Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Principles of Neoplasia > Flashcards

Principles of Neoplasia Flashcards

1
Q

• New, abnormal growth of tissue
– E.g. granulation tissue is new “normal” reparative growth
• Growth rate exceeds and is uncoordinated with the rest of the body
• Growth continues at the expense of the host

A

Neoplasm

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

– the study of tumors

– the diagnosis and treatment of cancer

A

Oncology:

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

: A hamartoma, not a true neoplasm

A

Hemangioma

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

Do most cancer cells grow faster than normal cells?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
= the organ specific 
neoplastic cells
– determines the neoplasm’s 
biologic behavior
= the component from which the 
tumor derives its name
A

Parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q 
= the connective tissue and 
blood vessels
– Crucial to the growth of the 
neoplasm, since it carries the 
blood supply and provides 
support for the growth of 
parenchymal cells.
A

Stroma

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

• Abnormal cell growth that is uncontrolled, with the potential to invade or spread
to other parts of the body.
– Cause often lies in structural changes of DNA

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • Generates own growth signals
  • Ignores signals not to grow
  • Evades apoptosis: normal cells die when their time is up
  • Limitless replication potential
  • Angiogenesis: allows the tumor to sustain itself
  • Invasion/metastasis: ultimate goal of cancer cells
A

Cancer cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q 
• The term means “to 
form backwards”
•implies 
dedifferentiation, or loss of the 
structural and functional 
differentiation of normal cells
• is the most extreme 
disturbance in cell growth
A

anaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
• Disorderly, but non-neoplastic 
proliferation
• Encountered primarily in epithelium
• A loss in the uniformity of individual 
cells and in their architectural 
orientation
• Typically implies a precancerous 
condition, however, all do 
not necessarily progress to cancer
A

dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which Type of cancer most commonly metastasize via lymphatic route to regional lymph nodes?

A

Carcinoma

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

Which Type of cancer most commonly metastasize via hematogenous route to lungs?

A

Sarcoma

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

Carcinomas metastasize via ____ route

A

Lymphatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sarcomas metastasize via ____ route

A

Hematogenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which type of cancer is mesenchymal?

A

Sarcoma

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

Which type of cancer is epithelial?

A

Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

____ is the development of tumor blood supply

A

Angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Mixed tumor (pleomorphic adenoma) of 
parotid gland implanted during surgery
A

Transplantation:

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

Benign tumor of blood vessels

A

Heamngioma

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

WHich germ layer forms skin, oral mucosa, and adnexa?

A

Ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

WHich germ layer forms muscle, fat, and bone?

A

Mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

WHich germ layer forms lining of respiratory tract, GI, GU tracts, and liver and pancreas?

A

Endoderm

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

Carcinomas and adenomoas arise from what 2 germ layers?

A

Ecto and endoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sarcomas arise from what germ layer?

A

Mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Osteomas and osteosarcomas arise from what germ layer?

A

Mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

____ is a neoplasm

A

Tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

A malignant neoplasm

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

= a benign neoplasm of glandular epithelial origin

A

Adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

= a malignant neoplasm of glandular epithelial origin

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

= a malignant neoplasm of mesodermal tissue origin (connective tissue) –
bone, cartilage, smooth muscle, skeletal muscle, nerve, adipose tissue

A

Sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Tumors of lymphocytes

A

Burkitt lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Primitive tumor of kidney

A

Wilm’s tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Primitive tumor of bone

A

Ewing sarcoma

34
Q

Do benign neoplasms transform into malignant?

A

Rarely

35
Q

Are sarcomas more frequent in young or old?

A

Young

36
Q

Are carcinomas more frequent in young or old?

A

Old

37
Q 
• Developmental, non-neoplastic 
overgrowth of normal tissue at a site 
where the tissues are normally 
expected to be found
– Vs. Choristoma:
• Developmental non-
neoplastic overgrowth of 
normal tissue at an abnormal 
site abnormalities
A

Hamartoma

38
Q

• A developmental, non-neoplastic overgrowth of normal tissue at a
site where the tissues are NOT normally expected to be found
• Heterotopic tissue

A

Christoma

39
Q 
• A tumor containing tissues from all three 
germ layers
• Generally arise in gonadal tissues
• Ovary most common
• “Dermoid cyst” of the ovary
– Benign cystic teratoma
– May contain a variety of tissues 
including hair, teeth, bone, cartilage, 
thyroid, etc.
A

Teratoma

40
Q

Using grading, is a well differentiated tumor grade 1 or 4?

A

1

41
Q

Using grading, is a poorly differentiated tumor grade 1 or 4?

A

4

42
Q

_____ is a measure of how localized or spread a malignant neoplasm is
-most important predictor of prognosis

A

Staging

43
Q

Stage ____

– Single lymph node region

A

Stage 1

44
Q

Stage ______
– Multiple lymph node regions
– Same side of diaphragm

A

Stage 2

45
Q

Stage ______

– Disseminated disease

A

• Stage IV

46
Q

Stage ______
– Multiple lymph node regions
– Both sides of diaphragm

A

• Stage III

47
Q

A ____ grade tumor behaves aggressively

A

High grade

48
Q

A ____ grade tumor behaves in an indolent manner

A

Low grade

49
Q

What are the 2 groups of genes controlling growth?

A

Proto-oncogenes and TSG

50
Q

At what point of the cell cycle do TSGs act?

A

G1 checkpoint

51
Q

– normal function is to suppress cell proliferation

A

Tumor suppressor genes

52
Q

– normal function is to promote cell proliferation

A

Proto-oncogenes

53
Q

Is TSG dominant or recessive?

A

Recessive

54
Q

Is proto oncogene, dominant or recessive?

A

Dominant

55
Q

________ act as brakes on
cell proliferation
• Mutations must
create a loss-of-function if they are to have
an effect on cell proliferation
• Two copies of each gene, one paternal, one
maternal
• A loss-of-function mutation in one copy
leaves one functional copy
• A loss-of-function mutation in both copies
results in loss of all braking power, allowing
the cell to undergo unrestricted
proliferation
• act in a recessive
manner

A

Tumor suppressor genes

56
Q

act as
accelerators for cell proliferation
• Mutations in must create
a gain-in-function if they are to have an
effect on cell proliferation
• There are two copies of each gene, one
paternal, one maternal
• A gain-in-function mutation in one copy is
all that is required to promote cell
proliferation
• A gain-in-function mutation in one copy
accelerates the cell cycle, allowing the cell
to undergo unrestricted proliferation
• act in a dominant manner

A

• Proto-oncogenes / oncogenes

57
Q

The following are _______:
– P53
– Rb

A

TSG

58
Q 
The following are \_\_\_\_\_\_:
– RAS: MEN IIb
– cMYC: Burkitt lymphoma
– bcr/abl fusion gene (Philadelphia chromosome): Chronic Myelogenous 
Leukemia (CML)
– Neurofibromin: Neurofibromatosis
A

Protoncogenes

59
Q 
• No role in the normal cell 
cycle
• DNA damage causes a 
rapid rise in protein
• cell cycle arrest in G1, 
allowing time for DNA 
repair by binding the 
cyclin/CDK complex via 
p21
• If the DNA damage 
cannot be repaired, the 
cell is instructed to 
undergo apoptosis
A

p53

60
Q 
•\_\_\_ gene codes for a 
protein that acts as a 
brake, creating a 
checkpoint near the end 
of G1
• G1 checkpoint is a pause 
that assures DNA is 
repaired and the cell is 
prepared to enter the S 
phase
• Mutations inactivate the 
protein
loss of function and 
loss of a brake
A

Rb

61
Q

Are TSGs or proto-oncogenes 2 hits to cause oncogenic activity?

A

TSGs

62
Q 
• Germ-line mutation in p53 (first hit)
• A second hit eliminates all p53 
activity
• 25x the risk of cancer at usual sites as 
general population (lung, colon, 
breast ...)
• Arise at earlier age and in multiple 
organ systems
• Same cancers as the general 
population
A

Li-Fraumeni Syndrome

63
Q 
• Malignant neoplasm of retina
• Familial form: multiple tumors in retinas 
of both eyes occurring in first few weeks 
of infancy
– Germline mutation of one Rb allele 
(first hit) plus a somatic mutation of 
the second allele (second hit)
• Sporadic form –single tumor in one eye 
sometime in early childhood
– Both inherited alleles normal. 
Somatic mutation in both alleles 
(double hit)
A

Retinoblastoma

64
Q

How many alleles must be mutated to turn a proto oncogene to an oncogene?

A

1 hit

65
Q 
• Normal function of \_\_\_\_
protein: receive a growth-
promoting signal from cell 
surface receptors and forward 
the it through the cytoplasm to 
the nucleus
• After the signal is sent by the 
active GTP form of it, it 
normally flips back to the 
inactive GDP form ending the 
signal
• Mutations that abolish the 
ability to flip back to the 
inactive state result in a 
continuous signal to proliferate 
when no signal has been 
received from the cell surface
A

RAS

66
Q

• _____ gene and its protein play an active role in shepherding the cell
through G1
• Cells lacking it will not progress to S phase
• Overexpression of it promotes inappropriate cellular
proliferation
– Burkitt lymphoma

A

c-myc

67
Q

• Novel (new) protein (bcr/abl) formed with tyrosine kinase activity
• False signal sent to nucleus instructing it to enter the cell cycle and proliferate
• Acts as an oncogene
• Created by a 9 to 22 translocation that places the abl gene (chromosome 9) next
to the bcr region (chromosome 22)
Chronic myelogenous leukemia (Philadelphia chromosome)

A

BCR/ABL gene

68
Q 
• Translocation t(9:22)
• Proto-oncogene abl on long arm 
chromosome 9(q34)
• Transposed to bcr region (breakpoint 
cluster region) on chromosome 
22(q11)
Results in bcr-abl fusion gene
Gene product is abnormal bcr-abl
tyrosine kinase
• Induces cell proliferation
• Therapeutic intervention:
– Gleevec (Imatinib mesylate) 
binds to the site of the tryosine
kinase activity (tyrosine kinase
A

Philadelphia Chromosome –Chronic Myelogenous Leukemia (CML)

69
Q 
• Translocations, t(8:14) is the 
most common
• c-myc proto-oncogene on 
chromosome 8 has a role in cell 
cycle progression
• Immunoglobulin gene 
promoters cause overexpression 
of c-myc
• Overexpression of c-myc
oncogene promotes 
inappropriate cellular 
proliferation
A

Burkitt’s lymphoma

70
Q 
Normal function of \_\_\_\_
protein: receive a growth-
promoting signal from cell 
surface receptors and forward 
the it through the cytoplasm to 
the nucleus
A

RAS

71
Q 
\_\_\_\_\_\_\_ facilitates 
conversion of RAS from active 
to inactive state 
• Loss of its function 
RAS tagged in active, signal-
emitting state
A

Neurofibromin

72
Q 
\_\_\_\_\_\_ proto-oncogene codes for 
a tyrosine kinase receptor
– mis-sense mutation of the 
receptor causes activation 
of the receptor protein 
causing the receptor 
monomers to dimerize
• Mimicks the effect caused by 
binding of ligand
• Activating (gain-in-function) 
mutation that sends a 
continuous signal to the 
nucleus to transcribe cyclins in 
the absence of growth factor
A

RET

73
Q

Is cancer itself inherited?

A

No

74
Q

Is an increased risk for cancer inherited?

A

Maybe

75
Q

Autosomal recessive inherited mutations of
DNA repair genes
• Predisposition to UV-B associated
malignancies of the skin (Squamous cell
carcinoma, Basal cell carcinoma, Melanoma)
• Cancer not inherited, but susceptibility to
cancer is inherited

A

Xeroderma pigmentosum (XP)

76
Q

• Chemicals: Polycyclic hydrocarbons
• Viruses
– Epstein-Barr Virus
– Human Papilloma Virus ***
– Must be transcriptionally active
• Carcinoma of uterine cervix: high risk strains inactivate p53, Rb TSGs
• Oropharyngeal squamous cell carcinoma
• Medical/dental diagnostic radiation: Thyroid shielding
• Nuclear radiation: Nuclear weapons, nuclear accidents
• Actinic (UV) radiation: Skin cancer

A

Carcinogens

77
Q

– Symptoms/disease due to the presence of cancer in the body, but not due to
the local presence of cancer cells

A

Paraneoplastic syndrome

78
Q

: Parathyroid hormone-related protein (PTHRP)

A

Hypercalcemia

79
Q

: verrucous hyperkeratosis of skin

A

Acanthosis nigricans

80
Q

– A pathologic state characterized by weight loss and anorexia that
accompanies some infections and neoplastic diseases
– weakness and wasting of the body due to severe chronic illness
– sustained production of tumor necrosis factor contributes to Cachexia

A

Cachexia:

Pathology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions