Brainscape's Knowledge GenomeTM

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


See full index

Term 3: Immunology/Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is neoplasia?

A

-new growth that is NOT under the normal control mechanisms

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

What is desmoplasia?

A

=fibrous stroma present in some cancers

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

What are the two basic components of all tumors (benign or malignant)?

A
  1. Neoplastic cells that constitute the tumor parenchyma
  2. Reactive stroma made up of connective tissue, blood vessels, and variable numbers of cells of the adaptive and innate immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What makes a tumor benign?

A
  • gross and microscopic appearances are considered relatively innocent, implying that it will remain localized,
  • will not spread to other sites
  • is amenable to local surgical removal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the general rules for naming a benign tumor?

A

“root word” + _oma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a polyp?

A
  • a tumor that projects into a lumen, usually GI tract

- usually benign

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

A rhabdomyoma is a:

A. Malignant tumor of smooth muscle
B. Benign tumor of fat
C. Benign tumor of skeletal muscle
D. Malignant tumor of collagen

A

C. Benign tumor of skeletal muscle

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

What are the general rules for naming a malignant tumor?

A

-“Root word” + carcinoma or sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a mixed tumor?

A
  • a divergent differentiation of a single neoplastic clone in a tumor
  • contain epithelial components scattered within a myxoid stroma that my contain cartilage or bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a Hamartoma?

A
  • A disorganized by benign-appearing masses composed of cells indigenous to the particular site
    e. g. A pulmonary chondroid hamartoma contains islands of disorganized but histologically normal cartilage, bronchi, and vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a Choristoma?

A
  • A heterotopic rest of cells
  • developmental, not a metastasis
    e. g. A small nodule of well-developed and normally organized pancreatic substance may be found in the submucosa of the stomach, duodenum, or small intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the common exceptions to the benign vs cancer naming conventions?

A

Lymphoma – malignant tumor of lymphoid cells

Hepatoma – malignant liver tumor

Neuroblastoma – malignant tumor of primitive neural tissue

Wilms tumor – malignant renal tumor

Ewing sarcoma – malignant bone tumor

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

What does differentiaton mean in context of tumors?

A

How closely the tumor resembles normal tissue

**we do not talk about differentiation in benign tumors

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

What is anaplasia?

A
  • lack of differentiation in tumors

- so poorly differentiated, we can’t tell what organ it came from

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

What are the histological characteristics of malignant anaplasia?

A

Pleomorphism

Hyperchromasia

High nuclear:cytoplasmic (N:C) ratio

Prominent nucleoli

High mitotic rate, abnormal mitotic figures

Tumor giant cells

Loss of normal orientation

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

What is pleomorphism ?

A
  • variability in size and shape
  • range from small to tumor giant cells (variability in size)

**not to be confused with normal giant cells

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

What is hyperchromatism?

A

-A lot of DNA chromatin (very dark)

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

What is a papilloma?

A

-benign tumor with “finger-like” projections on a surface into a lumen

**don’t confuse with polyp, it is a subclass of polyps

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

What does Sarcoma mean?

A

-the tumor is derived from mesenchymal tissues

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

What does carcinoma mean?

A

-the tumor is derived from epithelial tissue

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

What is dysplasia? Is it reversible?

A
  • loss of uniformity of cells, loss of normal architecture
  • Usually applied to epithelial surfaces
  • dysplasia is reversible, but may be a precursor to malignant transformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does Carcinoma in Situ mean?

A

-dysplastic features involving the whole thickness of the epithelium, but no invasion into deeper tissue

**not actually a carcinoma, malignancy occurs when it invades past the basement membrane

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

Why do benign tumors usually develop a rim of compressed fibrous tissue called a capsule?

A

-benign tumors grow and expand slowly

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

________ unequivocally marks a tumor as malignant.

A

-metastasis

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

What increases the likelyhood that a tumor is metastasizing?

A
  • lack of differentiation
  • aggressive local invasion
  • rapid growth
  • Large size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is hematogenous spread of a cancer?

A
  • metastasis via the blood vasculature

* more common in Sarcomas

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

Is dysplasia reversible?

A

Yes

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

What is the most common abnormality of protooncogenes in human tumors?

A
  • point mutation in the RAS family of genes

* 15-20% of all human malignancies contain mutated versions

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

What does the activated RAS protein do?

A
  • RAS is a protooncogene
  • a member of a family of small G proteins that bind guanosine nucleotides
  • Stimulates downstream regulators of proliferation, in favor of proliferation
  • efforts to find an inhibitor of this protein are difficult due to vague structure and pathways
30
Q

What do BRAF and PI3K do?

A
  • Protooncogenes
  • BRAF and PI3K are serine/threonine protein kinases
  • Mutation in these genes Remove inhibition of apoptosis
31
Q

What is the cause of Chronic Myelogenous Leukemia? How is it treated?

A
  • ABL gene translocated from chromosome 9 to 22, where it fuses with BCR gene
  • codes for rogue tyrosine kinase

**Treated with imatinib mesylate, inhibits the rogue kinase

32
Q

How is the MYC oncogene involved in carcinogenesis?

A
  • it activates genes that are involved in proliferation & is expressed in virtually all eukaryotic cells
  • in some contexts, MYC upregulates expression of telomerase

**MYC is one of a handful of transcription factors that can act together to reprogram somatic cells into pluripotent stem cells

33
Q

The orderly progression of cells through various phases of cell cycle is orchestrated by _________________.

A

cyclin-dependent kinases (CDKs)

34
Q

What are some examples of tumor suppressor genes (TSGs)?

A
  • Rb (retinoblastoma)
  • p53
  • BRCA 1 & 2
  • APC
  • NF1/2, TGF-beta, WT-1, PTEN, VHL
35
Q

What does activated and inactivated Rb do? Which point in the cell cycle does it control?

A
  • Inactivated: Allows transcription
  • Activated: Cycle halts
  • stops at the G1->S check point
36
Q

What are the two ways in which Rb can be compromised?

A
  • Loss-of-function mutations involving both RB alleles
  • A shift from the active hypophosphorylated state to the inactive hyperphosphorylated state by gain-of-function mutations that upregulate CDK/cyclin D activity or by loss-of-function mutations that abrogate the activity of CDK inhibitors
37
Q

What does p53 normally do?

A
  • tumor suppressor gene
  • regulates cell cycle progression, DNA repair, cellular senescence, and apoptosis
  • serves as the focal point of a large network of signals that sense cellular stress

**is the most frequently mutated gene in human cancers

38
Q

What is Li-Fraumeni syndrome?

A

-inheritance of a mutated copy of p53, which predisposes individuals to malignancies (one copy is already out of the picture)

=25x greater chance to develop cancer

-cancer often developed at a young age

39
Q

How does p53 fight neoplastic transformation (3 ways)?

A
  • Activation of temporary cycle arrest (quiescence)
  • Induction of permanent cell cycle arrest (senescence)
  • Triggering of programmed cell death (apoptosis)
40
Q

How does the MDM2 protein affect p53?

A
  • it stimulates the degradation of p53

* MDM2 gene is amplified in 1/3 of sarcomas

41
Q

How does HPV cause cancer?

A
  • binds p53 and promotes its degradation

* Also occurs in several DNA viruses

42
Q

How does a tumor’s p53 status affect cancer treatment techniques?

A
  • Irradiation and conventional chemotherapy mediate their effects by inducing DNA damage and apoptosis
  • Tumors with normal p53 alleles are more likely to be killed by such therapy than tumors with mutated p53
43
Q

What are Adenomatous polyposis coli genes (APC)?

A

Adenomatous polyposis coli genes (APC) are a class of tumor suppressors whose main function is to down-regulate growth promoting signals

**mutations common in colorectal carcinomas, as well as liver cancer

44
Q

What disease is associated with germ-line APC mutations?

A
  • Familial adenomatous polyposis

- pt develops thousands of polyps in teens and 20’s

45
Q

What are the four classes of normal growth regulatory genes?

A
  1. Growth promoting proto-oncogenes
  2. Growth inhibiting tumor suppressor genes
  3. Genes that regulate Apoptosis
  4. Genes involved in DNA repair
46
Q

What are driver mutations?

A

-mutations that contribute to the development of the malignant phenotype

47
Q

Aberrant DNA methylation is responsible for __________.

A

The silencing of tumor suppressor genes

48
Q

What are the eight key changes in the molecular basis of malignancy?

A
  1. Self sufficiency in growth signals
  2. insensitivity to growth-inhibitory signals
  3. Evasion of apoptosis
  4. Limitless replicative potential
  5. Sustained Angiogenesis
  6. Ability to invade or metastasize
  7. Defects in DNA repair
  8. Altered Cellular metabolism
49
Q

What are oncogenes?

A

-genes that promote autonomous cell growth in cancer cells

**unmutated cellular counterparts are called proto-oncogenes

50
Q

What cancers are associated with exposure to arsenic?

A
  • lung carcinoma

- skin carcinoma

51
Q

What cancers are associated with exposure to Asbestos

A
  • Lung, esophageal, gastric, and colon carcinoma

- Mesothelioma (malignancy of the pleural surfaces)

52
Q

What cancers are associated with exposure to benzene?

A

Acute Myeloid Leukemia

53
Q

What cancers are associated with exposure to Beryllium?

A

-Lung Carcinoma

54
Q

What cancers are associated with exposure to Cadmium?

A

-Prostate Carcinoma

55
Q

What cancers are associated with exposure to Chromium compounds?

A

-Lung carcinoma

56
Q

What cancers are associated with exposure to Nickel Compounds?

A

-Lung & oropharyngeal carcinoma

57
Q

What cancers are associated with exposure to Radon?

A

-Lung Carcinoma

58
Q

What cancers are associated with exposure to Vinyl Chloride?

A

-Hepatic Angiosarcoma

59
Q

What are passenger mutations?

A

Mutations that lead to genomic instability greatly increase the frequency of mutations

60
Q

Tumors that recur after therapy almost always have _______ genotype than the original tumor

A

a different

61
Q

What are Protooncogenes?

A
  • genes that promote normal cell growth and development

- Over expression of these genes can lead to neoplasia

62
Q

What is the JAK-STAT mutation?

A
  • Associated with several myeloproliferative disorders
  • Point mutation in JAK2
  • This aberration activates transcription factors of the STAT family which promote the growth factor-independent proliferation and survival of tumor cells
63
Q

Dysregulation of ____ occurs in Burkitt Lymphoma.

A

MYC

64
Q

Why is it important that MYC can upregulate the expression of Telomerase?

A

Telomerase is one of several factors that contribute to the endless replicative capacity

**MYC is one of a handful of transcription factors that can act together to reprogram somatic cells into pluripotent stem cells

65
Q

What growth factors are involved in tumor angiogenesis?

A
  • VEGF

- bFGF

66
Q

Even if a solid tumor possesses all of the genetic aberrations that are required for malignant transformation, it cannot enlarge beyond 1 to 2 mm in diameter unless it has the capacity to induce ____________.

A

Angiogenesis

67
Q

What is the dual effect of angiogenesis on tumor growth?

A
  • Provides nutrients and oxygen

- newly formed endothelial cells stimulate the growth of adjacent tumor cells by secreting growth factors

68
Q

Why are lung and colorectal cancers frequently resistant to radiation and chemotherapy?

A

Lung and colorectal cancers frequently carry mutated p53 copies

69
Q

What does the grading of a tumor represent?

A
  • the degree of differentiation
  • Well, moderately, or poorly differentiated

=Histologic

70
Q

What does the staging of a tumor represent?

A

=anatomic

-Size of tumor and extent of spread

(I = localized, IV = extranodal mets)

Term 3: Immunology/Pathology (17 decks)

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