Hehi Test 3 - Neoplasms: Carcinogenesis

Front 1

Cancer is the ___ leading cause of death in the US.

Back 1

2nd

(heart dx #1)

Front 2

Most common cancer deaths in
Men:
Women

Back 2

Men: 1) lung & bronchus 2) prostate
Women 1) lung & bronchus 2) breast

Front 3

Cancer death rates most common by race and ethnicity

Men:
Women:

Back 3

AA men
White Women

Front 4

Primary site:

Back 4

where cancer began, may metastisize to another area

Front 5

Cancer incidence in children, most common sites?

Back 5

1) Leukemia
2) Brain

Front 6

Most common cancer in the US?

Back 6

Colon

Front 7

Cell Cycle
G1 -
S -
G2 -
M -

Back 7

Process of splitting into 2 cells

G1- growth phase 1 - growth and metabolic roles
S - Interphase - DNA replication
G2 - growth phase 2 - Growth and preparation for mitosis
M - mitotic phase - prophase, metaphase, anaphase, telephase

Front 8

Defects in what 2 processes can cause neoplasia (abnormal growth)?

Back 8

1) Proliferation: inherent adaptive mechanism for replacing body cells when old cells die or additional ones are needed.

2) Differentiation: process of specialization whereby new cells develop the structure and function of cells they replace.

Front 9

Proliferation involves cell division and reproduction of 200 or more cell types that can be divided into 3 types. What are the 3 types?

Back 9

1) Well differentiated - neurons, skeletal muscle, cardiac - unable to reproduce
2) Parent or progenitor - continually divide and reproduce
3) Stem cells (undifferentiated) - can be triggered to enter the cell cycle and produce progenitor cells
(primary component of BMT -bone marrow transplant)

Front 10

Process of differentiation

Back 10

Stem cell -> progenitor cell -> specialized cell

Front 11

Characteristics of benign and malignant neoplasms

Back 11

1) PARENCHYMAL TISSUE - fuctional component of the organ, and are the COMPONENT FOR WHICH THE TUMOR IS NAMED.
2) STROMA: supporting tissue (connecting tissue, BV, lymph structures) - PROVIDES SUPPORT FOR TUMOR SURVIVAL AND GROWTH

Front 12

tumors are named by adding "-oma" to___

Back 12

the parenchymal tissue from which the tumor orginates

Front 13

Carcinoma

Back 13

used to describe a malignant tumor of epithelial tissue origin

Adenoma - benign
Adenocarcinoma - malignant

Front 14

Carcinoma in Situ

Back 14

severe dysplasia

early form of carcinoma defined by the absence of invasion of surrounding tissues. cells are proliferating in their normal habitat

Front 15

Cancer cells vs. normal cells

Back 15

Cancer cells:
-loss of contact inhibition
- inc in growth factor secretion
- inc in oncogene expression (gene that can transform into tumor cells)
- loss of tumor suppression genes

Normal cells:
- oncogene expression is rare
- intermittent or coordinated growth factor secretion
- presence of tumor suppressor genes

Front 16

Benign vs. Malignant Neoplasms

Back 16

Benign:
- slow progression
- may come to a standstill or regress
- well defined capsule (usually grow w/in)
- failure to metastasize
- well differentiated and resemble cells of tissue origin

Malignant:
- grow rapidly/ spread widely
- kill regardless of location
- compress and rob normal tissue
- liberate enzymes and toxins
- lack cell differentiation
- solid and hematologic

Front 17

metastasize

Back 17

development of a secondary tumor distant from a primary tumor

Front 18

angiogenesis

Back 18

ability of the tumor to produce blood vessels w/in the tumor

TAF - tumor angiogenesis factor

Front 19

Tumor growth is affected by

Back 19

- # of cells that are actively moving through the cell cycle
- duration of the cell cycle
- # of cells that are being lost compared to the # of cells that are being developed
- growth fraction: ratio of dividing cells to resting cells in all tissues

Front 20

How do "cancer genes" cause disharmony in cells?

Back 20

- autonomous growth
- insensitivity to growth inhibitory signals
- evasion of apoptosis
- limitless replication
- sustained angiogenesis
- invasion and metastasis

Front 21

dysplasia

Back 21

disorderly cell growth

Front 22

Hypertrophy

Back 22

larger cells, not more cells, they just become larger (ie: fa cells expanding)

Front 23

Anaplasia

Back 23

lack of cell differentiation in cancer cells

Front 24

Autonomous growth

Proto-oncogene:

Back 24

a normal gene whose product promotes cell growth

Front 25

Autonomous growth

Oncogene

Back 25

mutated proto-oncogene - causes cell to grow autonomously

Front 26

Autonomous growth

Oncoprotein

Back 26

the product of an oncogene

Front 27

Autonomous growth in normal cells:
How is it different in cancer cells?

Back 27

Normal
growth factor binds to receptor -> activates signal transducing protein -> activates 2nd messager who talks to nuclear transcription factors -> DNA transcription -> cyclins move the cell through the cell cycle -> CELL DIVIDES

CANCER CELLS: CELL DIVIDES ON ITS OWN
- growth factors may be made by cell itself
- receptors overexpressed or always on
- signal transducing proteins may always be on
- nuclear transcription factors may always be expressed
- cyclins may be overactive

Front 28

Example of autonomous growth - RAS gene is a transduction protein, a mutated RAS is always on - therefore what is happening?

Back 28

there are always transducing signals and the cell is always dividing

Front 29

Tumor supressor genes:

what happens when there is a mutation of these genes?

example: RB gene does what?

Back 29

normal genes whose products act as "brakes" on the cell cycle.

you lose the brakes!

RB gene stops cells at G1. A mutant RB is inactive and lets cells pass through G1.

Front 30

Causes of cancer?

Back 30

not a single cause!

hereditary
chemical and environmental
cancer causing viruses
immunologic defects

Front 31

Oncogenesis:

- protocogenes:
- anti-oncogenes:

Back 31

genetic mechanism whereby normal cells are transformed into cancer cells

- protocogenes: growth promoting regulatory genes
- anti-oncogenes: growth inhibiting regulatory genes

Front 32

What is the tumor suppression gene that is most common?

Back 32

p53

altered p53 has in been found in 1/2 human cancers

Front 33

How does p53 work?

Back 33

"guardian of the genome"
If a cells DNA is damaged p53 causes a pause in the cell cycle (via RB) so DNA can be repaired. If DNA damage is irreparable p53 causes cell to die.

Front 34

What suppressor gene has been found to be completely or partially absent in the presence of lung, breast, and colon cancers?

When is this gene particulary subject to mutation?

Back 34

FHIT - Fragile Histidine Triade Protein

Cigarette smoke

Front 35

Carcinogenesis - 3 stages of cancer as a multistage process

Back 35

1) Initiation: DNA alteration or cell change.
2) Tumor Promotion: single mutated -> formation of tumor
3) Tumor Progression: development of malignancy (if tumor suppression genes are mutated growth becomes uncontrollable)

Front 36

ploidy:

Back 36

single sets of chromosomes within a cell

Front 37

How does skin cancer develop?

Back 37

Cells damaged by the sun can die and be replaced by normal cells, but if cells die near a mutated cell then the mutated cell can replicate and fill the area.

Front 38

Successful DNA repair is accomplished by what two genes?

Back 38

FHIT
p53

Front 39

Cancer staging TNM system
T
N
M

Back 39

Tumor - how far the primary tumor has grown locally
Nodes - if the CA has spread to local lymph nodes
Metastasis - if CA has spread to other parts of the body.

A number is given for each of the TNM characteristics. Higher the number the more progressive and invasive

Front 40

- Grading of CA tells you

Back 40

the aggressiveness of the CA

Front 41

Staging tells you what 3 things?

Back 41

Location, degree of metastasis, and size of tumor

Front 42

Why is a health history important to know r/t to cancer?

Back 42

there are hereditary DNA repair defects

Front 43

2 Types of carcinogens

1) Direct reacting agents:
2) Indirect reacting agents:

Back 43

1) direct: do not require activation in the body to become carcinogenic

2) Indirect: PROCARCINOGENS: become carcinogenic only after metabolic conversion

Front 44

IARC (International Agency for Research on Cancer) the most widely used system for classifying carcinogens (part of WHO)

Back 44

the most widely used system for classifying carcinogens (part of WHO)

Groups
1: carcinogenic to humans
2A: probably
2B: possibly
3: unclassifiable as to carcinogenity in humans
4: probably not

Front 45

9 major correlates of cancer

Back 45

- overweight and obesity
- low consumption of fruits and vegtables
- physical inactivity
- smoking
- alcohol use
- Unsafe sex
- Urban air pollution
- use of solid fuels indoors
- contaminated healthcare injections

Front 46

2 highest correlates for cancer death?

Back 46

Tobacco
Diet

Front 47

Nulliparous women and cancer at highest risk for what?

Back 47

nulliparous women > 50 and still menstruating have a high risk for breast cancer

Front 48

Most common common oncovirus (virus that causes a cell to become cancerous)?

Back 48

HPV

Front 49

Epstein-Barr Virus (EBV)

Back 49

causes infectious mononucleosis
associated w/:
-lymphomas in immunosuppressed persons
-nasopharyngeal carcinomas
-Burkitt lymphoma (Africa & New Guinea
- cofactor for Hodgkin disease (30yrs after infection)

3rd world mostly affects children
industrialized nations 50% of the people are affected.

Front 50

In the US 30% of ____ cancers are r/t HBV or HCV.

Back 50

Liver

Front 51

Course of Hep. B & C

Back 51

Hep B:
more likely to cause symptoms, full recovery, small % go on to be carriers, vaccine available

Hep C:
less likely to be symptomatic, chronic infections, more cancer risk, silent epidemic, no vaccine

Front 52

T or F: HIV causes cancer.

Back 52

False - does not appear to DIRECTLY cause cancer

HIV increases a person's risk of getting several types cancer, esp those linked to HHV-8 and HPV.

Front 53

Kaposi's sarcoma HHV-8 virus

Back 53

common in AIDS pts and in transplant recipients; contains 81 genes;

agent co-infecting along with HIV

Incidence:
HIV+ men 25-30%
HIV- women 3-4%
HIV+ hemophiliacs 2-3%

Front 54

Human Adult T-cell Leukemia viruses

HTLV-1:

HTLV-2:

Back 54

HTLV-1: sexually transimitted, endemic to Japan, Carribbean; causes adult T-cell leukemia (Sezary T-cell leuk.)

HTLV-2: T varient of hairy cell leukemia; Native Amerindian pop; seroprevalence is over 50%

Front 55

What bacteria is linked to MALT lymphoma and gastric carcinoma?

Back 55

Helicobacter pylori

overlie the gastric epithelial cells; cause 90% duodenal ulcers; 80% gastric ulcers

cellular and hurmoral immune responses are activated but the bacteria still manage to persist lifelong unless eradicated by antibiotics

Front 56

T or F: Chlamydia trachomatis causes cancer.

Back 56

False

Women who have had a past infection may be at greater risk for cervical cancer, but has not been shown that it causes cancer by itself.
It may work with HPV in some way that promotes cancer risk.

Front 57

External factors that increase risk for cancer

Back 57

-Chemical carcinogenesis
-Physical Agents (radiation, chronic irritation
-Dietary factors
-Immune Function
-Age
-Genetic risk