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DMD 5246 > Bikman - Neoplasms > Flashcards

Bikman - Neoplasms Flashcards

1
Q

Benign tumor

A 
Remains localized; easily removed.
•	Small
•	Slow growing
•	Non-invasive
•	Well-differentiated
•	*Local growth*
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2
Q

Malignant tumor

A 
Cancer.
Invasive and destructive to adjacent tissue.
•	Large
•	Usually faster growing
•	Invasive
•	Poorly differentiated
•	Metastasis
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3
Q

Examples of benign tumors

A

Adenoma
Leiomyoma
Chondroma

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4
Q

Adenoma

A

Benign tumor in glandular cells

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5
Q

Leiomyoma

A

Benign tumor in SM cells

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6
Q

Chrondroma

A

Benign tumor in chondrocytes

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7
Q

Papilloma

A

Nipple or finger-like fronds

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8
Q

Polyp

A

Projects outward, forming a lump

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9
Q

Cystadenoma

A

Has hollow spaces inside (may be filled with fluid)

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10
Q

Histiologic characteristics of malignant tumors

A 
Anaplasia
Pleomorphism
Prominent nuclei
Hyperchromatism
High nuclear to cytoplasmic ratio
May be aneuploid
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11
Q

Anaplasia

A

Complete lack of differentiation

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12
Q

Pleomorphism

A

Cells aren’t shaped the right way

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13
Q

Malignant Tumors

A

Carcinoma

Sarcoma

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14
Q

Carcinoma

A

Malignant tumor in epithelial tissue

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15
Q

Adenocarcinoma

A

Malignant tumor of glandular cells

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16
Q

Squamous cell carcinoma

A

Malignant tumor of squamous cells

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17
Q

Sarcoma

A

Malignant tumor in mesenchymal tissue

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18
Q

Chondrosarcoma

A

Malignant tumor of chondrocytes

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19
Q

Angiosarcoma

A

Malignant tumor of BVs

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20
Q

Rhabdomyosarcomma

A

Malignant tumor of skeletal tissue

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21
Q

Mixed tumors

A

Show divergent differentiation

Pleomorphic adenoma
Fibroadenoma

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22
Q

Pleomorphic adenoma

A

Mixed tumor

Glands + Fibromyxoid stoma (fibroblasts + mucous)

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23
Q

What are some malignancies that sound benign?

A

Lymphoma
Mesothelioma
Melanoma
Seminoma

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24
Q

What are some non-tumors that sound like tumors?

A

Hamartoma (mass of disorganized indigenous tissue)

Choristoma (‘normal’ cells growing elsewhere)

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25
Q

What are some names that seem to come out of nowhere?

A

Leukemia

Hydatidiform mole

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26
Q

What is differentiation? Are malignant or benign cells well or poorly differentiated?

A

The degree to which a cell resembles the cell of origin.

Benign: well differentiated
Malignant: poorly differentiated

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27
Q

What are some features of anaplasia?

A 
Pleomorphism
Hyperchromatic, large nuclei
Bizarre nuclear shapes
Lots of mitoses and atypical mitoses
Architectural anarchy
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28
Q

What is dysplasia and what is it used to describe?

A

Disorderly growth

Used to describe disorderly changes in non-neoplasic epithelial cells

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29
Q

What is CIS and what are some of its features?

A

Carcinoma in situ.
A severe form of dysplasia, which isn’t yet cancer, but like a step right before cancer.

Features:
Pleomorphism
Hyperchromatic
Lots of mitoses
Architectural anarchy
30
Q

What factors does the rate of growth depend on?

A

Blood supply
Hormonal factors
Growth fraction (portion of cells that are actively dividing)

31
Q

What is metastasis and what does it depend on?

A

Development of secondary tumor implants in distant tissues.

Depends on:
Degree of differentiation of tumor
Type of tumor
Size of tumor

32
Q

What are the three means of metastasis?

A

Seeding
Lymphatic spread
Hematogenous spread

33
Q

What is seeding and what is an example of a cancer that spreads this way?

A

Tumor invades body cavity.
Bits break off and implant on peritoneal surfaces.

Ovarian cancer spreads this way.

34
Q

What is lymphatic spread and what is an example of a cancer that spreads this way?

A

Tumor spreads to local lymph nodes.
Sentinel lymph node first.
Moves through thoracic duct.
Empties into subclavian vein.

Carcinomas tend to spread this way.

35
Q

What is hematogenous spread and what is an example of a cancer that spreads this way?

A

Veins are easier to invade than arteries.
Liver and lungs are the most common metastatic tumors.
Some tumors like other sites better:
- Prostate –> bone
- Most lung cancers –> adrenals, brain

Sarcomas like to spread this way (but so do carcinomas).
Sarcomas metastasize to the lungs this way.

36
Q

What is the most common cancer in men and women?

A

Men: Prostate
Women: Breast

37
Q

What is the deadliest cancer in men and women?

A

Both: Lung

38
Q

What are environmental variables in cancer and what type are they typically linked to?

A 
Sun = skin 
Smoking = lung
Alcohol = liver, pancreas, breast cancers
39
Q

How are insulin resistance and cancer related?

A

The more insulin resistant an individual is, the more likely they are to develop cancer or to have a poor prognosis.

40
Q

What is the “Warburg effect”?

A

Cancer cells use glucose.
Insulin resistance/T2 Diabetes is a ‘perfect storm’ for cancer.

Glucose and insulin provide the fuel and allow growth for cancer.

41
Q

What are the three categories of heredity in cancer?

A
  1. Inherited cancer syndromes
  2. Familial cancers
  3. Syndromes of defective DNA repair
42
Q

What are some examples of inherited cancer syndromes?

A

Tend to be Autosomal Dominant.

Retinoblastoma
Familial polyposis coli
Neurofibromatosis

43
Q

What are some examples of familial cancers?

A

Breast
Colon
Ovary
Brain

Occur earlier with greater mortality

44
Q

What are some examples of syndromes of defective DNA repair (hereditary cancer)?

A

Tend to be Autosomal Recessive

Xeroderma pigmentosum

45
Q

What are paraneoplastic syndromes?

A

The indirect effects of a tumor that occur distant to the tumor.

  • Likely a consequence of proteins, polypeptides, or hormones secreted by the tumor
  • Usually precede dx/ID of malignancy
  • Can be a sign of malignancy

(The body is experiencing consequences of the tumor)

46
Q

What are the three most common neoplastic syndromes?

A

Endocrinopathies
Nerve and Muscle Syndrome
Dermatologic Disorders

47
Q

What are mutations that can cause proto-oncogenes to transition to oncogenes?

A 
Pathogens
Toxins
Radiation
Aging
Sexual Activity
Physical Inactivity
48
Q

Where are the two checkpoints in the cell cycle?

A

Between G2 and M

Between G1 and S

49
Q

What phase of the cell cycle does p53 and Rb regulate?

A

G1

50
Q

What is the function of p53 and Rb?

A

Inhibit the cell cycle

51
Q

What is the function of Ras?

A

To inhibit p53 and Rb, thus allowing the cell cycle to start up

52
Q

What do oncogenes cause that contribute to cancer?

A
  1. Autonomous growth
  2. Insensitivity to growth inhibitory signals
  3. Evasion of apoptosis
  4. Limitless replication
  5. Sustained angiogenesis
  6. Invasion and metastasis
53
Q

What are the causes of autonomous growth? Which oncogene is compromised to allow for this?

A
  • Increased secretion of growth factors (autocrine stimulation)
  • Increased growth factor receptors
  • Signal from cell-surface receptor it mutated into the on position
  • Activation of cell signals that drive the cell cycle

Ras is mutated, which allows for autonomous growth.

54
Q

Proto-oncogenes vs. Oncogenes

A

Proto-oncogenes - A normal gene whose product limits cell growth

Oncogenes - mutated proto-oncogenes that allow cells to grow unchecked. Cells lose the ability to restrict growth

55
Q

Which proto-oncogene is the “Guardian of the genome”?

A

p53

Most common mutation

56
Q

What are the four main apoptotic proteins that can undergo mutation? What happens when they mutate?

A

Fas
Executioner caspases
BCL2 family
p53

Cells become immortal when these proteins mutate

57
Q

Autonomous Growth

A

Cancer cells

  1. Make their own growth factors
  2. Receptors may be overexpressed or always on
  3. Signal-transducing proteins may always be on
  4. Nuclear transcription factors may always be expressed
  5. Cyclins may be overactive
58
Q

Insensitivity to growth inhibition

A

Proto-oncogenes –> Oncogenes –> Oncoprotein

Oncogenes - cells lose the ability to restrict growth
p53 and Rb allow cells to grow unchecked, when they usually would be stopped

59
Q

Evasion of apoptosis

A

Apoptotic proteins are mutated and allow cancer cells to become immortal

60
Q

Limitless replication

A

Telomere shortening leads to cell cycle arrest
- p53 and Rb

Stem cells and cancer cells use telomerase to maintain telomere length

61
Q

Sustained angiogenesis

A

Tumors need blood to deliver enormous amounts of nutrition.
Tumor cells secrete VEGF (primary angiogenic hormone)
Can’t grow over 1-2cm without a blood supply

Tumor BVs are abnormal (chaotic)

62
Q

Invasion and Metastasis

A

To invade, cells must:

  1. Loosen contact between cells
  2. Degrade ECM
  3. Migrate
63
Q

Where do circulating cancer cells usually settle?

A

Nearest capillary bed

Some display tropism (preference for certain sites)

64
Q

What are some necessary steps to cancer?

A
  • Accumulation of multiple mutations (Avg # is 90)

- Mutations within cell cycle checkpoint/guardian gene

65
Q

Chromosomal translocation vs. deletion

And genetic damage from them

A

Translocations - more commonly in hematopoietic malignancies; Philadelphia chromosome

Deletions - deletion of part or all of a chromosome; usually a tumor suppressor gene (p53); Retinoblastoma

Genetic damage:

  • Subtle - invisible on a karyotype (point mutation)
  • Large - visible on a karyotype (duplication)
66
Q

Chemical carcinogens
Direct acting vs. Indirect acting

What do they bind/affect and what are important targets?

A

Direct

  • Lethal as is
  • Most are chemotheraphy drugs
  • Cause secondary malignancy (i.e. leukemia)

Indirect
- Require a chemical conversion: hydrocarbons, aflatoxin B, nitrites

Both bind and affect DNA
Important targets: p53, Ras

67
Q

How does radiation contribute to cancer development?

A

Emission from x-rays, radioisotopes, and other radioactive sources.
Exposure causes gene mutations and chromosome aberrations.
- Causes pyrimidine dimers formation
- Repair pathways usually fix it, but they can become overwhelmed

i.e. Squamous cell carcinoma, melanoma

68
Q

What viral infections can contribute to cancer development? Which cancers?

A 
HTLV-1: T-cell lymphoma
HPV:  Cervical and oropharyngeal cancers
EBV:  Various lymphomas
HBV and HCV:  Hepatocellular carcinoma
H. pylori:  Gastric cancer, lymphoma
69
Q

Grading

A

Appearance
Pathological evaluation
Can reveal mitosis, pleomorphism, necrosis, etc.
LESS useful than staging

70
Q

Staging

A

Metastasis
TNM system
MORE useful than grading

DMD 5246 (3 decks)

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