Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

familial breast cancer is?

25% of breast cancers

A

family history is present but negative for BRCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hereditary breast cancer is?

10% of all breast cancers

A

BRCA1 or BRCA2 positive or TP53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

a susceptability gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

25

age 30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

PR

progesterone receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

luminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

treatment of luminal cancer

A

antiestrogenic therapy like tamoxifen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

most luminal cancers metastisize to the ?

A

bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

what chromosome?

A

HER2 gene on the chromosome 17q

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
HER2 cancers is the most common subtype of breast cancer in patients with germinal _ mutations. this is known as?
TP53 mutations Li-Fraumeni syndrome- sarcomas, leukemia, brain tumors
26
can HER cancers be ER positive?
yea or not, dont get too confused with this if it is ER positive it has a better prognosis than if it was negative
27
the only common molecular mechanism for HER2 overexpression is?
gene amplification ## Footnote they have complex interchromosomal rearrangements, high mutational load
28
HER2 carcinomas are diagnosed by?
detecting HER2 overexpression with immunochemistry or HER2 gene amplification by insitu hybridization
29
how do we treat HER2 cancers
with antibodies that bind and block HER2 activity (HER2 targeted therapy)
30
Decribe the TNBC pathway
1. BRCA1 mutation 2. TP53 mutation 3. P53 signature 4. BRCA1 inactivation 5. DCIS 6. Triple Negative Breast Cancer ## Footnote estrogen independent pathway and no HER2 amplification- 15% of all breast cancers
31
TNBC have a _ like gene expression because many of the genes that comprise this signature are normally expressed in basally located myoepitheleal cells
basal-like
32
possible precursor lesion for TNBC ?
lobular epithelial cells that are ER negative and p53 positive resemble serous tubal intraepithelial corcinoma in the fallopian tube with a BRCA1 mutation
33
TNBC shares genetic features with what?
serous ovarian carcinomas and serous tubal intraepitheal carcinomas
34
TBNC is more likely to present with? (different than luminal cancer)
palpable mass: less likely to be detected on mammography because it grows in the period betwen screenings
35
how do we treat TNBC and do they recurr
cytotoxic therapy yes they reoccur (first 8 years after diagnosis)
36
TNBC mestasizes where?
brain and visceral sites agreesive tumors that typically end in death
37
what approaches have been made to subclassify breast cancer into clinically meaningful subtypes
1. circos plots of genomic abnormalities 2. mRNA gene spression profiles (red= more mutations) 3. immuno-histochemistry for specific proteins 4. respective morphology
38
what immunochemistry proteins are spescific for luminal cancer, HER2+ cancers, and TNBC
luminal: ER and Ki67 HER2: HER2 TNBC: basal keratins
39
_ breast cancers have the lowest rate of recurences in the first 10 years
luminal
40
almost all recurrences of _ breast cancer occur within the first 8 years
TNBC
41
_ breast cancers show a mixed pattern with both early and late peaks of reoccurence
HER2+ cancers late peak: due to aquired resistance?
42
describe the spectrum of luminal cancers
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 ## Footnote PR is upregualted by estrogen and ER
43
luminal B has association with what mutation, and staining for what?
BRCA2 Ki67 staining
44
does luminal A or luminal B metastize to bone
luminal A
45
how do luminal A and luminal B differ in reponse to treatment?
luminal A has a good response to anti-estrogenic therapy luminal B- 10% need chemotherapy ## Footnote luminal B has higher expression of genes related to cellular proliferation
46
how does estrogen promote luminal breast cancer?
increases local growth factors like TGFBa, platelet derived growth factor, fibroblast growth factor, and stimulates breast growth
47
the proliferation of breast epithelium leads to accumulated _ damage
DNA
48
repeated _ increase the risk of developing cancer and damage may become fixed
cycles
49
once premalignant and malignant changes are present in luminal cancers _ stimulate growth of these cells and aid in tumor development
hormones (estrogen futher complicated/develops the cancer)
50
is there a morphologic pattern associated with HER2 cancers?
no ## Footnote poorly differentiated
51
variation in gene expression among HER2 cancers is largely based on?
ER status and differing lecels of expression of ER related genes
52
what pharmaceutical agent can help treat HER2+ cancers
herceptin (it is a monoclonal antibody that inhibits HER2) ## Footnote not all respond to targeted therapy because resistance can occur
53
who is most likely to get TNBC
african american women, hsitpanics, young premenopausal women
54
due to high proliferation and rapid growth TNBC are likely to present with palpable mass in the interbal between mammographic screenings
just know that (one year they are fine, the next year they have a large mass)
55
almost all breast malignancies are _ (SCC/Adenocarcinomas)
adenocarcinomas
56
all breast carcinomas arise from cells in the?
TDLU
57
carcinoma in situ by definiton is? 2 parameters-
a clonal proliferaction that is confied to ducts and lobules with NO extension beyond the basement membrane and the myoepithleal cells are preserved
58
DCIS is detected mammographically as?
micro Ca+ calcificatons that extend throughout the duct system | NOT as a mass!!
59
DCIS can present as a mass (usually just calcium) if ?
if it is associatd with fibrosis or nipple discharge
60
what is the nautral history of DCIS?
difficult to determine: mastectomy and radiation is curative
61
how many people with DCIS end up dying from metastasis
1-3% ## Footnote the deposittion of CA+ is variable and some might be missed?
62
risk factor for DCIS to reoccur?
high nuclear grade and necrosis extend of disease positive surgical marigins
63
what can decrease the rate of recurrence of DCIS
radiation and tamoxifen (along with ressection)
64
what is the most common type of DCIS
comedo type
65
comedo type DCIS presents as? | on mammography
linear brnaching og calification
66
on histology comedo type DCIS present with what 2 things?
1. tumor cells with pleomorphic high grade nuclei 2. central area of necrosis + calcifications in the ducts
67
pagets disease of the nipple arises from
malignant cells in the duct involved with DCIS
68
pathology of pagets disease of the nipple
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
paget cells are redilty detected by?
nipple biopsy or cytologic preparatios of exudate
70
clinical presentation of pagets disease of the nipple
unilateral erythematous eruption of a scale crust on the breast with pruritis palpable mass? ## Footnote commonly mistaken for eczema
71
paget disease of the nipple carcinomas (mass and are invasive) are assocated with what subtype of cancer?
ER negative and HER positive
72
lobular carcinoma insitu is a clonal proliferation of cells that growa in a discohesive patter due to mutations in?
CDH1 that leads to a loss of tumor suppressor adhesion protein E-cadherin ## Footnote CDH1 mutation E-cadherin negative bilateral
73
does LCIS have mammographic findings?
typically no
74
LCIS almost always expresses what subtype of cancer
ER and PR positive HER2 negative
75
_ incidence has not changed since mammographic screening
LCIS
76
how does LCIS look morphologically?
samll rounded, loosely cohesive cells that ill and expand in the acini of a lobule
77
LCIS cell extend into the adjacent duct by _ spread
pagetoid ## Footnote pagetoid: spread of neoplastic cells between the basement membrane and overlying luminal cells
78
_ cells are commonly present in LCIS
mucin positive signet ring cells
79
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
pectoralis dermis
80
when the breast tumor involves the central protion of the breast retraction of the _ may develop
nipple
81
breast carcinomas have a wide variety of morphologic apperance: 1/3 are and 2/3 are
1/3: special histological types 2/3: ductal/no special type NST/NOS
82
invasive carcinoma is graded using the _ score
Nottingham Histologic Score
83
invasive carcinomas of the breast are scored for _, _, and _
tubular formation nuclear pleomorphism mitotic rate
84
what are the multiple subtypes of invasive breast carcinoma that are recognised by distincitve morphologies 5 of them
1. lobular carcinoma 2. medullary carcinoma 3. mucinous/colloid carcinoma 4. tubular carcinoma 5. inflammtory carcinoma
85
lobular carcinoma has a loss of _ and has characteristic mestatasis where?
CHD1 (Ecadherin) metastasize to peritoniem, retroperitoneum, leptomeninges, GI tract, and ovaries/uterus ## Footnote like LCIS
86
medullary pattern carcinomas are of interest because they look like they have a _ mutation
BRCA1 hypermythlation mutation ## Footnote similar to TNBC but have a better prognosis
87
why do medullary pattern carcinomas have a better prognosis than TNBC?
they have a large number of infiltrating lymphocytes suggesting improved outcomes may be related to the host immune system response
88
mucinous/colloid carcinoma is soft and rubbery and has a consitency of?
pale gray blue gelatin
89
how do mucinous carcinomas look histologically
tumor cells arranged in clusters within large lakes of mucin
90
inflammatory carcinomas have higher incidence in?
african americans
91
presentation of inflammtory carcinomas and prognosis
peau d'orange from extensive plussing of lymp spaces with carcinoma cells poor prognosis ## Footnote cancer cells plug the dermis
92
male breast cancer is usually at _ stage at presentation
high
93
risk factors for male breast cancer
estrogen exposure
94
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)
carcinoma en cuirasse (carcinoma of the breastplate)
95
invasive carcinoma of no special type looks like what?
haphazard stromal invasion, irregular margins on immaging, exuberant demoplsatic stromal response (very hard like cutting a carrot)

ENRP II (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions