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Week 7 Foundations of Medicine > Neoplasm Lecture Oct 8 > Flashcards

Neoplasm Lecture Oct 8 Flashcards

1
Q

What does neoplasmia mean?

A

It means “new growth”

an abnormal mass ot tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which invoked the change.

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2
Q

What is a hamartoma?

A

It’s a non-neoplastic disorganized aggregate of mature tissues which is indigenous to the site of origin

(some can be neoplasms, but not all!)

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3
Q

What is a choristoma?

A

A heterotopic rest of mature cells

so mature cells that should be in one spot are in the wrong spot - sometimes you get pancreatic tissue in the submucosa of the stomach- it’s a developmental thing.

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4
Q

How do benign and malignant neoplasms differ?

A

THe key difference is that benign neoplasia cannot spread to other tissues, while malignant neoplasms have the capability of spreading (they don’t necessarily have to)

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5
Q

Which tend to be more locally invasive? benign or malignant neoplasms?

A

malignant - they ten to destroy adjacent structures

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6
Q

What are neoplasms made up of?

A

a clonal neoplastic population of parenchymal cells along with varying amounts of stroma

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7
Q

What does the differentiation of a neoplasm refer to?

A

the extent to which the neoplastic parenchymal cells resemble the normal parenchymal cells (morphologically and functionally)

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8
Q

What are the 6 classes of neoplasms based on cell/tissue of origin

A
  1. epithelial orgigin
  2. mesenchymal origin
  3. hematopoietic or lymphoid origin
  4. melanocytic origin
  5. CNS
  6. Germ Cell origin
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9
Q

What are malignant epithelial neoplasms called?

A

carcinomas

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10
Q

For mesenchymal tumors, what are the malignant ones called?

A

sarcomas

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11
Q

FOr melanocytic tumors, what are benign neoplasms called? What are malignant ones called?

A

benign = nevi

malignant = melanomas

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12
Q

If a benign epithelial neoplasm shows glandular differentiation, what are they called?

If they are cystic, what are they called?

If they form papillary structures what are they called?

A

glandular = adenomas

cystic = cystadenomas

papillary = papillomas

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13
Q

Malignant epithelial neoplasms that show squamous differentiation are called what?

Malignant epithelial neoplasms showing glandular differentiation?

A

squamous = squamous cell carcinomas

glandular = adenocarcinomas

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14
Q

If a tumor shows more than one type of differentiation, showing both epithelial and mesenchymal differentaion, what are they called?

A

pleomorphic

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15
Q

Germ cell tumors are called what?

A

teratoma - they have differentiation in all three germ cell layers

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16
Q

Which are more differentiated, benign or malignant neoplasms?

A

benign

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17
Q

Which has a higher mitotic rate, benign or malignant neoplasms?

A

malignant neoplasms

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18
Q

When is the term “anaplastic’ used to describe a tumor?

A

When it’s very undifferentiated

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19
Q

As malignant tumors become less differentiated, growth rate _____.

A

growth rate increases

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20
Q

What is the growth fration of a tumor?

A

the proportion of cells within the tumor population that is in the proliferative pool

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21
Q

Which are more likely to be affected by usual chemotherapeutic agents, tumors low high growth rates, or tumors with low growth rates?

A

tumors with high growth rates are more likely to be affected.

Low growth rate tumors can be regractory to these therapies

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22
Q

What is a desmoplasia?

A

Most invasive tumors like carcinomas can elicit a fibrous stromal response called desmoplasia - its the host tissue reaction to the tumor

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23
Q

What does it mean for a carcinoma to be in the “in situ” stage?

A

This is the stage where a malignant epithelial neoplasm hasn’t penetrated the basement membrane yet

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24
Q

What does “dysplasia” refer to?

A

The disordered growth and cytologic changes seen in epithelium

this is NOT a carcinoma yet, but can progress to one

these often arise in metaplstic epithelium

The big example is dysplasia of the cervix in response to HPV infection before the carcinoma develops

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25
Q

Metastatic spread can occur through which three pathways?

A
  1. Direct seeding of a body cavity or surface
  2. Lymphatic spread (often for carcinomas)
    Note that a LN could just be enlarged because of a reaction to the tumor - not metastatic spread - do a biopsy
  3. Hematogenous spread - sarcomas do this (through the blood)
    Note that it could seed the next capillary bed down or go to an organ is preferentially seeds
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26
Q

Which cancers have the highest incidence in men?

Highest incidence in women?

A

Men: prostate, lung, colon

Women: breast, lung, colon

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27
Q

What cancer causes the most deaths in both men and women?

A

lung

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28
Q

Which are more significant in sporadic cancers: genetic factors or environmental factors?

A

environmental factors

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29
Q

THe genetic predispositions to cancer fall into these three categories:

A
  1. autosomal dominant inherited cancer syndromes
  2. Defective DNA-repair
  3. Familial cancers - exact mutations and mode of inheritance unclear
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30
Q

What are wome nonhereditary predisosing conditions for cancer?

A

Chronic inflammation
(as in ulcerative colitis, H pylori gastritis, and viral hepatitis)

viral infection

exposure to carcinogens

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31
Q

What is the key initiating event in all examples of carcinogenesis?

A

You need nonlethal genetic damage (a mutation)

then the tumor must be formed by clonal expansion of a single precursor cells that has incurred genetic damage

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32
Q

Which four classes of normal regulatory genes are the principal targets in genetic damage?

A
  1. growth-promoting proto=oncogenes
  2. growth-inhibitin tumor suppressor genes
  3. genes that regulate programmed apopotisis
  4. genes involved in DNA repair
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33
Q

how do tumors become increasingly aggressive over time?

A

they develop as multiple mutations accumulate independently in different cells - leading to subclones with varying abilities to grow, invade and metastasize nad resist treatment

34
Q

Are tumors homogenous or heterogeneous?

A

for the most part, by the time they become clinically evident, they are extremely heterogeneous

this makes treatment tricky

it also means you can’t assume you know everything about a tumor just based on a needle biopsy

35
Q

What are the 8 fundamental changes in cell physiology that together determine the malignant phenotype?

A
  1. self suffiency in growth signals
  2. insensitive to growth-inhibition
  3. evasion of apopotisis
  4. limitless replicative potential
  5. sustained angiogenesis
  6. ability to invade and metastasize
  7. defects in DNA repair
  8. Escape from immune attack
36
Q

What causes the bast majority of cancer deaths?

A

metastases

37
Q

What allows for a tumor fo be self sufficient in growth signasl?

A

the oncogenes make all the proteins necessary for proliferation

38
Q

How many alleles need to become mutant in order to turn on an oncogene and cause a tumor?

A

only one

it’s a gain of function mutation

39
Q

what mutation is associated with chronic myelogenous leukemia?

what treatment was developed once we figured this out?

A

THe BCR-ABL translocation from chr 9 to chr 22

it increases tryosine kinase activity

treatment is now a tyrosine kinase inhibitor - imitinib mesylate (gleevac)

40
Q

Which proto oncogene is mutated in breast cancer?

A

HER (ERBB2)

If Her2/neu is present, it’s an overexpression of the epidermal growth factor receptor.

It can be treated with herceptin (trastuzumab)

41
Q

What is the protooncogene mutation in KRAS responsible for?

A

persistent activation of the RAS signal, resulting in colon cancer

42
Q

What is mutated if a tumor is insensitivt to growth inhibition or escapes sensecence?

how many alleles need to be locked out?

A

a tumor suppressor gene

both alleles need to be knocked out in a cell because it’s a loss of fucntion mutation

43
Q

What will the expression of an oncogene in an otherwise normal cell lead to?

A

quiescence - permament cell cycle arrest

the tumor suppressor genes are still working, so they stop the shit

44
Q

What tumor suppressor gene is mutated in familial polyposos (CRC)?

A

APC

it’s responsible for degrading the transcription factor beta-catenin

if it’s working, you don’t get proliferation

45
Q

Which tumor supressor gene is mutated in breast cancer?

A

BRCA

it regulates DNA repair

46
Q

What tumor suppressor gene is mutated in retinoblastoma?

A

Rb

47
Q

Which tumor suppressor gene is the “molecular policement” that prevents the propagation of genetically damaged cells?

A

p53

48
Q

How do B cell lymphomas evade apopotisis?

A

They are produced by a translocation that results in the overexpression of Blc2, which inhibits the release of cytochorme c from the mitochondria

49
Q

Do tumors that just evade apoptosis show a higher or lower growth rate?

A

lower - they don’t proliferate rapidly to form the tumor, they just don’t die

50
Q

How can a tumor cell game limitless replicative potential?

A

Most normal cells ahve a capacity for doublings which is determined by the progressive shortneing of the telomeres

Many neoplasms up-regulate the expression of telomerase, which promotes the maintenance of telomere length regardless of the number of divisions

51
Q

Why does the up regulation of telomerase result in a cacner cell having a clomplex karyotype?

A

With telomerase, the checkpoints that would usually stahl growth don’t work

withou checkpoints, the DNA repair pathway is inappropriatley activated and you get the formation of dicentric chromosomes

then at mitosis, the dicentric chromosomes are pulled apart and you get lots of double stranded breaks

these breaks then activate DNA repair pathways which leads to the random association of double stranded ends and the formation of more dicentric hromosomes

they just keep doing this over and over again and generate massive chromosomal instability and numerous mutations

52
Q

How do tumor cells promote angiogenesis for their own growth?

A

they upregulate angiogenic factors like VEGF

53
Q

How does angiogenesis help the tumor metastasize?

A

the new blood vessels are often abnormal and leaky, so they have easy access to circulation

54
Q

What two major steps are involved in the production of metastases?

A
  1. invasion of the ECM (degrading the basement menebrane and penetratind the ECM - is requires attachment of the tumor cells to ECM proteins)
  2. Intravasation into blood vessels and vascular dissemination, homing and then colonization
55
Q

What are some examples of a cancer caused by a mismatch reapri defects?

A

hereditary nonpolyposis colon cancer syndrome

56
Q

What is the dominant mode of immunity when it comes to anti-tumor mechanisms?

A

Cell mediated!

THe body doesn’t really make antibodies against tumor antigens (although we can make them as treatments)

57
Q

What are some ways a tumor cell can avoid the cell mediated immune attack?

A

use antigen negative variants

reduce expression of NHC

Lack the costimulatory molecules needed to activate the T cells

immunosuppression

mask your antigens

kill the cytotoxic t cells

58
Q

What are the ways chromosomes can change in cancer?

A

translocations (gene overexpression by swaping regulatory elements or having two unrelated sequences on dif chromosomes recombina nd form a hybrid fusion gene - as in CML)

deletions

reduplication and amplification of proto oncogene DNA sequences - leads to activation and overexpression

59
Q

What are the two steps required for chemical carcinogenesis?

A
  1. exposure of cells to a sufficient dose of a carcinogenic agent causing permament DNA damage/mutation
  2. Additional exposure to a promoter to enhance the proliferation of the damaged cells
60
Q

What is the difference between a direct acting carcinogen and an indirect acting carcinogen?

A

a direct actin requires no metabolic conversion to become carcinogenic

indirect acting agents need metabolic conversion of a procarcinogen to become active

61
Q

Although any gene can be the target of ac hemical carcinogen, what are the key targets usually?

A

oncogenes and suppressor genes

RAS and p53 are examples

62
Q

What are some forms of radiation carcinogenesis?

A
  1. ionizing electromagnetic radiation - x rays, gamma rays, particular radiation
  2. UV rays (Especially UVB) is increased risk of skin cancer through formation of pyrimidine dimers in DNA
63
Q

What is the warburg effect?

A

Cancer cells shift their glucose metabolism to aerobic glycolysis and use a lot of glucose

this can be used to visualize tumors on PET when patient sare injected eith fluorodeosyglucose which is a non-metabolizing derivative of glucose that will be taken up into tumor cells and then fluoresce to be visualized

64
Q

What is the basis for the “multistep carcinogenesis” idea?

A

cancer results from the accumulatino of multipl mutations in steps.

sometimes the steps need to happen in specific orders too

65
Q

Both benign and malignant tumors can cause clinical problems including….

A

Location and impingement on adjacent structures.

Functional activity such as hormone synthesis or the development of paraneoplastic syndromes.

Bleeding and infections when the tumor ulcerates through adjacent surfaces.

Symptoms that result from rupture or infarction.

Cachexia or wasting (seen in cancer).

66
Q

What is cachexia and what causes it?

A

It is a hypermetabolic state which presents as progressive loss of body fat and lean muscle mass along with weakness and anorexia

this is likely due to the action of soluble factors –cytokines - that result in a catabolic state along with a supressed appetitie

it’s not that the tumor is using up all thier nutrients

67
Q

what are paraneoplastic syndromes?

A

symptoms that cannot be explains by the local or distant spread of the tumor OR by hormones that are indigenous to the tissue from which the tumor arose

68
Q

What are some major paraneoplastic syndromes?

A

venous thrombosis

hypercalcemia

hypoglycemia

69
Q

What does the grading of a cancer take into account?

A

Grading is based on the degree of differentiation of the tumor cells (and sometimes the # of mitoses seen by light microscopy)

grades can be numerical (with 4 being the least differentiated)

or they can be graded describptively (well differentiated, moderately differentiated, poorly differentiated)

70
Q

What does staging of cancers take into account?

A

it’s based on the size/degree of invations, extent of spread to LNs, and the presence of abscence of distinct blood born metastases

it’s a T, N, M classification

71
Q

What is the first step in pathological diagnosis of a neoplasm?

A

obtaining a sample containing the tumor

72
Q

What are some of the different ways you can sample a tissue?

A
  1. incisional or excisional biopsy or lesions
  2. needle or punch biopsy with a hollow core needle
  3. musocal biopsy through endoscopy or colonoscopy
  4. Ctystoloy smear - cells are aspirated with a fine needle and syringe

For blood or body fluid…

  1. Blood smear
  2. Bone marrow aspiration smear
  3. Bone marrow core needle biopsy
  4. Cytology slide (aspirate fluid)
  5. cell block (aspirate fulid and hen centrifuge down to a pellet and process as tissue)
73
Q

HOw is immunohistochemistry used for in the laboratory diagnosis of cancer?

A

It uses pre-formed antibodies to allow for the detection of cell products or surface markers on the tissue being examined

it’s useful to categorize undifferentiated tumors

also useflu to determining the site of origin of a tumor

by detectin molecules that have prognostic of therapeutic significance, it can guide treatment (as in Her2/neu expression being treated with hercepfin)

74
Q

What is flow cytometry used for in the diagnosis of cancer?

A

It’s a technique that allows for the quanitfication of cells in a stream of fluid by passing them by an electronic detection devide

different cells are laveles with different lfuorescent antibodies

as the cells are detected and counted, so are the fluoescent signals so you can count different cells within a whole population

this is useful mainly for the luekmeias and lymphomas becase the blood cells all have different marker antigens that can be tagged

75
Q

What are some reasons to use molecular diagnosis of cancer?

A
  1. diagnose malignant neoplasms that are defined by their specific genetic abnormality - like CML
  2. Test the progrnosis of malignant neolasms because some tumors with certain genetic markers are known to respond to therapy and others aren/t
  3. Detect the minimal residual disease - sometimes you won’t be able to tsee any more cancer cells by other methods, but testing the bone marrow for genetic markers of the cancer cells will
  4. Diagnosies of a hereditary predisposition to cacner - like BRCA testing
76
Q

What does the OncotypeDX do for breast cancer patients?

A

It looks at 21 genes and determines a recurrence score which can be sued to determine the liklihood of a breast cancer recurrence - such considerations are important in developing a treatment plan

77
Q

What is the concept behind a tumor marker?

A

a tumor marker is a protine that a malinant cell will secrete into the blood or body fluid that can be measured to revel the presence of a tumor

they’re helpful for monitoring the effectiveness of treatment and looking for relapse

78
Q

What is the main issue with tumor markers?

A

they are often secreted in both malignant and non-malignant conditions (like PSA)

79
Q

Increasing the prevalence increases the utility of a test because it increases the positive predictive value. How can one change the prevalence in a population though?

A

You can’t in the population as a whole obviously, but you CAN increase the prevalence in the population being screened by only screening patients who have a liklihood of actually having the disease

80
Q
A

Week 7 Foundations of Medicine (8 decks)

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