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82 Cards in this Set

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Neoplasia
new growth
What are the two components all tumors, basic and malignant have?
1. parenchyma - proliferating NEOPLASTIC cells
2. Stroma - connective tissue, blood vessel (supporting tissue for tumor to grow in)
What determines the biological behavior of a neoplasm?
The origin of the neoplasm - whether it is neuroectodermal, epithelial, or mesenchymal (this is the parenchymal cell type)
How are tumors classified?
according to their cells of origin
VIP
How many types of cells do most cancers originate from?
One - they are monoclonal
Although the behavior and pathological consequences of a tumor are a result of its parenchymal origin, what does the growth an evolution of a tumor depend on?
Stroma of the tumor
What are the names of benign and malignant tumors of mesenchymal and epithelial origin?
Mesenchymal: B-Fibroma, M-Sarcoma

Epithelial: B-adenoma, papilloma; M-carcinoma
What are mixed tumors?
tumors with more than one neoplastic cell type but only from one germ line
VIP

What are two types of mixed tumors?
1. salivary gland tumors
B-pleomorphic adenoma, M-malig. mixed tumor
2. fibroadenoma - breast tissue mixed tumor
What are teratomas?
tumors with cellular elements from more than 1 germ layer
Where are teratomas most commonly found in the body?
In the midline of the body
What sex is most likely to get a teratoma?
Female
What is dysplasia? What types of cells exhibit dysplasia?
When cells lose both uniformity and normal architecture. This is an indicator of a pre-cancerous cell.
What is an anaplastic cell? What does this mean if an anaplastic cell is in a tumor?
a poorly differentiated cell, meaning that it looks primitive and do not resemble normal cells. Having anaplasia in a tumor usually means that the tumor is malignant, although a malignant tumor need not be anaplastic
Four characteristics of a malignant tumor?
1. marked pleomorphism (variation in cellular size and shape)
2. hyperchromatic nuclei (dark)
3. mitoses
4. less differentiated (does not look like other cells)
If a tumor metastasizes does that mean it is malignant?
YES!
To sarcomas usually spread via lymphatics?
Not usually?
Does sarcomas or carcinomas spread via blood?
Both do
What is a classic organ where many metastasis go?
The lung
What percentage of death does cancer account for?
23% of all deaths in US
For those people born in 1985, what portion of males and females will die of cancer?
Males - 1/4
Females - 1/5
What is the most common incidence of cancer in women and men?
Women - breast, 32%

Men - prostate, 33%
What is the most common cancer women and men die of?
Women - lung 25%

Men - lung 31%
Over the last 70 yrs, what cancer in women has increased in rate and what one has decreased?
Increased - lung
Decreased - uterine
Over the last 70 yrs, what cancer in men has increased (2)in rate and what one has decreased
Increased - lung and prostate (from fatty diets)
Decreased - stomach
Eating what can increase the rate of breast cancer?
High fatty diet
Which country has the highest rate of breast cancer? Lowest?
Highest - US and Northern Europe

Lowest - japan
Where are the highest rates of stomach cancer found?
Japan
At what age range is patient most succeptable to bone, brain, and leukemia cancers?
1-14y/o
At what age range is patient most succeptable to carcinomas and sarcomas?
55-75y/o
As we increase in age which type of tumor, epithelial or mesenchymal, is more likely to occur?
Epithelial
VIP

Three autosomal dominant cancers
1. familial adendomatous polyps of colon
2. familial retinoblastoma
3. Neurofibromatosis
VIP

Two familial cancers (causing a predisposition):
1. Breast
2. Ovarian
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Two autosomal recessive cancers due to a defective DNA repair system (enzyme defect):
1. xeroderma pigmentosa
2. ataxia telangiectasia
What four types of cancers have a pre-cancerous disorder that can be identified?
1. oral
2. bronchogenic
3. colon
4. cervical
What are protooncogenes?
Growth promoting targets of genetic damage.
VIP
What is the most common abn of a dominant oncogene?
RAS oncogene mutation
What is RAS?
A oncogene that controls cell prolifation and other cell components. To be active it must be bound to GTP.
What are GAP's and how to they relate to RAS?
GAP's are GTP-ase activating pathways) that prevent over expression of RAS.
What does NF-1 do?
It inhibits RAS -- keeps it as RAS-GTP
What does p53 do?
It is the "keeper of the genome" - recognizes DNA damage and either fixes it or induces bax to apoptose it.
VIP

What is the two-hit hypothesis?
In retinoblastoma, for example, there is first a genetic mutation (first hit) inherited from parent as autosomal DOMINANT
But before condition is developed a second hit must occur as a mutation in one of the many retinal cells which already carry the first mutation.
PT: both alleles of the RB locus must be activated (2 hits) for the development of retinoblastoma. Therefore the cancer develops only when cells become homozygous for the mutant allele (when cell loses its heterogenicity for a normal RB gene (LOH).
RB gene is a RECESSIVE cancer gene
What is BCl-2?
An anti-apoptotic gene that results in cell accumulation.
What is APC?
A tumor suppressor gene often mutated in colorectal cancer.
What is a RAS PROTEIN?
A protein regulating a cell that is often overstimulated by mutants causing an increase chance of cancer
VIP

What is doubling time?
Amount of time it takes for the number of tumor cells to double.
Are tumor cells cell cycles different in length than regular cells?
No tumor cells have the same cell cycle length however they are more readily induced to go into the cycle.
What is a tumors growth fraction?
Proportion of cells that are in the proliferative pool at any one given time.
What is true growth of tumors?
Dynamic equilibruim between cell production and loss
What enzyme to many cancers express to maintain growth?
Telermerase inhibitors
VIP VIP

If you add teleomeres to a growing tumor how is it effected?
It will be able to complete more cycles ----> greater heterogenity
How can a tumor ever be heterogenic?
Tumors start off as monoclonal but with time they form tumor cell subclones (becoming heterogenic) by the time they are ready to invade.
What produces FGF and VEGF and what do they do?
FGF (fibroblastic growth factor) and VEGF (vascular endothelial) are made by tumors as well as inflammatory cells (tumor can take advantage of this).
How do some drugs target inhibiting migration of tumors?
By using collagenase inhibitors
What are nm23, KISS, and KA-1?
Metastasis suppressor genes
VIP VIP VIP

What is Cushing's syndrome a paraneoplastic syndrome of? Mechanism
1. small cell carcinoma of the lung
2. adrenal tumors
3. pancreatic cancer

Mechanism: ACTH
What are four antitumor effector mechanism body employs?
1. cytoxic T-cells
2. NK cells
3. macrophage
4. hormonal mechanisms
VIP VIP VIP

What is Hypercalcemia a paraneoplastic syndrome of? Mechanism?
1. squamous cell carcinoma of lung
2. breast cx
3. adult t-cell leukemia
4. ovarian cx

Mechanism: Parathyroidism
VIP VIP VIP

What is dermatomyosistitis a paraneoplastic syndrome of? Mechanism?
broncogenic carcinoma
breast cx
ovarian cx

Mechanism: immunologic
What is tumore grading based on?
1. amt of cell differentation
2. amt of pleomorphism
3. loss of architecture
4. mitotic index

Use these four to estimate aggressiveness of tumor
What is staging of a tumor based on? What is the system used?
Staging - gross features
"TNM" system:
T: size of tumor, T1 2 3 4
N: extent of spread to lymphnodes, N0 1 2 3
M: presence of metastasis or not, M0 M1
How is neuro graded differently from other tumors?
Grade is stage since those tumors do not involve lymphatics, size doesn't matter, usually don't metastasize.
What is carcinoembryonic antigen a marker of?
Colon, pancreas, lung, stomach, or breast cancer
What is alpha fetoprotein a marker of?
Liver cx, tumor of yolk sac remnants, gonadal tumors.
Tumor associated markers are best for determining what?
recurrence of cancer - not primary diagnosis
Of chemical carcinogens there are direct acting carcinogens. How do they work?
They are highly reactive electrophiles that interact with neutrophilic sites on normal cell, permanently damaging the DNA.
What are "ultimate carcinogens"?
Carcinogens formed from activated procarcinogens.
What type of damage do chemical carcinogens cause?
Nonlethal genetic damage
What augments the carcinogenicity of chemicals?
Promoters - they facilitate the induction of cell proliferation in cells that have been "initiated" by chemical carcinogens.
Can chemical carcinogens act in concert with virues and radiation to induce neoplasms?
Yes
What determines the potency of a chemical carcinogen?
Its inherient reactivity of its electrophilic derivative and the balance between activation and inactivation rxns.
Does all carcinogen induced changes in DNA stay permenantly?
No, most can be repaired.
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What is required to convert a procarcinogen into an ultimate carcinogen?
cytochrome p450 - so any mutations that encode these enzymes can cause formation of ultimate carcinogens.
What are three main targets of chemical carcinogens?
1. RAS
2. p53
3. cytochrome p450
Since promoters are nonmutagenic, how do they contribute to tumorigenesis?
Promoters require inducers (?)
Which is the more potent carcinogen: direct-acting (alkylating) or procarcinogens (polycyclic aromatic hydrocarbons)?
Procarcinogens
What does the dose of the chemical carcinogen do to the probabilty of getting cancer?
The larger the dose the greater the incidence
What is xeroderma pigmentosa and how is it related to radiation?
It is a defect in a DNA repair enzyme that causes an increased suseptability to radiation.
Explain what cancer arises from oncogenic virus: Human T-cell leukemia virus. Who is affected? How is it transfered?
Causes T-cell leukemia. Common in SE asia and Japan. It is similar to the HIV virus in that it targets CD4 t-cells and is transmitted in the same way.
Explain what cancer arises from oncogenic virus: Infectious Hep B virus?
Hepatocellular carcinoma -

It is not a DNA virus but is strongly linked to this cancer
Explain what cancer arises from oncogenic virus:
Epstein Barr Virus
Burkitt's lymphoma and nasopharyngeal Cx
What proteins are effected in HPV?
E6 and E7, these are present only when other tumor suppressor proteins are disabled.

E6 = degrades p53
E7 = degreades RB & p21