1. Biology is the only subject in
which mul3plica3on is the same
thing as division…

2. A Karyotype is an Arranged Picture of Chromosomes At Their
Most Condensed State
A normal
human
karyotype
Note that almost all chromosomes come in homologous pairs.
Boy or
girl?

4. DNA Chemistry
Looks like snot to me!

5. Chromosome Structure
Single DNA strand
+ proteins
Chromosome arm
Centromere
Chromosome arm

6. Chromosome Structure
Two identical
chromosomes Single DNA strand
+ proteins
Chromosome arm
Centromere
Chromosome arm

7. Chromosome Structure
Two identical
chromosomes Single DNA strand
+ proteins
Chromosome arm
Centromere
Chromosome arm
Before duplication

8. Chromosome Structure
Two identical
chromosomes Single DNA strand
+ proteins
Chromosome arm
Centromere
Chromosome arm
Before duplication After duplication

9. Mutations

10. Mutations
 Point mutations

11. Mutations
 Point mutations
 single base change

12. Mutations
 Point mutations
 single base change
 base-pair
substitution

13. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation

14. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change

15. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code

16. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code
 missense

17. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code
 missense
 change amino acid

18. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code
 missense
 change amino acid
 nonsense

19. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code
 missense
 change amino acid
 nonsense
 change to stop codon

20. Mutations
 Point mutations
 single base change
 base-pair
substitution
 silent mutation
 no amino acid change
 redundancy in code
 missense
 change amino acid
 nonsense
 change to stop codon
When do mutations
affect the next
generation?

21. Point mutation leads to Sickle cell anemia

22. Point mutation leads to Sickle cell anemia
Missense!

23. Sickle cell anemia
 Primarily Africans
 recessive inheritance pattern
 strikes 1 out of 400 African Americans

24. Sickle cell anemia
 Primarily Africans
 recessive inheritance pattern
 strikes 1 out of 400 African Americans
hydrophilic
amino acid

25. Sickle cell anemia
 Primarily Africans
 recessive inheritance pattern
 strikes 1 out of 400 African Americans
hydrophilic hydrophobic
amino acid amino acid

26. Chloride channel
transports chloride through
Effect on Lungs protein channel out of cell
normal lungs Osmotic effects: H2O follows Cl-
airway
Cl- Cl- channel
H 2O
cells lining
lungs
cystic fibrosis
Cl-
H 2O
bacteria & mucus build up
thickened mucus
hard to secrete
mucus secreting glands

27. Deletion leads to Cystic fibrosis

28. Deletion leads to Cystic fibrosis

29. Deletion leads to Cystic fibrosis
delta F508

30. Deletion leads to Cystic fibrosis
delta F508
loss of one
amino acid

31. Chromosomal abnormalities

32. Chromosomal abnormalities
 Incorrect number of chromosomes

33. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction

34. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis

35. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis
 breakage of chromosomes

36. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis
 breakage of chromosomes
 deletion

37. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis
 breakage of chromosomes
 deletion
 duplication

38. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis
 breakage of chromosomes
 deletion
 duplication
 inversion

39. Chromosomal abnormalities
 Incorrect number of chromosomes
 nondisjunction
 chromosomes don’t separate properly
during meiosis
 breakage of chromosomes
 deletion
 duplication
 inversion
 translocation

40. Nondisjunction
2n

41. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
2n

42. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
2n

43. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
2n

44. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

45. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

46. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

47. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n n
n

48. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

49. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

50. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

51. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n

52. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n n-1

53. Nondisjunction
 Problems with meiotic spindle cause errors in
daughter cells
 homologous chromosomes do not separate
properly during Meiosis 1
 sister chromatids fail to separate during Meiosis 2
 too many or too few chromosomes
2n n-1
n+1

54. Down syndrome

55. Down syndrome
 Trisomy 21

56. Down syndrome
 Trisomy 21
 3 copies of chromosome 21

57. Down syndrome
 Trisomy 21
 3 copies of chromosome 21
 1 in 700 children born in U.S.

58. Down syndrome
 Trisomy 21
 3 copies of chromosome 21
 1 in 700 children born in U.S.
 Chromosome 21 is the
smallest human chromosome

59. Down syndrome
 Trisomy 21
 3 copies of chromosome 21
 1 in 700 children born in U.S.
 Chromosome 21 is the
smallest human chromosome
 but still severe effects

60. Down syndrome
 Trisomy 21
 3 copies of chromosome 21
 1 in 700 children born in U.S.
 Chromosome 21 is the
smallest human chromosome
 but still severe effects
 Frequency of Down
syndrome correlates
with the age of the mother

61. Down syndrome & age of mother
Incidence of
Mother’s age Down Syndrome
Under 30 <1 in 1000
30 1 in 900
35 1 in 400
36 1 in 300
37 1 in 230
38 1 in 180
39 1 in 135 Rate of miscarriage due to
40 1 in 105 amniocentesis:
 1970s data
42 1 in 60 0.5%, or 1 in 200 pregnancies
44 1 in 35
 2006 data
46 1 in 20 <0.1%, or 1 in 1600 pregnancies
48 1 in 16
49 1 in 12

62. Genetic testing

63. Genetic testing
 Amniocentesis in 2nd trimester

64. Genetic testing
 Amniocentesis in 2nd trimester
 sample of embryo cells

65. Genetic testing
 Amniocentesis in 2nd trimester
 sample of embryo cells
 stain & photograph chromosomes

66. Genetic testing
 Amniocentesis in 2nd trimester
 sample of embryo cells
 stain & photograph chromosomes
 Analysis of karyotype

67. Genetic testing
 Amniocentesis in 2nd trimester
 sample of embryo cells
 stain & photograph chromosomes
 Analysis of karyotype

68. Klinefelter’s syndrome

69. Klinefelter’s syndrome
 XXY male

70. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births

71. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile

72. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics

73. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development

74. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development
 lack of facial hair

75. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development
 lack of facial hair
 tall

76. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development
 lack of facial hair
 tall
 normal intelligence

77. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development
 lack of facial hair
 tall
 normal intelligence

78. Klinefelter’s syndrome
 XXY male
 one in every 2000 live births
 have male sex organs, but
are sterile
 feminine characteristics
 some breast development
 lack of facial hair
 tall
 normal intelligence

79. Jacob’s syndrome male

80. Jacob’s syndrome male
 XYY Males

81. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births

82. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome

83. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average

84. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active

85. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active
 normal intelligence, slight learning disabilities

86. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active
 normal intelligence, slight learning disabilities
 delayed emotional maturity

87. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active
 normal intelligence, slight learning disabilities
 delayed emotional maturity
 normal sexual development

88. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active
 normal intelligence, slight learning disabilities
 delayed emotional maturity
 normal sexual development

89. Jacob’s syndrome male
 XYY Males
 1 in 1000 live male
births
 extra Y chromosome
 slightly taller than
average
 more active
 normal intelligence, slight learning disabilities
 delayed emotional maturity
 normal sexual development

90. Trisomy X

91. Trisomy X
 XXX

92. Trisomy X
 XXX
 1 in every 2000 live births

93. Trisomy X
 XXX
 1 in every 2000 live births
 produces healthy females

94. Trisomy X
 XXX
 1 in every 2000 live births
 produces healthy females
 Why?

95. Trisomy X
 XXX
 1 in every 2000 live births
 produces healthy females
 Why?
 Barr bodies

96. Trisomy X
 XXX
 1 in every 2000 live births
 produces healthy females
 Why?
 Barr bodies
 all but one X chromosome is inactivated

97. Turner syndrome

98. Turner syndrome
 Monosomy X or X0

99. Turner syndrome
 Monosomy X or X0
 1 in every 5000 births

100. Turner syndrome
 Monosomy X or X0
 1 in every 5000 births
 varied degree of effects

101. Turner syndrome
 Monosomy X or X0
 1 in every 5000 births
 varied degree of effects
 webbed neck

102. Turner syndrome
 Monosomy X or X0
 1 in every 5000 births
 varied degree of effects
 webbed neck
 short stature

103. Turner syndrome
 Monosomy X or X0
 1 in every 5000 births
 varied degree of effects
 webbed neck
 short stature
 sterile

104. Changes in chromosome structure

105. Changes in chromosome structure
replication
error of

106. Changes in chromosome structure
 deletion
replication
error of

107. Changes in chromosome structure
 deletion
replication
error of

108. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment

109. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication

110. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication

111. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment

112. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
crossing over
error of

113. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
error of

114. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
error of

115. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
 reverses a segment
error of

116. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
 reverses a segment
error of

117. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
 reverses a segment
error of
 translocation

118. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
 reverses a segment
error of
 translocation

119. Changes in chromosome structure
 deletion
replication
error of
 loss of a chromosomal segment
 duplication
 repeat a segment
 inversion
crossing over
 reverses a segment
error of
 translocation
 move segment from one chromosome
to another

120. Mother cell
Nucleus with un‐ Stages Of Mitosis
condensed
chromosomes
Equator of
Interphase the cell
Poles of
Disappearing Two
the cell
nuclear Prophase daughter
membrane Mito3c cells
spindle Metaphase
Anaphase
I.P.M.A.T.
Telophase

121. GeIng it right
chromosomes (stained orange)
in kangaroo rat epithelial cell
→notice cytoskeleton fibers

122. GeIng it right
 What is passed
on to daughter
cells?
 exact copy of
gene3c material
= DNA
 mitosis
chromosomes (stained orange)
in kangaroo rat epithelial cell
→notice cytoskeleton fibers

123. Interphase

124. Interphase
 90% of cell life cycle
 cell doing its “everyday job”
 produce RNA, synthesize proteins/enzymes
 prepares for duplica3on if triggered

125. Interphase
 90% of cell life cycle
 cell doing its “everyday job”
 produce RNA, synthesize proteins/enzymes
 prepares for duplica3on if triggered
I’m working here!

126. Interphase
 90% of cell life cycle
 cell doing its “everyday job”
 produce RNA, synthesize proteins/enzymes
 prepares for duplica3on if triggered
I’m working here!
Time to divide
& multiply!

127. Mito3c Chromosome
 Duplicated chromosome

128. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds

129. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres

130. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA

131. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous
chromosomes

132. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous
chromosomes
homologous = “same information”

133. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous
chromosomes
single-stranded homologous = “same information”

134. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous homologous
chromosomes chromosomes
single-stranded homologous = “same information”

135. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous homologous
chromosomes chromosomes
single-stranded homologous = “same information”
double-stranded

136. Mito3c Chromosome
 Duplicated chromosome
 2 sister chroma8ds
 narrow at centromeres
 contain iden8cal
copies of original DNA
homologous homologous
chromosomes chromosomes
sister chromatids
single-stranded homologous = “same information”
double-stranded

137. Coordina3on of
cell division
 A mul3cellular
organism needs to
coordinate cell
division across
different 3ssues &
organs

138. Checkpoint control system

139. Checkpoint control system
 Checkpoints
 cell cycle controlled by STOP & GO chemical
signals at cri3cal points
 signals indicate if key cellular
processes have been
completed correctly

140. Ac3va3on of cell division

141. Ac3va3on of cell division
 How do cells know when to divide?
 cell communica3on signals
 chemical signals in cytoplasm give cue
 signals usually mean proteins
 ac3vators
 inhibitors

142. “Go‐ahead” signals
 Protein signals that promote cell growth &
division
 internal signals
 “promo3ng factors”
 external signals
 “growth factors”

143. “Go‐ahead” signals
 Protein signals that promote cell growth &
division
 internal signals
 “promo3ng factors”
 external signals
 “growth factors”
 Primary mechanism of control
 phosphoryla3on
 kinase enzymes
 either ac3vates or inac3vates cell signals

145. Growth Factors and Cancer

146. Growth Factors and Cancer
 Growth factors can create cancers
 proto‐oncogenes
 normally ac3vates cell division
 growth factor genes
 become oncogenes (cancer‐causing) when mutated
 if switched “ON” can cause cancer
 example: RAS (ac3vates cyclins)
 tumor‐suppressor genes
 normally inhibits cell division
 if switched “OFF” can cause cancer
 example: p53

147. Problems with cell division
Normal Cell

148. Problems with cell division
Normal Cell
Obeys strict rules
Divides only when told to
Dies rather than misbehaving
Stays close to home

149. Problems with cell division
Normal Cell
Obeys strict rules
Divides only when told to
Dies rather than misbehaving
Stays close to home
Careful with chromosomes

150. Problems with cell division
muta8ons
Normal Cell
Obeys strict rules
Divides only when told to
Dies rather than misbehaving
Stays close to home
Careful with chromosomes

151. Problems with cell division
muta8ons
Normal Cell
Obeys strict rules
Divides only when told to
Dies rather than misbehaving
Stays close to home
Careful with chromosomes

152. Problems with cell division
muta8ons
Normal Cell Cancer Cell
Obeys strict rules Disobeys rules
Divides only when told to Divides at will
Dies rather than misbehaving Bad behavior doesn’t kill
Stays close to home Wanders aimlessly
Careful with chromosomes

153. Problems with cell division
muta8ons
Normal Cell Cancer Cell
Obeys strict rules Disobeys rules
Divides only when told to Divides at will
Dies rather than misbehaving Bad behavior doesn’t kill
Stays close to home Wanders aimlessly
Careful with chromosomes Careless with chromosomes

154. p53 — master regulator gene
p53 allows cells
with repaired
DNA to divide.
p53
protein DNA repair enzyme
p53
protein
Step 1 Step 2 Step 3
DNA damage is caused Cell division stops, and p53 triggers the destruction
by heat, radiation, or p53 triggers enzymes to of cells damaged beyond repair.
chemicals. repair damaged region.
abnormal
p53 protein
cancer
Step 1 Step 2 cell
DNA damage is The p53 protein fails to stop Step 3
caused by heat, cell division and repair DNA. Damaged cells continue to divide.
radiation, or Cell divides without repair to
damaged DNA. If other damage accumulates, the
chemicals. cell can turn cancerous.

155. p53 — master regulator gene
NORMAL p53
p53 allows cells
with repaired
DNA to divide.
p53
protein DNA repair enzyme
p53
protein
Step 1 Step 2 Step 3
DNA damage is caused Cell division stops, and p53 triggers the destruction
by heat, radiation, or p53 triggers enzymes to of cells damaged beyond repair.
chemicals. repair damaged region.
abnormal
p53 protein
cancer
Step 1 Step 2 cell
DNA damage is The p53 protein fails to stop Step 3
caused by heat, cell division and repair DNA. Damaged cells continue to divide.
radiation, or Cell divides without repair to
damaged DNA. If other damage accumulates, the
chemicals. cell can turn cancerous.

156. p53 — master regulator gene
NORMAL p53
p53 allows cells
with repaired
DNA to divide.
p53
protein DNA repair enzyme
p53
protein
Step 1 Step 2 Step 3
DNA damage is caused Cell division stops, and p53 triggers the destruction
by heat, radiation, or p53 triggers enzymes to of cells damaged beyond repair.
chemicals. repair damaged region.
ABNORMAL p53
abnormal
p53 protein
cancer
Step 1 Step 2 cell
DNA damage is The p53 protein fails to stop Step 3
caused by heat, cell division and repair DNA. Damaged cells continue to divide.
radiation, or Cell divides without repair to
damaged DNA. If other damage accumulates, the
chemicals. cell can turn cancerous.

157. Development of Cancer

158. Development of Cancer
 Cancer develops only aber a cell experiences ~6 key
muta3ons (“hits”)
 unlimited growth
 turn on growth promoter genes
 ignore checkpoints
 turn off tumor suppressor genes (p53)
 escape apoptosis
It’s like an
 turn off suicide genes
out-of-control
 immortality = unlimited divisions car with many
 turn on chromosome maintenance genes systems failing!
 promotes blood vessel growth
 turn on blood vessel growth genes
 overcome anchor & density dependence
 turn off touch‐sensor gene

159. Tumors

160. Tumors
 Mass of abnormal cells
 Benign tumor
 abnormal cells remain at original site as a lump
 p53 has halted cell divisions
 most do not cause serious problems &
can be removed by surgery
 Malignant tumor
 cells leave original site
 lose aeachment to nearby cells
 carried by blood & lymph system to other 3ssues
 start more tumors = metastasis
 impair func3ons of organs throughout body

161. Categories of Cancer
Solid cancers
 Carcinoma – body 3ssues e.g. skin
 Sacroma – connec3ve 3ssues e.g. car3lage
Fluid cancers
 Lymphoma – nodes of lympha3c system
 Leukemic – blood related
Semi Fluid cancers
 Myelomas – bone marrows

162. Naming Cancers
Cancer Prefixes Point to Location
Prefix Meaning
adeno- gland
chondro- cartilage
erythro- red blood cell
hemangio- blood vessels
hepato- liver
lipo- fat
lympho- lymphocyte
melano- pigment cell
myelo- bone marrow
myo- muscle
osteo- bone

163. What causes these “hits”?
 Muta3ons in cells can be triggered by

164. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on

165. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on
 chemical exposure

166. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on
 chemical exposure
 radia8on exposure

167. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on
 chemical exposure
 radia8on exposure
 heat

168. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on  cigareKe smoke
 chemical exposure
 radia8on exposure
 heat

169. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on  cigareKe smoke
 chemical exposure  pollu8on
 radia8on exposure
 heat

170. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on  cigareKe smoke
 chemical exposure  pollu8on
 radia8on exposure  age
 heat

171. What causes these “hits”?
 Muta3ons in cells can be triggered by
 UV radia8on  cigareKe smoke
 chemical exposure  pollu8on
 radia8on exposure  age
 heat  gene8cs

172. Detecting Cancer
Pathology
Proteomic profile
Patient’s
tissue
sample or Genomic profile
blood
sample

173. Viruses
Virus
inserts
and
changes
Cancer-linked genes for
virus cell growth

174. Examples of Human Cancer Viruses
Some Viruses Associated with Human Cancers

175. Population-Based Studies
Regions of Highest Incidence
U.K.:
Lung
cancer
JAPAN:
Stomach
cancer CANADA:
Leukemia
U.S.:
CHINA: Colon
Liver cancer
cancer
BRAZIL:
Cervical
AUSTRALIA: cancer
Skin
cancer

176. DNA Mutation
A woman
DNA
CA AG C T A A C T
without her man
Normal gene
is nothing
CA AG C G A A C T
Single base change
CA A G G CG C T A A C T
Additions
C
T
CA A G A A C T
Deletions

177. DNA Mutation
A woman
DNA
CA AG C T A A C T
without her man
Normal gene
is nothing
CA AG C G A A C T
♂: A woman
Single base change
without her man,
is nothing
CA A G G CG C T A A C T
Additions
C
T
CA A G A A C T
Deletions

178. DNA Mutation
A woman
DNA
CA AG C T A A C T
without her man
Normal gene
is nothing
CA AG C G A A C T
♂: A woman
Single base change
without her man,
is nothing
CA A G G CG C T A A C T
Additions
♀: A woman,
C
T
without her, man
CA A G A A C T
is nothing
Deletions

179. Tradi3onal treatments for cancers

180. Tradi3onal treatments for cancers
 Treatments target rapidly dividing cells
 high‐energy radia3on
 kills rapidly dividing cells
 chemotherapy
 stop DNA replica3on
 stop mitosis & cytokinesis
 stop blood vessel growth

181. New “miracle drugs”
 Drugs targe3ng proteins (enzymes) found only in
cancer cells
 Gleevec
 treatment for adult leukemia (CML)
& stomach cancer (GIST)
 1st successful drug targe3ng only cancer cells
without with
Gleevec Gleevec
Novartis

182. DNA NORMAL CELL
damaging
agents Successful DNA repair
DNA damage Cell Death
INITIATION
Failure of DNA repair
INITIATED CELL
PROMOTION
Cell Prolifera8on/
AND
Altered
PROGRESSION Differen8a8on
Prolifera8on
Cancerous Addi8onal
Muta8ons
MALIGNACY

183. An3oxidants

184. Flavonoids are
Phenolics
 Flavonoids
 Many are
an3oxidants
 Deeply pigmented
fruits and
vegetables
 Lycopene from
tomatoes

186. Anthocyanins are Flavonoids
 Eat a variety of
colored fruits and
vegetables to get
an3‐oxidants
Pomegranate
Acai-berry

187. Many Flavonoids are
An/‐oxidants
 Flavonoids are
an3oxidants
 An3oxidants are
chemicals that destroy
free radicals
 Free radicals are reac3ve
molecules that destroy
DNA, proteins and faey
acids in cells
Blueberries

188. Chocolate
 Theobromine cacoa
 Theobromine
 Nectar of the gods
 The feel‐good
flavonoid in dark
chocolate