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Pathophysiology > Biology of Cancer (Quiz 2) > Flashcards

Biology of Cancer (Quiz 2) Flashcards

1
Q

Neoplasia definition

A

New Abnormal Growth; could be either benign or malignant (also known as a tumor)

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2
Q

Tumor definition

A

New abnormal growth; could be either benign or malignant (same as neoplasia)

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3
Q

Malignant definition

A

Cancer “crab”, can invade and destroy adjacent structures and spread to distant sites

  • fatal without treatment
  • destructive where they’re at
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4
Q

Benign definition

A
  • “relatively innocent”

- remain localized, does not spread distantly (not a whole lot of destruction)

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5
Q

Neoplasia

A
  • new abnormal growth
  • loss of responsiveness to normal growth controls (autonomy)
  • behave as parasites:
  • compete with normal cells for their metabolic needs
  • increase in size tumor not individual cells regardless of their local environment and the nutritional status of their host
  • spolied king w/peasants example
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6
Q

Nomenclature of benign tumors

A
  • benign tumors are designated with suffix -oma added to the cell type (example fibroma, adenoma)
  • names based on cells of origin: adenoma (glandular), cystadenoma (mass on a hollow organ)
  • two important exceptions are lymphoma and melanoma which are both malignant
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7
Q

Nomenclature of malignant tumors

A

main categories:

  • sarcoma
  • carcinoma
  • lymphomas and leukemias
  • multiple myeloma
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8
Q

-sarcoma

A

connective tissue origin

-e.g: fibrosarcoma, osteosarcoma

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9
Q

-carcinoma

A

epithelial origin

-e.g. adenocarcinoma

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10
Q

lymphomas & leukemias

A 
lymphomas = solid mass of tissue
leukemias = proliferate in bloodstream and bone marrow
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11
Q

multiple myeloma

A

malignant cancer

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12
Q

risk factors for cancer

A
  • genetics and cancer-prone families
  • viral causes (HPV)
  • bacterial causes (helicobacter pylori)
  • tobacco use
  • diet
  • alcohol consumption
  • sexual and reproductive behavior (increase risk for cervical cancer)
  • air pollution (free radicals)
  • occupational hazards
  • ultraviolet radiation (skin cancer)
  • ionizing radiation
  • sex hormones
  • others
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13
Q

how is diet a risk factor for cancer?

A
  • xenobiotics (substitute acts like a drug, hormone or toxin)
  • nitrates (lunchmeats)
  • low fiber (colon cancer risk)
  • obesity
  • omega 6 fatty acid: increases risk
  • omega 3 fatty acids: decreases risk
  • many others
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14
Q

Carcinogenesis

A
  • origin or production or development of cancer
  • normal cell division, proliferation, and differentiation is strictly regulated by genetic control
  • regulatory genes “turn on” resting cells so that they will divide, and “turn off” proliferating cells
  • damage of these genes leads to carcinogenesis
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15
Q

damage of what kind of genes leads to carcinogenesis?

A

mutations of:

  • genes that encode growth factors
  • genes that encode growth factor receptors
  • genes that regulate apoptosis
  • genes that regulate repair of damaged DNA
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16
Q

Oncogenes

A

regulatory genes, that if damaged may lead to neoplasia

  • proto-oncogenes
  • tumor suppressor genes
  • “proof-reading” genes
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17
Q

Proto-oncogenes

A

genes that in their normal, non-mutant state, lead to proliferation of cells (code for various pro-growth signals)

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18
Q

Tumor suppressor genes

A

Genes that in their normal, non-mutant state, stop excessive cell proliferation (code for various antigrowth signals)

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19
Q

“proof-reading” genes

A

genes that code for DNA error repair enzymes

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20
Q

Telomere

A

normal cap on DNA at the end of a chromosome

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21
Q

Telomerase

A

an enzyme that can build the telomere back up (turned off in every adult cell except sperm cells)

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22
Q

Cancer transformation requires multiple mutations

A
  • self-sufficiency in growth signals
  • insensitivity to antigrowth signals
  • evading apoptosis (via telomerase)
  • limitless replicative potential
  • sustained angiogenesis (new blood vessels form to supply it)
  • tissue invasion and metastasis
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23
Q

transformation

A

the process by which a normal cell becomes a tumor cell

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24
Q

Tumor progression

A
  • transformation occurs
  • benign tumors may further mutate into malignant tumors
  • many tumors become more aggressive and acquire greater malignant potential over time
  • subpopulations of cells can develop
  • most benign tumors stay benign
  • frequently reproduces
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25
Q

Differentiation

A
  • process by which cells become different from each other
  • normal cells become irreversibly more specialized
  • as they become more differentiated, they may lose their ability to replicate
  • genes that are normally “turned off” during differentiation can be mutated or reactivated by carcinogenic agents
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26
Q

oncology

A

backwards embryology

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27
Q

three germ layers

A

epiderm (skin, neuro)
mesoderm (musculoskeletal)
endoderm (digestive, urinary)

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28
Q

totipotent cell

A
  • undifferentiated

- has the potential to become anything

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29
Q

multipotent cell

A

germ lines

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30
Q

pluripotent stem cell

A

more stem-ish than others

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31
Q

Unipotent cell

A

white blood cells (cells that can only differentiate into one type of cell)

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32
Q

Differentiation of tumor cells

A

-extent to which the tumor cells resemble their normal forebears, both morphologically and functionally

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33
Q

differentiation of benign tumors

A
  • well differentiated and closely resembles their normal counterparts
  • may produce functional hormones, etc.
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34
Q

Differentiation of malignant tumors

A
  • range from well-differentiated to totally undifferentiared (anaplastic)
  • a spectrum
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35
Q

Dysplasia

A
  • dysplasia is a disorderly but non-neoplastic proliferation of (usually epithelial) cells
  • loss of uniformity (pleomorphic)
  • loss of architectural orientation
  • mitotic figures more abundant & in abnormal locations
  • mild to moderate dysplastic changes may be reversible
  • dysplastic changes are often found adjacent to cancerous foci “pre-cancerous”
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36
Q

Carcinoma in SItu

A
  • contained in one spot
  • pre-invasive epithelial tumors (NOT pre-cancerous)
  • have not yet broken through the basement membrane
  • may be erroneously confused with benign tumors
  • may be non-invasive for variable periods of time before progressing to invasive carcinomas
  • e.g. cervix, breast (DCIS)
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37
Q

benign vs. malignant differentiation

A

B: well differentiated and grow slower
M: well to poorly differentiated and grow faster
*anaplasia in worst of malignant only

38
Q

benign vs. malignant rate of growth

A

B: slow
M: varies
-lots of exceptions to this rule

39
Q

benign vs. malignant local invasion

A

-differs from local growth
B: no
M: yes

40
Q

benign vs. malignant metastasis

A

B: no
M: varies

41
Q

anaplasia

A

cells show the most extreme disturbances in cell growth

  • total loss of differentiation
  • cells have no recognizable patterns of orientation to each other
  • the more anaplastic a tumor, the less likely it is to have specialized functional activity
42
Q

pleomorphism

A

cells show marked variation in size and shape (many size and many shapes)

43
Q

Nuclei in anaplastic cells

A
  • nuclei are very hyperchromic (dark & big) and large

- nuclei are variable and bizarre in size and shape

44
Q

mitoses in anaplastic cells

A

numerous and abnormal

45
Q

Rate of growth

A
  • benign tumors grow slowly and malignant tumors grow much faster
  • rate of growth of malignant tumors correlates with their level of differentiation
  • malignant tumors show wide variation in their rate of growth (may grow slowly for years, then suddenly grow rapidly)
  • rapidly growing cancers often contain central areas of ischemic necrosis because the tumor’s blood supply fails to keep pace
46
Q

Exceptions to the rate of growth

A
  • benign tumors influenced by circulating hormone levels

- pressure constraints

47
Q

Tumor angiogensis

A
  • tumors cannot enlarge beyond 1-2mm in diameter unless they are vascularized
  • cancers which “outgrow” their vascular supply develop necrotic centers
  • clinical importance:
  • intratumor microvascular density is a prognostic factor in breast cancer
  • angiogenesis inhibitors have potential for use in treatment in the future
48
Q

Central necrosis

A

typically only found; very rapidly growing, very dangerous cancers

49
Q

Cell (growth) cycle

A 
G0= "non-pregnant"
G1-S-G2-M= pregnancy of a cell
50
Q

Kinetics of tumor cell growth

A
  • doubling time
  • growth fraction
  • population statistics
51
Q

Doubling time

A

Cells may be triggered to cycle more often, but do not complete the cycle more rapidly

52
Q

Growth fraction

A

the proportion of cells within the tumor that are replicating

53
Q

new cells > # cells lost

A

increase in population

54
Q

new cells = # cells lost

A

population stays the same

55
Q

new cells < # cells lost

A

decrease in population

56
Q

Clinical importance of tumor growth kinetics

A

chemotherapy

  • almost all agents in current use, work by killing any cell in the cell growth cycle (colon cancer has a low growth fraction, so its relatively resistance to chemotherapy)
  • need increased growth fraction in order for chemo to really work
  • debulking the tumor by surgery or using radiation can cause the surviving cells to of into active growth which makes them more susceptible to chemotherapy (primitive approach, antigens are the future)
  • contact inhibition (cancer some do some don’t but all normal cells have)
57
Q

Local growth of benign tumors

A
  • benign tumors remain localized at site of origin and slowly expand
  • benign tumors do not have the ability to infiltrate, invade or metastasize
  • most, but not all, benign tumors develop an enclosing fibrous capsule that separates them from the normal tissue
  • malignant tumors never do
  • benign tumors do their own thing
  • malignant tumors invade locally and harm surrounding cells
58
Q

Local invasion by cancers

A
  • cancers grow by progressive infiltration, invasion, destruction and penetration of the surrounding tissue
  • similar to plants putting down roots (force sheets or finger-like projections along lines of least resistance, pressure from the growing mass leads to local tissue death which further aids the spread)
59
Q

malignant tumor process of invasion

A
  • have high levels of lytic enzymes
  • use these enzymes to kill cells that are in the way
  • proteases, lysosomes, collagenases, etc
  • cause significant damage to the normal extracellular matrix
  • malignant tumor cells have decreased cell to cel adhesion (metastasis) and increased cell motility (pseudopodia)
60
Q

Biology of tumor cells

A
  • biochemical differences are seen (metabolism of liver tumor cells is much simpler than that of adult liver cells)
  • tumor cells are better adapted to survive under unfavorable conditions (can test for it in the blood, require less oxygen, so fewer mitochondria and better tolerate lactic acid by-products)
  • don’t contain all enzymes or produce all the proteins that normal cells do
61
Q

Growth properties in cell culture

A
  • cancer/tumor cells have less stringent nutritional requirements (may be “immortal”)
  • normal cells have a finite lifespan
  • normal cells exhibit contact inhibition
  • malignant cells tend to pile up and form aggregates and nodules
  • normal cells require firm support for growth (anchorage-dependent)
  • cancer cells can float suspended in clumps (anchorage-independent)
62
Q

Metastasis

A
  • spread of cancer cells from a primary site of origin to a distant site
  • cancers vary in their ability to metastasize (more likely to have large neoplasms and anapestic neoplasms)
  • location of metastases may or may not be easily predicted by the location of the primary tumor
63
Q

3 steps of metastasis

A
  1. Invasion and penetration into blood vessels, lymphatic vessels, or body cavities (get released from the original mass)
  2. Transport to a second site “shedding”
  3. Arrest, adherence, and proliferation at the secondary site (single cell or clump: safer for cancer)
64
Q

CAM

A

cellular adhesion molecule

65
Q

Metastatic spread

A
  • malignant neoplasms disseminate by one of three pathways
  • seeding
  • lymphatic speed
  • hematogenous spread
66
Q

Seeding

A
  • occurs in natural body cavities
  • characteristic of ovarian cancers
  • enhanced by lack of intracellular adhesion
  • like a flower, seeds fall down
67
Q

Lymphatic spread

A
  • more typical of carcinomas (epithelial origin which doesn’t need blood supply)
  • depends on the primary site and the natural lymphatic drainage of the the site (carcinoma of breast -> axillary lymph nodes)
  • “skip metastasis”
68
Q

Hematogenous

A
  • more typical of sarcomas
  • arteries are less readily penetrated than are veins (thinner wall and lower pressure)
  • the liver (intestinal cancer) and lungs are the most frequently involved secondary sites (small diameter, gets stuck)
  • appears to be tissue-specific homing of some tumor cells
  • metastasis is not a one time event
69
Q

Effects of tumors on the host

A
  • location and size
  • hormone production
  • ulceration
70
Q

location and size

A

1 cm pituitary adenoma or a 5 mm lieomyoma in the wall of a renal artery (decreased blood flow and increased BP)

71
Q

hormone production

A

pancreatic islet cell tumor (makes insulin), thyroid tumor (hyperthyroidism), adrenal tumor

72
Q

Ulceration

A

through a surface causing bleeding and secondary infection

73
Q

Clinical manifestations of cancer

A
  • cancer cachexia: a wasting syndrome
  • progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia
  • degree of cachexia usually correlates to the cancer’s size and aggressiveness
  • cancer patients have an increased basal metabolic rate
74
Q

Clinical manifestations of cancer: pain

A
  • usually little or no pain in early stages
  • pain occurs in 60-80% of terminally ill patients
  • pressure, obstruction, invasion of a sensitive structure, stretching of visceral surfaces, tissue destruction, and inflammation can all contribute to pain
  • pain is influenced by fear, anxiety, sleep loss, fatigue and physical deterioration
75
Q

fatigue

A

the most frequently reported symptom (decrease in supply of ATP combined with increase need for ATP)

  • probably related to nutritional status, decreased muscle contractility, secondary biochemical changes, etc
  • described by cancer patients as tiredness, weakness, lack of energy, exhaustion, inability to concentrate, depression, lack of motivation, etc.
76
Q

Cancer grading and staging

A

T- tumor
N- nodes
M- metastases

77
Q

T

A

primary tumor; the number equals the size of tumor and its local extent

78
Q

T0

A

free of tumor

79
Q

T1

A

lesion < 2cm in size

80
Q

T2

A

lesion 2-5 cm

81
Q

T3

A

beyond organ

82
Q

N

A

lymph node involvement; a higher number means more nodes and involved

83
Q

N0

A

no nodes involved

84
Q

N1

A

adjacent nodes

85
Q

N2

A

distant nodes

86
Q

M

A

extent of distant metastases

87
Q

M0

A

no metastases

88
Q

M1

A

demonstrable metastases

89
Q

Morbidity

A

of cases

90
Q

Mortality

A

of deaths

Pathophysiology (11 decks)

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