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Patho II > The Breast > Flashcards

The Breast Flashcards

1
Q

what are the 2 major structures of the breast?

A

ducts (connect lobules to nipples)
lobules

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2
Q

what are the 2 types of breast epithelial cells?

A

luminal -In center

myoepithelial- around luminal

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3
Q

when do the breast ducts and first development of lobules start?

A

puberty - ovarian estrogen and progesterone induction

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4
Q

What are the two types of stroma ?

A
  • Interlobular
  • Intralobular
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5
Q

when do breasts fully develop and what contributes?

A

pregnancy: progesterone, prolactin → permanent ↑ in lobule #/size

oxytocin → myoepithelial differentiation and proliferation

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6
Q

Following lactation total breast size decreases due to?

A

due to apoptosis of epithelium and lobule atrophy

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7
Q

what happens to breast tissue after menopause?

A

atrophy of lobules & ducts
↓ in fibrous connective tissue
↑ adipose tissue content

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8
Q

where do carcinomas and fibroadenomas happen in the breast?

A

carcinomas: lobules & ducts
fibroadenomas: intralobar stroma
- Stroma: is the part of a tissue or organ with a structural or connective role. It is made up of all the parts without specific functions of the organ - for example, connective tissue, blood vessels, nerves, ducts, etc. The other part, the parenchyma, consists of the cells that perform the function of the tissue or organ.

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9
Q

what are the 3 classes of benign breast lesions and examples of each?

A
  1. non-proliferative:
    - simple breast cyst (fluid filled mass, not proliferative- no risk of malignancy)
  2. proliferative without atypia:
    - fibroadenoma

→small increased risk of developing breast cancer in certain sitauations

  1. atypical hyperplasia: (proliferative with atypia)
    - atypical ductal & lobar hyperplasia (substantial ↑ risk of breast cancer)
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10
Q

Simple Breast Cyst:

Can it become malignant?

Where does the fluid filled masses come from?

A
  • no risk of becoming malignant because its non-proliferative
  • fluid filled masses derived from the terminal duct lobular unit
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11
Q

what kind of tissue is in a fibroadenoma?

A

glandular and fibrous

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12
Q

what kind of fibroadenomas are associated with increased cancer risk?

A

complex fibroadenomas slight ↑ risk with multi centric proliferative changes due to calcification

-usually only w. family hx

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13
Q

what are the 2 likely etiologies of fibroadenomas?

A

Hormonal:
-estrogen, progesterone, lactation during pregnancy

-EGF (human epidermal GF) receptors on surface: respond to EFG and GH

Genetics: MED12 gene

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14
Q

Simple Fibroadenoma

Composition?

is there an increase in cancer risk?

A
  • benign, solid tumors containing glandular as well as fibrous tissue
  • majority: no increased risk of dev. breast cancer
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15
Q

What is Estrogen and where does it come from?

A

steroid hormone derived from androgenic precursors androstenedione and testosterone via aromatization

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16
Q

what are the 3 kinds of naturally occurring estrogens?

A

estrone (E1): predominant form of circulating estrogen after menopause

17 ß-estradiol (E2): found primarly in premenopausal women and produced by theca and granulosa cells in the ovary

estriol (E3): Is the estrogen the placenta makes during pregnancy

17
Q

ER-α

predominantly found?

sustained stimulation and activation can lead to?

A

Predominant ER receptor in the uterus & mammary gland

-sustained stimulation and activation of receptor leads to ↑ breast & endometrial cancer risk

18
Q

ER-ß

Prodominantly expressed in ?

affect on cancer?

A
  • ovary, prostate (b - boys have it too)
  • -activates anti-proliferative and pro-apoptotic pathways in many cancer cells
19
Q

G-Protein Coupled Estrogen Receptor (GPER)

mediates ?

regulates ?

A

G-Protein Coupled Estrogen Receptor

mediates rapid estrogen signaling, expressed in ovary
→regulates follicle maturation

20
Q

HER2 Oncogene

Encodes for?

Function?

A

encodes HER2 receptor:

controls cell growth, differentiation, angiogenesis (activates GF pathways)–cell survival

21
Q

what percent of breast cancers express overamplification of HER2?

A

20%

22
Q

what are the 3 biologic subgroups of breast cancer?

A
  1. ER positive (80%)
  2. HER positive (20%)
  3. Triple Negative (ER-, PR-, HER2-)
23
Q

what should all females <60yo with triple negative breast cancer be tested for?

A

BRCA mutations

24
Q

what is HER2 and ER cross-talk?

A

-complex, bi-directional

treating only one of them if they are both positive amplifies the untreated one → resistance to therapy

25
Q

“Drivers” of cell proliferation and survival in majority of human breast cancers?

A

Estrogen Receptors (ER) & HER2 signaling pathways

26
Q

>95% of breast carcinomas are what kind of tumors?

A

adenocarcinomas

27
Q

what are the 2 in situ breast carcinomas? (in place)

A

ductal (most common)

lobular

28
Q

what are the 2 invasive breast carcinomas?

A

infiltrating ductal 76%

invasive lobular 8%

29
Q

What is a Ductal Carcinoma In Situ (DCIS)?

A

A proliferation of abnormal cells confined within the mammary ductal system

-no invastion

30
Q

what are the 3 nuclear grades of ductal carcinoma in situ (DCIS) and traits of each?

A

  1. high grade: no ERs or PRs, high proliferative rate, overexpression of HER2 oncogene, P53 mutation, angiogenesis (HER2+)
  2. intermediate grade
  3. low grade: ER and PR positive, low proliferative rate (EPR+)
    all: +/- necrosis
31
Q

what are the 3 grades of infiltrative ductal breast carcinoma?

A
  1. well-differentiated (G1): uniform cells, no mitosis
  2. moderately-differentiated (G2): some glandular differentiation, moderate mitotic activity
  3. poorly-differentiated (G3): no gland differentiation, significant mitotic activity

****the more poorly differentiated the INCREASE in chaotic architexture of cells

32
Q

Gold standard of dx for invasive ductal breast carcinoma?

A

biopsy

33
Q

what are most familial breast cancers?

A

80-90% BRCA1 & BRCA2

34
Q

what do normal BRCA genes do?

A

produce proteins to help repair DNA

35
Q

what are the major risk factors for sporadic (don’t involve BRCA genes) breast cancer?

A

hormone exposure and age

age (at menarche and menopause, reproductive hx - more preg. less risk, breastfeeding, and exogenous estrogen exposure)
gender
radiation exposure/chemicals with estrogen like effects

estrogen (↑ breast growth during puberty/menstrual cycles/pregnangy –> ↑ cells that can be cancerous)

36
Q

what are the 2 methods of computational investigation of DNA repair deficiency in sporadic breast cancer?

A

BRCAness profile -based on gene expression profiles between sporadic and familial tumors, influences management and txs for sporadic breast and ovarian cancers

→very important to know to give your patient the best chance at survival

sample-specific BRCA score: (homologous recombination DNA repair pathway)

37
Q

why should BRCAness and sample-specific BRCA scores be evaluated for sporadic breast cancers aka what is their clinical significance?

A

defects in HR DNA repair pathway are susceptible to alkylating chemo (causes DNA strand breaks)

in ovarian cancer, ↑ BRCA score more sensitive to chemo, better outcomes

Patho II (12 decks)

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