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TBL 1.1 Flashcards

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1
Q

What is the most common non-skin malignancy in women?


A

Breast cancer

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2
Q

What is the second most common cause of cancer deaths in the United States?

A

Breast cancer

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3
Q

What are the most important risk factors for sporadic breast cancers in women?


A

Estrogenic stimulation and age

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4
Q

What percentage of breast cancers are familial?


A

Approximately a quarter to a third

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5
Q

Which high-risk genes are associated with familial breast cancer?


A

BRCA1, BRCA2, and TP53

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6
Q

How are breast cancers classified into molecular groups?


A

Into luminal (ER-positive), HER2, and triple negative groups

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7
Q

What distinguishes luminal cancers group A from group B?

A

Group A has low proliferation, while group B has high proliferation

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8
Q

What characterizes HER2 cancers?


A

Overexpression of the HER2 receptor due to HER2 gene amplification

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9
Q

What is a defining feature of triple negative breast cancers (TNBCs)?


A

They lack ER and HER2 expression

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10
Q

What is the prognosis for TNBCs?


A

They carry a relatively poor prognosis

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11
Q

What type of carcinoma do almost all breast malignancies represent?


A

Adenocarcinomas

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12
Q

What are the terms used to describe subsets of breast carcinomas?


A

Ductal and lobular

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13
Q

From where do most breast carcinomas arise?


A

From cells in the terminal duct lobular unit

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14
Q

How was carcinoma in situ originally classified?


A

As ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS) based on the resemblance of involved spaces to normal ducts or lobules.

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15
Q

What does the term “lobular” refer to in current convention?


A

Invasive carcinomas that are biologically related to LCIS

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16
Q

What does carcinoma in situ refer to?


A

Cancer cells confined within ducts and lobules by a basement membrane

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17
Q

Why does carcinoma in situ have no capacity to metastasize?


A

Because the location precludes access to blood vessels and lymphatics

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18
Q

What is ductal carcinoma in situ (DCIS)?


A

A clonal proliferation of epithelial cells limited to ducts and lobules

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19
Q

How is DCIS typically detected?


A

Almost always by mammography

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20
Q

What percentage of carcinomas detected without mammography are in situ lesions?


A

Less than 5%

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21
Q

What percentage of carcinomas detected in mammography screened populations are in situ lesions?


A

15% to 30%

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22
Q

What are common findings associated with DCIS on mammography?


A

Calcifications associated with secretory material or necrosis

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23
Q

What is a rare presentation of DCIS?


A

Nipple discharge

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24
Q

What defines comedo DCIS?


A

Pleomorphic, high-grade nuclei and areas of central necrosis

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25
How does the architectural patterns of DCIS vary?

They vary in nuclear grade and the presence and extent of necrosis
26
What does micropapillary DCIS produce?

Complex bulbous protrusions without fibrovascular cores
26
What characterizes cribriform DCIS?

Rounded spaces filled with calcified secretory material
27
What is Paget disease of the nipple?

A rare [1% to 4% of cases] manifestation of breast cancer presenting as a unilateral erythematous eruption
27
What does papillary DCIS produce?

True papillae with fibrovascular cores that lack a myoepithelial cell layer
28
How do malignant cells in Paget disease extend from DCIS?

Within the ductal membrane via the lactiferous sinuses into nipple skin without crossing the basement membrane.
28
What are common symptoms of Paget disease of the nipple?

Pruritus and a scale crust
29
What is the significance of a palpable mass in women with Paget disease?

50% to 60% of women with Paget disease have a palpable mass, which is usually invasive carcinoma
30
What are the key features of ductal carcinoma in situ (DCIS)?

1. Clonal proliferation of epithelial cells limited to ducts and lobules 2. Myoepithelial cells are preserved, though may be diminished 3. Can spread throughout the ductal system 4. Detected almost always by mammography 5. Associated with calcifications or necrosis
31
What is the prognosis for women with Paget disease?

Prognosis depends on the features of the underlying carcinoma and is not affected by the presence or absence of paget disease.
32
What do we now know about Carcinoma in situ?

We now know that these growth patterns are not related to the cell of origin, but instead reflect differences in tumor cell genetics and biology.
32
What are the architectural patterns of DCIS and their characteristics?

1. Comedo DCIS: High-grade nuclei Areas of central necrosis 2. Cribriform DCIS: Rounded spaces filled with calcified secretory material 3. Micropapillary DCIS: Complex bulbous protrusions without fibrovascular cores 4. Papillary DCIS: True papillae with fibrovascular cores lacking myoepithelial cell layer
33
what does the term 'Ductal' refer to in current convention?

'Ductal' is used more generally for adenocarcinomas that cannot be classified as a special histologic type.
34
What can the lesion in Paget disease be mistaken for?

Eczema
35
What type of carcinoma is seen in paget disease?

The carcinomas are usually ER-negative and overexpresses HER2.
35
How is Paget disease detected? 

Paget cells are detected by nipple biopsy or cytologic preparations of the exudate.
36
Majority of women with paget disease that dont have a palpable mass have what? 

They have DCIS.
37
What is the genes BRCA1, BRCA2 and TP53 associated with?
DNA repair and genomic stability.
38
What does HER2 cancer respond well to?
HER2 inhibitors
39
What genes are affected in TNBCs?
BRCA1 is silenced and TP53 is mutated.
40
What can be the reason for innocuous in situ lesions to turn into invasive cancers?
Changes in the stromal cells rather than tumor cells.
41
What cells maintain the basement membrane?
Luminal cells, myoepithelial cells and stromal cells.
42
What happens to Myoepithelial cells in DCIS?
Preserved although may be diminished.
43
How much can the lesion spread in DCIS?
It can spread over an entire sector of the breast.
44
What does Periductal fibrosis do in DCIS?
It results in mamographic density or creates a vaguely palpable mass.
45
What is Comedo DCIS detected as?
As clustered or linear and branching areas of calcification.
46
What happens to nipple surface in paget disease of the nipple?
The tumor cells disrupt normal epithelial barrier and extracellular fluid seeps onto the surface.
47
What is the natural history of DCIS difficult to determine?

Because in the past all women were treated with mastectomy and the current method is largely curative.
48
What is the current practice for treating DCIS?

Surgical excision, usually followed by radiation
49
What is the rate of developing invasive cancer for women with small, low-grade DCIS if untreated?
About 1% per year.
50
How does invasive cancer that develops in the same breast quadrant relate to the associated DCIS?
It tends to have a similar grade and expression pattern of ER and HER2.
51
What is believed about patients with high-grade or extensive DCIS?

They have a higher risk for progression to invasive carcinoma.
52
What is the overall death rate for women with DCIS compared to the general population?

It is lower than that for women in the population as a whole.
53
What percentage of women with DCIS die from metastatic breast cancer?

1% to 3% of women.
54
Where may the origin of metastatic disease come from after a diagnosis of DCIS?

From a subsequent invasive carcinoma in the 1. ipsilateral or 2. contralateral breast or 3. occult foci of invasion that were not detected during DCIS diagnosis.
55
What is the cure rate of mastectomy for women with DCIS?

Greater than 95% of women.
56
What is the risk of recurrence in breast conservation compared to mastectomy?

Breast conservation has a slightly higher risk of recurrence. ( half is DCIS and half invasive carcinoma)
57
What are the major risk factors for recurrence of DCIS?
1. High nuclear grade and necrosis, 2. extent of disease, and 3. positive surgical margins.
58
Why is ensuring complete excision of DCIS not straightforward?
Its distribution in the breast is not reliably predicted by imaging and is usually not grossly evident at surgery.
59
What treatments reduce the risk of recurrence for DCIS?
Postoperative radiation therapy and tamoxifen. They are used for high risk patients.
60
What is the incidence of Lobular Carcinoma in Situ (LCIS) among all carcinomas?
1% to 6% of all carcinomas and it has not changed with the introduction of mammographic screening
61
How is LCIS typically discovered?
It is almost always an incidental biopsy finding because it is rarely associated with calcification or stromal reactions that produce mammographic densities.
62
What is the bilateral occurrence rate of LCIS when both breasts are biopsied?

20% to 40% of cases.
63
What is the relationship between atypical lobular hyperplasia, LCIS, and invasive lobular carcinoma?

The cells are morphologically identical.
64
What causes the observed loss of cellular adhesion in LCIS?

Dysfunction of E-cadherin.
65
What role does E-cadherin play in normal epithelial cells?

It is a tumor suppressing transmembrane protein that contributes to the cohesion of normal epithelial cells in breast and other glandular tissues.
66
What happens to E-cadherin in neoplastic proliferations
It may be lost through a variety of mechanisms, including mutation of the E-cadherin gene (CDH1).
67
What is the morphology of LCIS?
It consists of a uniform population of cells with oval or round nuclei and small nucleoli.
68
What type of cells are commonly present in LCIS?
Mucin-positive signet ring cells.
69
What shape of cells does E-cadherin result in LCIS?

It results in a rounded shape without attachment to adjacent cells.
70
What is commonly seen in breast ducts related to Pagetoid spread?

Presence of neoplastic cells between the basement membrane and overlying luminal cells.
71
What is the expression profile of LCIS?

It almost always expresses ER and PR and is HER2-negative.
72
What is the risk associated with LCIS?

It is a risk factor for developing invasive carcinoma in either breast but more in ipsilateral breast.
73
At what rate does invasive carcinoma develop after LCIS?

About 1% per year.
74
What is the treatment choice for invasive carcinoma developing after LCIS?

Bilateral prophylactic mastectomy, tamoxifen, or close clinical follow-up and mammographic screening.
75
What proportion of breast carcinoma can be classified into special histologic types?

About one-third.
76
What are the clinical features of DCIS?

1. Treated with mastectomy in the past 2. Current treatment is surgical excision followed by radiation 3. Untreated small, low-grade DCIS has a 1% per year risk of invasive cancer 4. High-grade or extensive DCIS has a higher risk for progression to invasive carcinoma 5. Overall death rate for women with DCIS is lower than the general population
77
What are the characteristics of LCIS?
1. Clonal proliferation of cells within ducts and lobules 2. Rarely associated with calcifications or stromal reactions 3. Bilateral occurrence in 20% to 40% of cases when both breasts are biopsied 4. Morphologically identical to atypical lobular hyperplasia and invasive lobular carcinoma 5. Loss of cellular adhesion due to E-cadherin dysfunction
78
What are the morphological features of LCIS?
Uniform population of cells with oval or round nuclei Presence of mucin-positive signet ring cells Lack of E-cadherin results in rounded shape without attachment Pagetoid spread is commonly seen in breast ducts Almost always expresses ER and PR, and is HER2-negative
79
What is Lobular Carcinoma in Situ (LCIS)?
Clonel proliferation of cells within ducts and lobules that grow in dyscohesive fashion.
80
What percentage DCIS is bilateral?
10 to 20%
81
Why is calcification absent in LCIS?
Necrosis and secretory activity is not seen
82
What protein that is needed for E-cadherin-mediated cellular cohesion is disregulated in LCIS?
Catenins

TBL-MSK (2 decks)

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