Transcript cancer
CANCER
A. THE NATURE OF
CANCER
def - sudden uncontrolled
growth of cells
1. FEEDS ON THE BODY’S
NUTRIENTS
RESULTS FROM
ANGIOGENESIS FORMATION OF NEW
BLOOD VESSELS
2. DEPLETES BODY’S
SUPPLY OF NUTRIENTS
AMINO
ACIDS, GLUCOSE,
FATTY ACIDS
3. BLOCKS PASSAGEWAY FOR
MATERIAL FLOW
4. DISRUPTS, OR PREVENTS
PROTEIN SYNTHESIS
5. SECRETE PROTEASES
LEADS
TO METASTASIS
6. BLOCKS
DIFFERENTIATION
CELLS
PRODUCED LACK
SPECIALIZATION, THEIR
FUNCTION IS THEREFORE
INHIBITED
7. NO CONTACT INHIBITION
LEADS
TO METASTASIS
CELLS MOVE OVER UNDER
AND THROUGH
NEIGHBORING CELLS
8. LACK ANCHORAGE
DEPENDENCY
CELLS
FLOAT FREELY
CELLS DO NOT REMAIN AT
ORIGINAL SITE
LEADS TO METASTASIS
9. GENETIC INSTABILITY
HIGH
MUTATION RATE
LEADS TO DRUG
RESISTANCE
CONTAIN GENETIC
ABBERRATIONS
10. GROWTH FACTOR
REQUIREMENTS ARE LOW
RECEPTORS
TO REGULATE
GROWTH MALFUNCTION
IT DOESN’T REQUIRE MUCH
TO INITIATE GROWTH
B. POSSIBLE CONTRIBUTING
FACTORS
1.
GENETIC PREDISPOSITION
2. CARCINOGENS
3. DIET
4. RADIATION
5. VIRUSES
C. MOLECULAR LEVEL
ONCOGENES – GENES THAT
TRIGGER RAPID CELL DIVISION
(GAS PEDAL)
FORM WHEN PROTO-ONCOGENES
MUTATE TO FORM ONCOGENES
1.
discovery
discovered
because of a viral link
to some cancers and also from the
ability to transfer genes from
cancer cells to normal cells
resulting in cancerous growth in
the previously normal cells. THIS
IS KNOWN AS
TRANSFORMATION
2. TUMOR SUPPRESSOR
GENES
GENES
THAT SUPPRESS CELL
GROWTH, KEEP IT IN CHECK
discovery from
the fusion of a normal cell
with a cancer cell resulting in no
cancer activity
ex. - retinoblastoma - arises from a
deletion of a gene on chromosome
#13
p53 gene
tumor
suppressor gene
found on chromosome #17
plays a role in lung, breast,
colon/rectal cancers some
leukemias and lymphomas - about
1 out of 3 cancers
3. DNA REPAIR GENES
OVER
130 HAVE BEEN IDENTIFIED
MAY BE INVOLVED IN MANY KINDS
OF CANCERS
XERODERMA PIGMENTOSUM
E. RESULTS
1.
GROWTH SURROUNDED BY
A MEMBRANE
2. ANGIOGENESIS
3. ENZYMES RELEASED BY
CANCER CELLS DISSOLVE
THE MEMBRANE
4. CANCER METASTASIZES
5.
CANCEROUS GROWTHS
SPRING UP ELSEWHERE
F. HOW CANCER ELUDES
THE IMMUNE SYSTEM
1.
CANCER CELLS ARE SELF
CELLS, SOMETIMES THE
CHANGE IN SURFACE
PROTEINS IS SO SLIGHT THAT
IT GOES UNNOTICED
2.
THEY CAN EMIT DECOY
ANTIGENS INTO THE
BLOODSTREAM IN HIGH
NUMBERS, AS ANTIBODY
BINDS TO DECOYS, TUMOR
GOES UNNOTICED
3.
NON COMPLEMENT
BINDING ANTIBODIES
SURROUND BUT DO NOT
HARM THE TUMOR
4.
PIECE OF TUMOR BREAKS
OFF - CLUMP IS DESTROYED,
IMMUNE SYSTEM’s
RESPONSE FOCUSED ON THE
CLUMP, TUMOR REMAINS - A
STATE OF SUPPRESSION
OCCURS
5.
ANTI-ANTIBODIES SHUT
DOWN AN ATTACK, ALONG
WITH T SUPPRESSOR CELLS
G. PREVENTION
1.
HABITS
smoking
excessive alcohol consumption
excessive exposure to the sun
diet (low fat, high fiber, low in
pickled, smoked, cured foods
2. POSSIBLE POSITIVE
ACTIONS
intake
of vitamins A, C, D,E
beta carotene
calcium
avoid exposure to carcinogens,
radiation, sunlight
H. WARNING SIGNS
CHANGE
IN
BOWEL/BLADDER HABITS
A SORE THAT DOES NOT
HEAL
UNUSUAL BLEEDING OR
DISCHARGE
Thickening
or lump in breast or
elsewhere
Indigestion or difficulty in
swallowing
Obvious change in wart or mole
Nagging cough or hoarseness
I. EARLY
DETECTION/SCREENING
PAP
SMEAR - cervical carcinoma
Breast/testicular self exam
Prostate/ colon-rectal exams
Mammography
Annual exams
Ames Test – for carcinogenicity
SOME
CANCERS CANNOT
BE OR ARE NOW
DIFFICULT TO DETECT AT
EARLY STAGES –
ESPECIALLY LUNG
CANCERS
J. TREATMENTS
1.
SURGERY
2. RADIATION
3. CHEMOTHERAPY
4. IMMUNOTHERAPY-active – ex
cancer vaccines and passive -ex
monoclonal antibodies
PROTON THERAPIES – easier
to aim, cancer cells poor at repair
6. ANGIOSTATIC DRUGS
7. GENE THERAPY
8. BONE MARROW
TRANSPLANTATION
9. HORMONE THERAPY –
tamoxifen to block estrogen
receptors in breast cancer
5.
10.
COMBINATION THERAPIES
11. HIGH INTENSITY
THERAPIES
12. PHOTODYNAMIC
THERAPY – photosensitizing
agent injected, remains in cancer cells
longer, 2-3 d later exposed to light
13. TARGETED THERAPIES
- Enzyme inhibitors
- Apoptosis inducing drugs
- gleevec
FUTURE?
GENE
THERAPY? PROBLEM OF
DELIVERY
MORE TARGETED
APPROACHES
CLASSIFY CANCER
ACCORDING TO THE
MUTATION, NOT THE
LOCATION
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