module D cancer

Created by bernikitty 

Upgrade to
remove ads

normal cells have limited cell division

cell must perform in predictable manner for homeostasis:
-divide, limited cell division
-mitosis for:
-- development of normal tissue
--replace lost or damaged normal tissue
--divide only when body conditions and nutrition are just right

Characteristics of Normal Cells

1. Have limited cell division
2. Undergo apoptosis
3. Show specific morphology
4. Have a small nuclear-cytoplasmic ratio
5. Perform specific differentiated functions
6. Adhere tightly together
7. Are non-migratory
8. Grow in an orderly and well-regulated
9. Are contact inhibited
10. Are euploid

apoptosis

programmed cell death, when DNA is bad, to ensure each organ has adequate # of cells at fxn peak

morphology

distinct and recognizable appearance, size, and shape

small nuclear-cytoplasmic ratio

normal cells have_______________________ nucleus is small compared to rest of cell

Perform specific differentiated functions

normal cells ______________ each has at least 1:
ex. RBC make Hgb to carry O2

adhere tightly together

normal cells ____________ make proteins that protrude from cell surface, allowing binding

Are non-migratory

normal cells are _____________ do not wander from one tissue to another (except RBC, WBC)

normal cells grow in an orderly and well-regulated manner

a.cell cycle
-divide when need for new cells, adequate nutrients, adequate space to divide
b. mitotic cell division
-division occurs in well-recognized pattern, cell cycle
-mitotic cell division makes one cell divide into 2 cells, cells are identical to each other and original cell
-cell cycle steps are tightly controlled, balance b/w protein promoting (cyclins) cell division and proteins (suppressor gene products) that inhibit

normal cells are contact inhibited

(a.k.a. density-dependent inhibition of cell growth), divides only when some of surface when not in direct contact w/another cell

cell cycle

divide when need for new cells, adequate nutrients, adequate space to divide

euploid

have 23 pairs of chromosomes

mitotic cell division

-division occurs in well-recognized pattern, cell cycle
-makes one cell divide into 2 cells, cells are identical to each other and original cell
-cell cycle steps are tightly controlled, balance b/w protein promoting (cyclins) cell division and proteins (suppressor gene products) that inhibit

Biology of Abnormal Cells

Characteristics of Benign Tumor Cells
-when cell growth or fxn is changed, cells are considered abnormal
-normal cells growing at wrong place or at wrong time
-moles, fibroids, endometriosis, skin tags

Characteristics of Benign Tumor Cells

1.Have continuous or inappropriate cell growth
2.Show specific morphology
-morphology: look like tissues they come from, retain morphology of parent cells
3.Have a small nuclear-cytoplasmic ratio
-have small nuclear-cytoplasmic ration
4.Perform specific differentiated functions
-perform differentiated fxns: perform same as parent cells
5.Adhere tightly together
-adhere tightly together, make fibrinectin to bind tightly
6.Are non migratory
7.Grow in an orderly manner
-rate of growth is normal, do not invade
8.Are euploid: have 23 pairs of chromosomes

Characteristics of Cancer Cells

1.Have rapid or continuous cell division, nearly continuously
2.Do not respond to signals for apoptosis
3.Show anaplastic morphology
w/o shape or differentiation
-usually small and round, esp the more malignant
4.Have a large nuclear-cytoplasmic ratio nucleus is larger
5. Lose some or all differentiated functions
-lose some or all of fxns, lose appearance of parent cell
6. Adhere loosely together
7.Are able to migrate
-migratory b/c not bound together
-many enzymes on cell surfaces, slip thru blood vessels and tissues
-able to spread from main tumor site to other body sites
8.Grow by invasion
-invasion and persistent growth make untx cancer cells deadly
9.Are not contact inhibited
10.Are aneuploid
-aneuploid: lose or gain chromosomes, can have more or less than 23 pairs

cancer cells

-abnormal, no useful function, harmful to normal body tissues

anaplastic morphology

w/o shape or differentiation
-usually small and round, esp the more malignant

cancer cells have a large nuclear-cytoplasmic ratio

nucleus is larger

Lose some or all differentiated functions

lose appearance of parent cell

aneuploid:

lose or gain chromosomes, can have more or less than 23 pairs

Cancer Development

1. Malignant transformation (the process of changing a normal cell into a cancer cell) occurs through the following steps:
a. initiation
b. promotion
c. progression

Carcinogenesis / Oncogenesis

-carcinogens: chg activity of a cell's genes so that cells become cancer cells:
--chemicals, physical, viruses
- --anything that can penetrate cell, can damage DNA and genes, can turn on genes that s/b suppressed, can turn of normal genes

Malignant transformation

(the process of changing a normal cell into a cancer cell) occurs through the following steps:
a. initiation
b. promotion
c. progression

initiation:

irreversible event that can lead to cancer development provided does not interfere w/cell's ability to divide

promotion:

cell can become cancer cell if cellular chgs during initiation are enhanced by promotion,

promoters

are substances that enhance growth of initiated cancer cells, may be hormones, drugs, chemicals

latency period:

time b/w initiation and development of overt tumor can range from months to years

progression:

after detectable tumor is formed (1cm) other events must occur:
--must develop own blood
--metastasis occurs when cancer cells move from the primary location by breaking off from the original group and establishing remote colonies.

tumor angiogenesis factor

(TAF) triggers capillaries and other blood vessels in area to grow new branches into tumor, ensure tumors continued nourishment

primary tumor:

original tumor, identified by tissue it came from (parent tissue)

metastasis

occurs when cancer cells move from the primary location by breaking off from the original group and establishing remote colonies. It occurs through many steps:
-i. extension into surrounding tissues
-ii. blood vessel penetration
-iii. release of tumor cells
-iv. invasion
-v. local seeding
-vi. blood-borne metastasis
-vii. lymphatic spread

extension into surrounding tissues:

secretion of enzymes that open up areas of surrounding tissue; pressure created as tumor increases in size can force cells to invade new territory;

blood vessel penetration

blood vessels can have large pores that allow tumor cells to enter blood and circulate

release of tumor cells

release of tumor cells b/c they are loosely held together

invasion:

circulate thru blood and enter tissues at remote sites, secondary tumors

local seeding:

shedding of cancer cells in local area of primary tumor

blood-borne metastasis:

released into blood stream (most common); clumps can become trapped in capillaries and damage wall and allow spread to surrounding tissue

lymphatic spread:

related to the number structure, and location of lymphatic nodes and vessels; primary sites rich in lymphatics have earlier spread

cancer: Diagnosis

-Xray, CT, MRI, ultrasonography
-only microscopic histologic exam reveals type of cell and difference from parent tissue
-tissue acquired thru biopsy, pap smear, sputum, lymph nodes

Grading

evaluates amt of differentiation, maturity, and estimates rate of growth based on mitotic rate
-most differentiated are least malignant (grade I)
-least differentiated are most malignant (grade IV)

Staging:

used to classify solid tumor and refers to relative size of tumor and extent of dz

Cytologic Examination

Specimens are collected by three basic methods:
a. exfoliation from an epithelial surface
b. aspiration of fluid from body cavities or blood
c. needle aspiration of solid tumors
d. Tumor Markers
-protein molecule that is detectable in serum or body fluids
-used as biochemical indicator of presence of malignancy
-small amts are found in normal body tissue or benign
-high amts are suspicious, follow up dx studies (PSA)
-PSA for men over 40, pap smears for women (not completely reliable)

exfoliation from an epithelial surface

(pap smear, bronchial washings)

aspiration of fluid from body cavities or blood

(WBCs to eval hematopoetic, CSF, pleural fluid)

needle aspiration of solid tumors

(breast, lung, prostate)

Tumor Markers

-protein molecule that is detectable in serum or body fluids
-used as biochemical indicator of presence of malignancy
-small amts are found in normal body tissue or benign
-high amts are suspicious, follow up dx studies (PSA)
-PSA for men over 40, pap smears for women (not completely reliable)

Oncologic imaging:

-Xray: least expensive, least invasib/c physical assessment cannot detect cancer b4 risk for metastasis, important in early dx
1. X-ray imaging
2. Computed tomography (CT)
3. Magnetic resonance imaging (MRI)
4. Ultrasonography
5.Nuclear imaging

early dx

physical assessment cannot detect cancer b4 risk for metastasis, important in _________.

X-ray imaging

least expensive, least invasive, method of choice (breast, lung, bone) to identify chgs, does not reveal lung tumors until size is threat to pt

Computed tomography (CT)

advance effectiveness of traditional xray by applying computers and mathematics, allows visualization of cross sections of anatomy, reveals subtle diff in tissue density and provide greater accuracy in tumor dx, especially useful in lymph node involvement

Magnetic resonance imaging (MRI)

involves computerized mathematical technology, pt placed in strong magnetic field, radio waves directed at pt, signals are transmitted based on tissue
characteristics that are analyzed and projected by computer, PET scans and SPECT create visual images by measuring electrical impulses from body structures

Ultrasonography:

safe and non-invasive, measures sound waves as bounce off body structures, gives image of normal anatomy or abnormalities, also used to guide needle biopsies, useful for detecting masses in dense breast tissues

nuclear imaging:

use specific radio isotypes w/special scanners, invasive safe dx method for identifying tumors, used to check for bone or other organ metastasis,

Direct Visualization

-invasive, but no use of radiography:
1.Sigmoidoscopy
2.Cytoscopy
3.Endoscopy
4.Bronchoscopy

Direct Visualization: sigmoidoscopy:

colon with flexible, fiber optic scope

Direct Visualization:cystoscopy:

viewing urethra and bladder

Direct Visualization: endoscopy:

viewing upper gi tract

Direct Visualization: bronchoscopy:

viewing tracheal bronchial tree
-suction, cauterize, treatment can be done as well

cancer: Laboratory Tests

-most test are used to rule out nutritional disorders or noncancerous conditions
-used in conjuction w/other tests to confirm or validate

cancer: Laboratory Tests: Liver:

elevated ALT, AST, LDN

cancer: Laboratory Tests: Protein tumor markers:

PSA, CEA

cancer: Laboratory Tests: liver metastasis:

a.alanine aminotransferase (ALT)
b.asparate aminotransferase (AST)
c.lactic dehydrogenase (LDH)

cancer: Laboratory Tests: Protein tumor markers

a. prostatic-specific antigen (PSA)
b. carcinoembryonic antigen (CEA)
V. Classification of Cancer

Histologic Analysis Classification

-appearance of cell and histological are evaluated

Histologic Analysis Classification: Grade I

(mild dysplasia): differ slightly from normal cells, well differentiated

Histologic Analysis Classification: Grade II:

cells more abnormal, moderately differentiated

Histologic Analysis Classification: Grade III:

cells very abnormal, poorly differentiated

Histologic Analysis Classification: Grade IV:

immature, primitive, undifferentiated, cell of origin difficult to determine

For many tumor cells, four grades are used:

Grade I (mild dysplasia)
Grade 11 (moderate dysplasia)
Grade III (severe dysplasia)
Grade IV (anaplasia)

Extent of Disease Classification

-extend and spread of dz is staging
-based on description of extent of dz rather than cell appearance

clinical staging

-0: carcinoma in situ, in normal place w/o invasion
-1: tumor limited to tissue of origin, localized growth
-2: limited local spread
-3: extensive local and regional spread
-4: metastasis

a. clinical staging

i. stage 0
ii. stage I
iii. stage II
iv. stage III
v. stage IV

TNM Classification System

is a standardization of the clinical staging of cancer used to determine the extent of the disease process of cancer

TNM: according to three parameters:

-tumor size (1-4)
-degree of regional spread to lymph nodes
-metastasis
-staging can be done initially or at intervals, to estab dx and determine tx plan, extent of dz process

surgical staging

i. tumor size (T)
ii. degree of regional spread to the lymph nodes (N)
iii metastasis (M)
c. surgical staging
d. carcinoma in situ

carcinoma in situ:

commonly used term, lesion w/all histological features of cancer w/o invasion, left untx will invade

Cancer Etiology and Genetic Risk: Oncogene Activation

Activation of proto-oncogenesis appears to be the same, regardless of the specific cause, in the mechanism of carcinogenesis. These proto-oncogenes were the genes that directed normal early embryonic development. At about 8 days after conception, these genes should normally be controlled forever. They are turned off, controlled or suppressed by "suppressor genes" that can act directly at the DNA level, preventing the proto-oncogene from being over-expressed. Another way that the suppressor genes work is by preventing cells from dividing, or maintaining control over the cell cycle.

Cancer Etiology and Genetic Risk: Oncogene Activation: Carcinogen exposure

-when normal cell is exposed, proto-oncogenes are over-expressed and turned on
oncogenes:
--can cause cells to change from normal to cancer cell
--gene in a virus that has the ability to induce a cell to become malignant
--part of every cell's normal makeup
--only a problem if activated after embryonic development
--Oncogenes

External Factors Causing Cancer

80% of cancers in north America are result of environmental or external factors:
1. Types of environmental, or external, carcinogens:
-a. chemical carcinogens
-b. physical carcinogenesis
-c. viral carcinogenesis
2. Dietary factors related to cancer development

Types of environmental, or external, carcinogens:

a. chemical carcinogens
b. physical carcinogenesis
c. viral carcinogenesis

chemical carcinogens

tobacco and alcohol appear to be mildly carcinogenic, however, can act as co- carcinogens and enhance activity (30%)

tobacco

-is single most important source of preventable carcinogens
-use both initiates and promotes cancer

tobacco and alcohol

co-carcinogens

physical carcinogenesis

-radiation
-chronic irritation
-ionizing
-ultraviolet (UV)

physical carcinogenesis: radiation:

ionizing and UV; ionizing radiation is found in rocks and soil, xrays; UV is type of solar radiation, tanning beds, UV do not penetrate as deeply as other, but can cause irritation
-ionizing
-ultraviolet (UV)

physical carcinogenesis: chronic irritation:

incidence of skin cancer is higher in people w/burn scars, chronically irritated tissues undergo frequent cell division and are at increased risk for spontaneous DNA mutation

physical carcinogenesis: viral carcinogenesis

-many viruses are suspected
-viruses can infect and break DNA chain

physical carcinogenesis: viral carcinogenesis: oncoviruses

(HBV, HPV, Epstein Barr can cause Birkett's lymphoma)

Dietary factors related to cancer development

-low fiber intake
-high intake of red meats and animal fats
-different preservatives, sweeteners, dyes

Personal Factors and Cancer Development:

A. Immune Function
B. Age
C. Genetic Risk

Personal Factors and Cancer Development: Immune Function

-immune system normally protects body from non-self cells, including cancer cells
-cell-mediated immunity protects from cancer (NK and helper T)
-organ transplant recipients take immunosuppressive drugs and therefore have higher incidences of cancer
-clients w/AIDS have an 80% chance cancer
1. Cell-mediated immunity
a. natural killer (NK) and helper T-cells
2. Organ transplant recipients

Personal Factors and Cancer Development: Age

Older adults must be aware of and report symptoms such as the seven warning signs of cancer:
1 change in bowel or bladder habits
2 a sore that does not heal
3 unusual bleeding or d/c
4 thickening or lump in breast or elsewhere
5 indigestion oe difficulty swallowing
6 obvious chg in wart or mole
7 nagging cough or hoarseness

Personal Factors and Cancer Development: Genetic Risk

-proto-oncogene must be overexpressed to an oncogene for cancer to occur
-in some people, sequence of proto-oncogene is different and it may allow some people to be predisposed

seven warning signs of cancer:

1) change in bowel or bladder habits
2) a sore that does not heal
3) unusual bleeding or d/c
4) thickening or lump in breast or elsewhere
5) indigestion oe difficulty swallowing
6) obvious chg in wart or mole
7) nagging cough or hoarseness

Cancer prevention activities can focus on:

Primary prevention or Secondary prevention

cancer: Primary prevention

-prevent actual occurrence of cancer
-skin protection during sun exposre, avoid tobacco, eliminate asbestos
-stop drinking w/smoking, chg unhealthy diets (low in fiber, high in fats)
-removing moles to prevent conversion, removing colon polyps
-mega doeses of vit C, aspirin

cancer: Secondary prevention

-use of screening strategies to detect cancer early
-regular screening: mammogram 40yo, breast self exam 40yo, colonoscopy 50yo, FOB test 50yo, PSA tests, DRE 50yo,
-do not reduce incidence but can reduce deaths

Primary prevention strategies

a. avoidance of known or potential carcinogens
b. modification of associated factors
c. removal of "at risk" tissues
d. chemo-prevention

Secondary prevention strategies

a. screening programs
B. Public education related to the prevention and detection of cancer:
-goal of public education is to motivate learner to change the pattern of behavior as necessary to achieve and maintain optimal state of health

Please allow access to your computer’s microphone to use Voice Recording.

Having trouble? Click here for help.

We can’t access your microphone!

Click the icon above to update your browser permissions above and try again

Example:

Reload the page to try again!

Reload

Press Cmd-0 to reset your zoom

Press Ctrl-0 to reset your zoom

It looks like your browser might be zoomed in or out. Your browser needs to be zoomed to a normal size to record audio.

Please upgrade Flash or install Chrome
to use Voice Recording.

For more help, see our troubleshooting page.

Your microphone is muted

For help fixing this issue, see this FAQ.

Star this term

You can study starred terms together

NEW! Voice Recording

Create Set