR

progesterone receptor

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17
Q

the major risk factor for luminal/ ER + cancer is?

A

estrogen exposure

estrogen increases local production of growth factors like TGFba, platelet derived growth factor, and expression of genes in breast epithelial cells stimulating proliferation

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18
Q

because estrogen increases cyclicly during reporductive years it has a direct correlation with what kind of breast cancer

A

luminal

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19
Q

treatment of luminal cancer

A

antiestrogenic therapy like tamoxifen

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20
Q

most luminal cancers metastisize to the ?

A

bone

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21
Q

do luminal cancers have a good prognosis?

A

yes, they respond well for decades to anti-estrogenic therapy, they are well differentiated and slow growing

well differentiated- look like normal cell type

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22
Q

describe the pathway for HER2+ breast cancers

A
  1. TP53 mutations
  2. HER2 amplification
  3. NO PRCURSOR
  4. DCIS
  5. HER+ cancer

20% of all breast cancers

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23
Q

her2 positive cancers arise through a pathway strongly associated with amplification of the ?

what chromosome?

A

HER2 gene on the chromosome 17q

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24
Q

HER2 also known as ERBB2 is a ?

A

receptor tyrosine kinase that promotes cell proliferation and opposes apoptosis by stumulating RAS and P13K-AKT signaling pathways

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25
Q

HER2 cancers is the most common subtype of breast cancer in patients with germinal _ mutations.

this is known as?

A

TP53 mutations

Li-Fraumeni syndrome- sarcomas, leukemia, brain tumors

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26
Q

can HER cancers be ER positive?

A

yea or not, dont get too confused with this

if it is ER positive it has a better prognosis than if it was negative

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27
Q

the only common molecular mechanism for HER2 overexpression is?

A

gene amplification

they have complex interchromosomal rearrangements, high mutational load

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28
Q

HER2 carcinomas are diagnosed by?

A

detecting HER2 overexpression with immunochemistry or HER2 gene amplification by insitu hybridization

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29
Q

how do we treat HER2 cancers

A

with antibodies that bind and block HER2 activity (HER2 targeted therapy)

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30
Q

Decribe the TNBC pathway

A
  1. BRCA1 mutation
  2. TP53 mutation
  3. P53 signature
  4. BRCA1 inactivation
  5. DCIS
  6. Triple Negative Breast Cancer

estrogen independent pathway and no HER2 amplification- 15% of all breast cancers

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31
Q

TNBC have a _ like gene expression because many of the genes that comprise this signature are normally expressed in basally located myoepitheleal cells

A

basal-like

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32
Q

possible precursor lesion for TNBC ?

A

lobular epithelial cells that are ER negative and p53 positive

resemble serous tubal intraepithelial corcinoma in the fallopian tube with a BRCA1 mutation

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33
Q

TNBC shares genetic features with what?

A

serous ovarian carcinomas and serous tubal intraepitheal carcinomas

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34
Q

TBNC is more likely to present with? (different than luminal cancer)

A

palpable mass: less likely to be detected on mammography because it grows in the period betwen screenings

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35
Q

how do we treat TNBC and do they recurr

A

cytotoxic therapy
yes they reoccur (first 8 years after diagnosis)

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36
Q

TNBC mestasizes where?

A

brain and visceral sites

agreesive tumors that typically end in death

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37
Q

what approaches have been made to subclassify breast cancer into clinically meaningful subtypes

A
  1. circos plots of genomic abnormalities
  2. mRNA gene spression profiles (red= more mutations)
  3. immuno-histochemistry for specific proteins
  4. respective morphology
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38
Q

what immunochemistry proteins are spescific for luminal cancer, HER2+ cancers, and TNBC

A

luminal: ER and Ki67
HER2: HER2
TNBC: basal keratins

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39
Q

_ breast cancers have the lowest rate of recurences in the first 10 years

A

luminal

40
Q

almost all recurrences of _ breast cancer occur within the first 8 years

A

TNBC

41
Q

_ breast cancers show a mixed pattern with both early and late peaks of reoccurence

A

HER2+ cancers

late peak: due to aquired resistance?

42
Q

describe the spectrum of luminal cancers

A

there are different histological grades and proliferation rates for luminal cancer

luminal A- low proliferation with ER+ and PR+ which are well differentiated and slow growing

luminal B- high proliferation has low ER+ and absent PR+ are more aggressive luminal tumors

PR is upregualted by estrogen and ER

43
Q

luminal B has association with what mutation, and staining for what?

A

BRCA2

Ki67 staining

44
Q

does luminal A or luminal B metastize to bone

A

luminal A

45
Q

how do luminal A and luminal B differ in reponse to treatment?

A

luminal A has a good response to anti-estrogenic therapy

luminal B- 10% need chemotherapy

luminal B has higher expression of genes related to cellular proliferation

46
Q

how does estrogen promote luminal breast cancer?

A

increases local growth factors like TGFBa, platelet derived growth factor, fibroblast growth factor, and stimulates breast growth

47
Q

the proliferation of breast epithelium leads to accumulated _ damage

A

DNA

48
Q

repeated _ increase the risk of developing cancer and damage may become fixed

A

cycles

49
Q

once premalignant and malignant changes are present in luminal cancers _ stimulate growth of these cells and aid in tumor development

A

hormones (estrogen futher complicated/develops the cancer)

50
Q

is there a morphologic pattern associated with HER2 cancers?

A

no

poorly differentiated

51
Q

variation in gene expression among HER2 cancers is largely based on?

A

ER status and differing lecels of expression of ER related genes

52
Q

what pharmaceutical agent can help treat HER2+ cancers

A

herceptin (it is a monoclonal antibody that inhibits HER2)

not all respond to targeted therapy because resistance can occur

53
Q

who is most likely to get TNBC

A

african american women, hsitpanics, young premenopausal women

54
Q

due to high proliferation and rapid growth TNBC are likely to present with palpable mass in the interbal between mammographic screenings

A

just know that (one year they are fine, the next year they have a large mass)

55
Q

almost all breast malignancies are _ (SCC/Adenocarcinomas)

A

adenocarcinomas

56
Q

all breast carcinomas arise from cells in the?

A

TDLU

57
Q

carcinoma in situ by definiton is?

2 parameters-

A

a clonal proliferaction that is confied to ducts and lobules

with NO extension beyond the basement membrane and the myoepithleal cells are preserved

58
Q

DCIS is detected mammographically as?

A

micro Ca+ calcificatons that extend throughout the duct system

NOT as a mass!!

59
Q

DCIS can present as a mass (usually just calcium) if ?

A

if it is associatd with fibrosis or nipple discharge

60
Q

what is the nautral history of DCIS?

A

difficult to determine: mastectomy and radiation is curative

61
Q

how many people with DCIS end up dying from metastasis

A

1-3%

the deposittion of CA+ is variable and some might be missed?

62
Q

risk factor for DCIS to reoccur?

A

high nuclear grade and necrosis
extend of disease
positive surgical marigins

63
Q

what can decrease the rate of recurrence of DCIS

A

radiation and tamoxifen (along with ressection)

64
Q

what is the most common type of DCIS

A

comedo type

65
Q

comedo type DCIS presents as?

on mammography

A

linear brnaching og calification

66
Q

on histology comedo type DCIS present with what 2 things?

A
  1. tumor cells with pleomorphic high grade nuclei
  2. central area of necrosis + calcifications in the ducts
67
Q

pagets disease of the nipple arises from

A

malignant cells in the duct involved with DCIS

68
Q

pathology of pagets disease of the nipple

A

DCIS in the duct ectends within the duct system vua the lactiferous sinuses into the nipple skin without crossinf the basement membrane

tumor cells disrupt the normal epitheliam barrier and allos extracellular fluid to seep out onto the nipple surface

69
Q

paget cells are redilty detected by?

A

nipple biopsy or cytologic preparatios of exudate

70
Q

clinical presentation of pagets disease of the nipple

A

unilateral erythematous eruption of a scale crust on the breast with pruritis

palpable mass?

commonly mistaken for eczema

71
Q

paget disease of the nipple carcinomas (mass and are invasive) are assocated with what subtype of cancer?

A

ER negative and HER positive

72
Q

lobular carcinoma insitu is a clonal proliferation of cells that growa in a discohesive patter due to mutations in?

A

CDH1 that leads to a loss of tumor suppressor adhesion protein E-cadherin

CDH1 mutation
E-cadherin negative
bilateral

73
Q

does LCIS have mammographic findings?

A

typically no

74
Q

LCIS almost always expresses what subtype of cancer

A

ER and PR positive

HER2 negative

75
Q

_ incidence has not changed since mammographic screening

A

LCIS

76
Q

how does LCIS look morphologically?

A

samll rounded, loosely cohesive cells that ill and expand in the acini of a lobule

77
Q

LCIS cell extend into the adjacent duct by _ spread

A

pagetoid

pagetoid: spread of neoplastic cells between the basement membrane and overlying luminal cells

78
Q

_ cells are commonly present in LCIS

A

mucin positive signet ring cells

79
Q

larger breast carcinomas may invade the _ muscle and become fixed to the chest wall or invade the _ which causes retraction and dimpling of the skin

A

pectoralis

dermis

80
Q

when the breast tumor involves the central protion of the breast retraction of the _ may develop

A

nipple

81
Q

breast carcinomas have a wide variety of morphologic apperance: 1/3 are and 2/3 are

A

1/3: special histological types
2/3: ductal/no special type NST/NOS

82
Q

invasive carcinoma is graded using the _ score

A

Nottingham Histologic Score

83
Q

invasive carcinomas of the breast are scored for _, _, and _

A

tubular formation
nuclear pleomorphism
mitotic rate

84
Q

what are the multiple subtypes of invasive breast carcinoma that are recognised by distincitve morphologies

5 of them

A
  1. lobular carcinoma
  2. medullary carcinoma
  3. mucinous/colloid carcinoma
  4. tubular carcinoma
  5. inflammtory carcinoma
85
Q

lobular carcinoma has a loss of _ and has characteristic mestatasis where?

A

CHD1 (Ecadherin)

metastasize to peritoniem, retroperitoneum, leptomeninges, GI tract, and ovaries/uterus

like LCIS

86
Q

medullary pattern carcinomas are of interest because they look like they have a _ mutation

A

BRCA1 hypermythlation mutation

similar to TNBC but have a better prognosis

87
Q

why do medullary pattern carcinomas have a better prognosis than TNBC?

A

they have a large number of infiltrating lymphocytes suggesting improved outcomes may be related to the host immune system response

88
Q

mucinous/colloid carcinoma is soft and rubbery and has a consitency of?

A

pale gray blue gelatin

89
Q

how do mucinous carcinomas look histologically

A

tumor cells arranged in clusters within large lakes of mucin

90
Q

inflammatory carcinomas have higher incidence in?

A

african americans

91
Q

presentation of inflammtory carcinomas and prognosis

A

peau d’orange from extensive plussing of lymp spaces with carcinoma cells

poor prognosis

cancer cells plug the dermis

92
Q

male breast cancer is usually at _ stage at presentation

A

high

93
Q

risk factors for male breast cancer

A

estrogen exposure

94
Q

in the absence of adequate surgery the majority of patients with breast cancer die wtih extensive local disease causing ulceration of the skin. _ is a dreaded complication of breast cancer (skin involvement)

A

carcinoma en cuirasse (carcinoma of the breastplate)

95
Q

invasive carcinoma of no special type looks like what?

A

haphazard stromal invasion, irregular margins on immaging, exuberant demoplsatic stromal response (very hard like cutting a carrot)

ENRP II (25 decks)

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