Neoplasia

Front 1

what is cell prolieration?

Back 1

normal cell replacment mechamism

Front 2

when do cells proliferate?

Back 2

- replace short life cells - skin, blood, etc
-increase tissue mass during growth
- tissue repair

Front 3

What are 3 types of cells?

Back 3

1. permanent - nuerons, cardiac muscle cells
2. Labile cells - constant renewal: blood cells, GI tract epi
3. stable cells- slow divisiojn, can be accelerated if needed. (ex liver cells)

Front 4

T/F : the total number of cells in the body remain constant

Back 4

true. normally # of cells produced = number that die

Front 5

what are growth factors?

Back 5

cells divide only when growth factors / hormones tell cell to divide

Front 6

Process of normal cell proliferation:

Back 6

1. growth factor binds to specific membrane receptor
2. transient activation of growth factor
3. activation of signal trandducing G-protein
4. transmission of signal by enzymes and 2nd messengers across cytosl to nucleaus
2. DNA --> cellular growth

Front 7

stages of cell cycle:

Back 7

1. G1 - interphase
2. synthesis - DNA replicates
3. G2 - preparation for dividing
4. Mitosis- prophase, metaphase, anaphase
- unofficial G0 phase - non dividing, quiescence

Front 8

what are tumor supressor proteins?

Back 8

proteins that control division checkpoints - usually stop division of mutated cells to prevent cancer.
Types:
-cyclins
cyclin-dept kinases
-cyclin inhibitors

Front 9

waht do cylins do?

Back 9

1. check that DNA has been correctly duplicated
2. make sure has made the proteins needed to separate chromosomes
3. measure wheather the cell has grown large enough to divide

Front 10

waht is pRB?

Back 10

a regulatory protien for cell cycle.. controled by CDK complex

Front 11

what are proto-oncogenes?

Back 11

regulate pathways for growth stimulation that activate genes for cell growth

Front 12

Where do cyclins check for DNA damage?

Back 12

1. between G1 and S
2. Between G2 and M

Front 13

swhat is the most comon target for genetic alteration in human cancers? (50%)

Back 13

P53 - a type of tumor supressor gene

Front 14

what does p53 do?

Back 14

prevents propagation of damaged cells by activating apoptosis genes.
-can also cause hypoxia

Front 15

what are the functions of telomeres?

Back 15

telemoeres are another control stystem. With each division of DNA, the telomere sequence is not duplicated and shorten with each cell cycle.

Front 16

other replication regulation mechanisms?

Back 16

1. contact inhibition
2. area code hypothessis - each cell has an "address" on its membrane, telling other cells where it should be
3. apoptosis of cells with damaged DNA - triggerd by p53

Front 17

what is apoptosis?

Back 17

controlled cell death whe n cell is damaged or control systems are deregulated
-ie oncogenes formed and tumor supressor genes inactivated

Front 18

what is telomerase?

Back 18

enzyme that is absense in most cells that overides telomere control system. promotes the creation of immortal cells wtih indefinate reliplication.

Front 19

what do DNA repair genes do?

Back 19

identifies nad repairs DNA.
detects mutations
(unlike tumor suprressor genes, do not control cell growth directly)

Front 20

what is cancer?

Back 20

a collection of disorders. many histological types

Front 21

what is carcinmoa?

Back 21

origin of tumor in epithelial tissue

Front 22

what is adenocarcinmoa

Back 22

orgin in ductal or glandular tissue

Front 23

what is oncogenesis?

Back 23

process of genetic and cytological changes that result intumor formation. Is a nulti-step rprocess requiring accumpulation of mutations, taht can be accelerated by hereditary genetic mutations

Front 24

what is neoplasia?

Back 24

when neoplasms proliferate to form new tissue, without signals from the body sayign tissue is needed and ignore signals to stop division. Often do not differentiate to do "job" or die off to keep cell # constant

Front 25

what are proto oncogenes?

Back 25

The normal genes that code for normal proteins used in cell division:
Growth factors
Growth factor receptors
G proteins
Enzymes that produce second messengers
Genes that turn the production of these proteins on and off

Front 26

what do proto-onco genes code for?

Back 26

Growth factors
-Growth factor receptors
-G proteins
-Enzymes that produce second messengers
-Genes that turn the production of these proteins on and off

Front 27

what are oncogenes?

Back 27

Oncogenesare mutated proto-oncogenes that code for abnormal proteins
-They still code for the proteins needed for cell division but they might produce
Too much of the protein
An abnormal protein
Protein that turns on all by itself
Protein that is made when it is not needed
Protein that cannot turn cell division off
Protein that should be made by a different cell

Front 28

proliferation without external growth signals can occur by:

Back 28

1. autocrine stimulation - cancer secretes growth factors that stimulate its own growth
2. upregulated growth factor receptors
3. activating mutation: signal cascade activated in "on" position

Front 29

How can you stop a cell from dividing?

Back 29

1. use drug to block growth factor receptors
2. use drug that inactivates growth factors
3. use drug that stops cell from producing growth factor

Front 30

what are main sources of DNA damage?

Back 30

1. Viruses (e.g.: HPV, HBV, HCV, EBV)
2. Bacteria (H. Pylori)
3. Gene-Environment Interaction

Front 31

What are specific environmental causes of DNA damage?

Back 31

Tobacco Use
Diet
Alcohol Consumption
Sexual and Reproductive Behavior
Air Pollution
Occupational Hazards
Ultraviolet Radiation
Ionizing Radiation
Hormones
Free-radicals

Front 32

what happens when differentiated cells mutate?

Back 32

form benign tumors :differentiated “working” tumors.

Front 33

what happens when undifferentiated, rapidly dividing cells mutate?

Back 33

they form rapidly dividing tumors—malignant tumors

Front 34

what kind of mutations result in poorly differentiated neoplasms?

Back 34

Early mutations cause poorly differentiatd and highly malignant neoplasms

Front 35

what are stages of oncogenesis?

Back 35

1. intiation - mutation occurs due to exposure to carcinogenic agent
2. promotion - mutated cells divide - unregulated growth
3. progression - tumor cells compete and develop more mutations, becoming more aggressive... become malignant

Front 36

When a well-differentiated cell mutates, is it more or less likely to become a malignant tumor?

Back 36

b.Less
The more differentiated a cell is when it mutates, the more likely it is to become a benign tumor. If poorly differentiated cells mutate, the tumor is more likely to become malignant.

Front 37

what kind of cells tohereditary cancer mutations occur in?

Back 37

germline cells

Front 38

what type of mutations are hereditary?

Back 38

tumor supressor genes or DNA repair genes.... individuals with mutations in these usually need few mutations for oncogenes to culminate

Front 39

what is the Theory of Accumulation of Mutations?

Back 39

“Multi-hit ”theory:
•After sufficient mutations: cancer occurs
•After mutation a cell may acquire some characteristics of cancer –permit progression to cancer after added hits

Front 40

how are benign tumors named?

Back 40

tissue name + "oma"

Front 41

how are malignant tumors named?

Back 41

epithelial tissue: tissue name + carcinoma
Mesenchymal tissue: tissue name + sarcoma

Front 42

what are characteristics of benign tumors?

Back 42

Contain cells that look like normal tissue cells
May perform the normal function of the tissue (like secreting hormones)
-This may lead to oversecretion
Usually have a capsule around them
Usually do not invade neighboring tissues
But they can damage nearby organs by compressin

Front 43

what are characteristics of malignant tumors?

Back 43

Contain cells that do not look like normal adult cells
These cells divide rapidly, so:
Tumors grow quickly
Cells mutate faster and can change type
The tumor does not have clear boundaries and sends “legs” out into surrounding tissue (the word cancer means “crab” and is based on these crablike legs)
Do not perform the normal functions of the organ
May secrete hormones associated with other tissues
Can compress and/or destroy the surrounding tissues

Front 44

how do tumors metastasize?

Back 44

cells must detach from their original location, invade a blood or lymphatic vessel, travel to a distant site, and establish a new cellular colony

Front 45

how do tumors have ability to metastasize?

Back 45

1. hide bw platelets
2. must have enzymes to destroy epithelial cells so can enter the blood vessel
3. must be near bllod or lymph vessel

Front 46

what is angiogenesis?

Back 46

the formation of new blood vessels, a process controlled by chemicals produced in the body that stimulate blood vessels or form new ones. Angiogenesis plays an important role in the growth and spread of cancer
Critical to the progression from in situ to metastasis
Mutated tumor cells either recruit or produce proteins that mobilize nearby angiogenic proteins

Front 47

what are the manifestations of cancer?

Back 47

1.Changes in organ function (organ damage, inflammation, and failure)
2.Local effects of tumors (e.g., compression of nerves or veins, gastrointestinal obstruction)
3. Ectopic hormones secreted by tumor cells (paraneoplastic disorders)
4. Nonspecific signs of tissue breakdown (e.g., protein wasting, bone breakdown)

Front 48

what changes in organ function can cancer cause?

Back 48

1. Organ damage - inflammation, or failure
2. Benign tumors may cause overproduction of normal organ secretions
3. Malignant tumors may occasionally cause overproduction (as in thyroid cancer), but more commonly decrease production of normal organ secretions

Front 49

Why do malignant tumors usually cause a reduction in the amount of hormones the affected organ produces?

Back 49

d.All of the above
Rationale:Effects of malignant tumors on the organ system include inflammation and damage, which ultimately lead to organ failure. In all cases the organ cannot function optimally, and is unable to secrete the normal/typical amount of hormones

Front 50

what are the local effects of tumor growth?

Back 50

1. bleeding
2. compression of blood vessels --> portal hypertension,
3. compression of lymph vessels -> edema, effusion
4. compression of hollow organs
5. compression of nerves - pain, paralysis

Front 51

what are Paraneoplastic Syndromes?

Back 51

is a disease or symptom that is the consequence of the presence of cancer in the body, but is not due to the local presence of cancer cells. These phenomena are mediated by humoral factors (by hormones or cytokines) excreted by tumor cells or by an immune response against the tumor. .
- Cancer cells produce hormones or hormone-like proteins

Front 52

what are the generalized effects of cancer?

Back 52

Cancer cachexia syndrome
Weight loss
Muscle wasting
Weakness
Anorexia
Anemia

Front 53

what are the stages in tumor development?

Back 53

1. genetic mutation
2. hyperplasia - overproduction of cells
3. dysplasia (stage 1)
4. dysplasia stage II - in situ neoplasia
5. invasive neoplasia (stage 3 - lymph node involvement
6. metastases (stage 4) - secondary tumors invading nopadjacent cells

Front 54

in TNM, what is T?

Back 54

Primary Tumor (T)
T0: No evidence of primary tumor
Tis: In situ
T1, T2, T3, T4: Size and/or extent of the primary tumor

Front 55

What is N?

Back 55

Regional Lymph Nodes (N)
N0: No regional lymph node involvement
N1, N2, N3: Number and/or extent of spread/involvement of regional lymph nodes

Front 56

Metastasis (M) in TNM?

Back 56

M0: No distant metastasis
M1: Distant metastasis

Front 57

look at schematic

Back 57

on final slide of neoplasm leacture

Front 58

what kind of cancer is a sarcoma?

Back 58

cancer of connective tissue

Front 59

what kind of cancer is a lymphoma

Back 59

cancer of lymphatic tissue

Front 60

what kind of cnacer is a leukenia?

Back 60

cancer of the blood-forming cells