1
Q
- Genetic abnormalities can already
be diagnosed even before birth
(within the womb)
A
Prenatal Cytogenetics
2
Q
- Genetic abnormalities can be
diagnosed after birth
A
Postnatal Cytogenetics
3
Q
- Babies are born at a normal
pregnancy but manifests a
genetic abnormality later in life
(either physical or mental
disabilities)
A
Childhood and Adult Cytogenetics
4
Q
_______ Syndrome
Features:
○ Flat nose bridge
○ Slanted eyes
○ Broad and prominent palpebral fissures
A
down
5
Q
Rate of biological eliminations:
○ __% of 45,X
A
95
6
Q
rate of biological eliminations
__% of Trisomy 13
A
90
7
Q
rate of biological eliminations
__% of Trisomy 18
A
80
8
Q
rate of biological eliminations: __% of Trisomy 21
A
65
9
Q
15% of recognized pregnancies end in
spontaneous fetal loss, 80% of which occur
during the ____trimester (first 3 months)
A
first
10
Q
- the most common
chromosomal error in spontaneous losses
A
45,X (Turner Syndrome)
11
Q
- the most common trisomy seen in
abortus
A
Trisomy 16
12
Q
INDICATIONS FOR __________ CYTOGENETICS:
1. Screening for maternal age-related risk
2. Family history of previous child with
chromosomal abnormalities
3. Abnormal levels of AFP (Alpha-fetoprotein)
in a screening test
A
PRENATAL
13
Q
- A fetal abnormality detected on ultrasound
- A parent who is a carrier of unbalanced
gametes - A parent who is a carrier of X-linked genetic
disorder
are indications for _________ cytogenetics
A
prenatal
14
Q
Karyotype analysis on both biological parents is used
to differentiate between an inherited rearrangement
and a ?
A
“de novo” anomaly in the child
15
Q
This pose less risk for
related impairment than “de novo” inheritance but
may recur in future pregnancies
A
Inherited rearrangement
16
Q
Approximately 0.6% - 1% if all newborns have
gross chromosomal abnormality
___________ cytogenetics
A
postnatal cytogenetics
17
Q
INDICATIONS FOR __________ CYTOGENETICS:
1. Presence of multiple congenital anomalies
2. Suspected aneuploidy (e.g: features of
Down Syndrome)
A
POSTNATAL
18
Q
● Some genetic disorders manifest in later life
● One of the most difficult diagnostic problem such
that other than cytogenetic studies, molecular
biochemical studies may be needed
____________CYTOGENETICS
A
CHILDHOOD AND ADULT CYTOGENETICS
19
Q
INDICATIONS FOR ______________
CYTOGENETICS
1. Unexplained mental retardation or
developmental delay
2. Suspected unbalanced autosome (ex:
Prader-Willi syndrome)
3. Suspected sex chromosomal abnormality
(ex: Turner syndrome)
A
CHILDHOOD AND ADULT
20
Q
- Suspected fragile-X syndrome
- Infertility – to rule out sex chromosomal
abnormality - Multiple spontaneous abortions – to rule
out the parents as carriers of balanced
translocations where both parents should
be evaluated
are indications for?
A
adult and chldhood cytogeneticx
21
Q
Defect on Chromosome 15
○ Insatiable appetite
○ Higher threshold for pain
what syndrome is thiz
A
prader-willi syndrome
22
Q
○ Outbursts of rage
○ There may be sleep disorders and
abnormalities
○ Compulsive behaviors such as
picking at the skin and even
psychoses
what syndrome iz this
A
prader-willi
23
Q
Defect on Chromosome 15
○ Uncontrollable laughing
○ Ataxia
○ Mental disabilities
○ Physical disabilities
what syndrome
A
angelman syndrome
24
Q
Specific chromosome rearrangements are directly
associated with ?
A
tumorigenesis
25
1. Confirm a clinical diagnosis
2. Monitor disease progression – relapse and
disease progression
3. Monitor patient’s response to therapy –
successful treatment results in cytogenetic
remission
are indicators for?
cancer cytogeneticx
26
a valuable tool in clinical oncology studies
FISH
27
In ______, we label the antibodies with
fluorescent dye that are used against the
antigen (mga chromosomal
abnormalities). If they bind together, they
will fluoresce
FISH
28
_________of signals - occur if the translocation
results in separation of two probes generating
two-different colored signals in place of the
original single-color signal
Splitting
29
________ of signals occur if the translocation results
in the relocation of 2 different probes into proximity
causing generation of a new color
Fusion (CENTRIC OR ROBERTSONIAN TRANSLOC)
30
t(9;22)(q34;q11.2)
acute lymphoblastic leukemia (ALL),
31
t(8:;21)(q22;q22)
acute myeloid leukemia (AML),
32
t(9;22)(q34.1;q11.2);
chronic myeloid leukemia (CML),
33
_____---- for BCR locus on chromosome
22
Green
34
___________________- will give two green and two red signals for the ABL and BCR alleles in each cell
Normal chromosome
35
formed with the
● fusion of green and red signals
A yellow signal
36
The ABL is located in the near end of the long arm
of chromosome 9 and the BCR gene is near the
centromere of the long arm of chromosome 22.
PHILADELPHIA CHROMOSOME
37
The chromosome break occurs in the ABL and
BCR gene which prompts the translocation.
PHILADELPHIA CHROMOSOME
38
The derivative chromosome 22 is also known as
the ?
Philadelphia chromosome
39
It detects all nucleated cells both normal
and abnormal,
FISH
40
Karyotyping can only be performed on
_______ cells
dividing
41
The ________- will identify the chromosomal abnormalities
karyotype
42
________ will establish the baseline frequency
of leukemic clones which can be used as
reference point for all the patients’ future
testing
FISH
43
__________- has also been used to study
leukemic cell lines
Multicolor FISH
44
Which of the following specimens is not used
for prenatal cytogenetic testing?
A. Umbilical cord blood
B. Fetal bladder aspirate
C. Amniotic fluid
D. Chorionic villi
B. FETAL BLADDER ASPIRATE
45
Although chromosomal abnormalities are
present in 1:3 conceptuses, only 6:1000 live
births manifest the disorder. Which of the
following explains this low incidence at birth?
A. Repair mechanism of recognized errors
B. Biological elimination of recognized errors
C. Poor identification of genetic abnormalities
D. Low interest on genetic abnormalities
B. Biological elimination of recognized errors
46
Genetic abnormalities are not seen in which of
the following individuals
A. Seemingly normal
B. With gross deformities
C. With confirmed genetic disorder
D. None of these
NONE
47
Philadelphia chromosome or abl-bcr fusion
gene is a diagnostic of which of the following
hematopoietic malignancy?
A. Acute myelogenous leukemia
B. Acute lymphoblastic leukemia
C. Chronic myelogenous leukemia
D. Chronic lymphocytic leukemia
C. Chronic myelogenous leukemia
48
Diseases with abnormal chromosomal number or alterations in structure of one or more chromosomes
cytogenetics disorders
49
complete sets of chromosomes with
none extra or missing.
The normal cells are diploid, having 2 sets of 23 chromosomes
euploidy
50
opposite of euploidy; where 1 or more individual chromosomes are with extra or missing from a euploid set
aneuploidy
51
missing pair of homologs
■ Ex: pair of chromosomes 6
nullisomy
52
1 chromosome is missing
■ Ex: Monosomy X (45,X); occurs at
embryonic stage; lethal
monosomy
53
3 copies of a particular
chromosome in an otherwise diploid cell
■ Ex: Trisomy 21 (47, XX or XY
+21); embryonic or fetal stage which may be lethal
trisomy
54
TRISOMY __ (DOWN SYNDROME)
● Mostcommon of the chromosomal disorders
● Majorcause of mental retardation
● Bands21q22.12-21q22.3
trisomy 21
55
➢ Mentalretardation
➢ Prominentepicanthic fold
➢ Flatfacial profile
➢ Simiancrease
➢ Congenitalheart defects
are manifestations of
trisomy 21
56
➢ Umbilicalhernia
➢ Intestinalstenosis
➢ Hypotonia→ muscleweakness→ called Floppy
babies
➢ Heartdefects (40%)
hypogonadism
are manifestations of
TRISOMY 21
57
Facial features of?
➢ Flatfaces ➢ Smallears ➢ Protrudingtongue
trisomy 21
58
Clinical manifestations of?
➢ Lowbirth weight
➢ Heartdefect
➢ Overlappingfingers
➢ Rockerbottomfeet
trisomy 18 Edward syndrome
59
Clinical manifestations of?
➢ Mentalretardation
➢ Microcephaly(smaller head)
➢ Microphthalmia(smaller eyes)
➢ Polydactyly(extra fingers)
➢ Cleftlip and palate
trisomy 13 patau syndrome
60
SEX CHROMOSOME ANEUPLOIDIES incidence:
1:500 livebirths
61
● Phenotypicallymilder than autosomal aneuploidies
● Subtle, chronic problems associated with sexual
development and fertility
● Difficultto diagnose at birth and usually
recognized at puberty
sex chromosome aneuploidies
62
● Difficultto diagnose at birth and usually
recognized at puberty (when secondary sex characteristics develop)
● Thehigher the number of X chromosomes in both
male and female, the higher the possibility of mental retardation
sex chromosome aneuploidies
63
➔ 47, XXX females and 47, XYY males
➔ Klinefelter Syndrome
➔ Turner Syndrome
➔ Pseudohermaphroditism
➔ Hermaphroditism
sex chromosome aneuploidies
64
● Oftengo undetected throughout life
● Incidence1:1000
● Fullyfertile and have chromosomally normal
children
47 XXX FEMALES AND 47 XYY MALES
65
● XXYmales have increased risk for behavioral
problems and are anti-social with criminal tendencies which has been negated by subsequent findings
47 XXX FEMALES AND 47 XYY MALES
66
Clinical manifestations of??
➢ Tallerthan average
➢ Somewith generalized learning difficulties
identified in school screening programs
47 XXX FEMALES AND 47 XYY MALES
67
● Oneof the most frequent sec chromosomal
disorders
● Incidence: 1:500 live male births
● Oneof the most common causes of hypogonadism
in male
KLINEFELTER SYNDROME
68
● Rarelydiagnosed before puberty
● Postpubertalhypogonadism
● Infertilitydue to small atrophic testicles with
hyalinized seminiferous tubules and azoospermia
KLINEFELTER SYNDROME
69
Clinical manifestations of?
➢ Distinctivebody habitus
➢ Talland thin with long legs
➢ Smallpenis
➢ Absenceof 2nd malesex characteristics
KLINEFELTER SYNDROME
70
➢ Gynecomastia(breast development)
➢ LowerIQ
➢ IncreasedFSH and estradiol
are clinical manifestations of
KLINEFELTER SYNDROME
71
○ Morephysical abnormalities
○ Cryptorchidism(testicles are
undescended)
○ Hypospadias(orifice of urethra is located
on the under surface of the penis
PolysomicX (47,XXY/48,XXXY)
○ cause din sha ng Klinefelter Syndrome
72
○ Prognathism
○ Severetesticular hypoplasia
○ Radioulnarsynostosis (connection
between radius and ulna - difficulty in movement
PolysomicX (47,XXY/48,XXXY)
73
● Mostcommon sex chromosomal anomaly in
female
● Onlyviable in live born monosomy
turner syndrome
74
Thecritical region for female differentiation is at the
region of the short arm just proximal to the centromere
○ ABSENCE→ ??
turner syndrome
75
➢ Lowposterior hairline
➢ Heartand renal anomalies
➢ Cubitusvalgus and shield chest
➢ Autoantibodyto thyroid (50%)
➢ Glucoseintolerance
➢ Obesity
are manifestations of
turner syndrome
76
_______ sex - determined presence or
absence of Y chromosome → IfY is present, individual is a
Genetic
77
______ sex - histologic characteristics of the gonads
→ Ifone has seminiferous tubules with developing sperm cells, individual is a male
→ Ifone has ovarian follicles, individual i s a female
gonadal
78
______ sex - depends on the presence of
derivatives of mullerian or wolfian ducts
ductal
79
__________produced by TDF initiates the male
developmental pathway
proteins
80
● Disagreementbetween gonadal (XX) and
phenotypic (male) sex
● Congenitaladrenal hyperplasia due to deficiency of
enzyme 21-hydroxylase
FEMALE PSEUDOHERMAPHRODITISM (XX MALE
81
Clinical features of?
➢ Normalovaries and internal genitalia
➢ Externalgenitalia is ambiguous or virilized
FEMALE PSEUDOHERMAPHRODITISM (XX MALE
82
Mostcomplex of all disorders of sexual
differentiation
○ Androgeninsensitivity/Testicular
feminization
■ Androgen receptor gene mutation,
located in the long arm: Xq11-Xq12
○ TDF/SRY is absent in the Y chromosome
due to translocation
MALE PSEUDOHERMAPHRODITISM (XY FEMALE)
83
Clinical features of
➢ Lackof any internal genitalia
➢ Blind vagina
➢ Testes in the abdomen or inguinal canal causing
infertility
MALE PSEUDOHERMAPHRODITISM (XY FEMALE)
84
● Exceedinglycomplex (sexual ambiguity)
● Truehermaphrodites = both ovarian and testicular
tissues (one on each side or ovotestes
HERMAPHRODITISM
85
● Extremelyrare
● Mostcommon karyotype: 46,XX (50%); the rest
mostly are mosaic: 46,XX/46,XY karyotype; rarely 46,XY
HERMAPHRODITISM
86
- Diseases with abnormal chromosomal number or
alterations in structure of one or more chromosomes
CYTOGENETIC DISORDERS
87
● Terminal deletion of the short arm of chromosome
4, del(4)(p16)
WOLF-HIRSCHHORN SYNDROME (4P-)
88
Clinical manifestations of?
➢ Microcephaly
➢ Frontal bossing
➢ Micrognathia (small jaw)
➢ Hypotonia
➢ Epicanthal folds
➢ Developmental delay
WOLF-HIRSCHHORN SYNDROME (4P-)
89
● Greek warrior facial helmet appearance due to
arched eyebrows, prominent glabella,
hypertelorism, and long beaked nose
WOLF-HIRSCHHORN SYNDROME (4P-)
90
● Special education and are at risk for seizures
➔ Diagnosis: Karyotyping and FISH
wolf-hirschhorn syndrome
91
● Deletion of the short arm of chromosome 5, del
(5)(p15)
CRI-DU-CHAT SYNDROME (5P-)
92
Clinical manifestations of?
➢ High-pitched cat like cry
➢ Low birth weight
➢ Slow growth
➢ Hypotonia
➢ Microcephaly
➢ Hypertelorism
➢ Epicanthal folds
➢ Cardiac anomalies
➢ Mental retardation
cri-du-chat syndrome
93
Patients have delayed development and may
reach cognitive and social level of a 5 or 6 year old
cri du chat syndrome
94
nvolve a fraction of a single
chromosome band (>500 kb) and may be large
enough to identify by karyotype analysis but most
may require FISH for detection
Microdeletions
95
involve a single to several
hundred base pair and are identified by molecular
technology
Molecular Deletions
96
- those that are due
to deletions that encompass several adjacent,
unrelated genes resulting in variable phenotypic
expression
Contiguous Gene Syndrome
97
● Deletion of the elastin gene (ELN gene) on the
proximal long arm of chromosome 7 (7q11.23)
● Unequal meiotic crossover → interstitial deletion
WILLIAM’’S SYNDROME
98
Elastin is important in:
○ Heart
○ Blood vessels
○ Skin
○ Vocal cords
→ is absent among these patients, thus the clinical
features except behavioral anomalies which may be
explained as a contiguous gene syndrome
what syndrome
william's syndrome
99
Clinical manifestations of?
➢ Low IQ with behavioral anomalies
➢ Hypersensitivity to sound
➢ Blue eyes with stellate pattern in the iris
➢ Prominent lips with hoarse voice
➢ Supravalvular aortic stenosis and other cardiac
defects
➢ Hypertension
➢ Premature aging of the skin
➢ Hypercalcemia
william's syndrome
100
● Due to del 8p24.11-q24.13, involving the TRPSI,
TRPSII, EXTgenes
LANGER-GIEDION SYNDROME
101
Clinical manifestations of?
➢ Craniofacial dysmorphism
➢ Exostosis
➢ Skeletal abnormalities
➢ Mild to severe mental deficiency
➢ Fine scalp hair
➢ Large and prominent ears
➢ Missing teeth
➢ Trichorhinophalangeal syndrome
langer-giedon syndrome
102
● Wilm’s tumor, Aniridia, Genitourinary defects, and
mental Retardation (75%)
● Deletion on the short arm of chromosome 11
(11p13.3) involving WT1 gene, AN2 gene causing
contiguous gene syndrome
WAGR SYNDROME
103
Deletion of one copy of PAX6 gene → aniridia &
MR; brain-derived neurotrophic factor (BDNF gene)
→ hyperphagia and obesity
wagr syndrome
104
Patients with _______has 1:3 chance of developing
Wilm’s tumor but patients with Wilm’s tumor have
1:50 chance of having aniridia.
aniridia
105
● del 13q14.1-q14.2, involving Rb gene
● May also occur by hypermethylation of the
promoter sequence
RETINOBLASTOMA
106
● Patients have risk of developing tumors of the
retinoblast cells of the eye
● PHL > 1:18000
● 90% diagnosed before 5 y/o
→ Diagnosis: Karyotyping or Southern Blot
retinoblastoma
107
● Best known microdeletion syndromes
● Share the same interstitial deletion of the proximal
long arm of chromosome 15 del(1)(q11.2-q13),
PRADER-WILLI AND ANGELMAN SYNDROME
108
● Broad Thum-Hallux syndrome, AD, mostly
acquired
● del 16p13.3, CREBBP gene, regulates cell growth
and division for normal fetal development: EP300
gene, small % of cases
RUBINSTEIN-TAYBI SYNDROME
109
Clinical manifestations of ??
➢ Beaked nose
➢ Prominent columella
➢ Hypoplastic maxilla
➢ Down slanted palpebral fissures
➢ Broad thumbs
➢ First toes
➢ Hirsutism
➢ Short stature
➢ Mental retardation
➢ Speech delay
RUBINSTEIN-TAYBI SYNDROME
110
● del 17p11.1, RAI1 gene
● Not inherited
● Deleted during formation of reproductive cells
SMITH-MAGENIS SYNDROME
111
Clinical manifestations of?
➢ Brachycephaly
➢ Broad nasal bridge
➢ Prominent jaw
➢ Short broad hands
➢ Hyperactivity
➢ Mental retardation
➢ Delayed speech
➢ Self-destructive behavior
smith-magenis syndrome
112
● Two stereotypic behaviors: spasmodic upper-body
squeeze or “self-hug” and hand licking and page
flicking “lick and flip”, are specific to SMS
→ Diagnosis: Karyotyping and or FISH
smith-magenis syndrome
113
● Microdeletion of the distal short arm of
chromosome 17 (17p13.3), involving the LIS1
gene, with the deletion of at least 2 genes
MILLER-DIEKER SYNDROME AND LISSENCEPHALY
114
_____________ is associated with profound mental
retardation and seizures
Lissencephaly
115
● Possible the most common microdeletion
syndrome, occurring in 1:4000 live births, but not
often recognized
● 3 Mb deletion on the proximal long arm of
chromosome 22 (22q11.2), GCSL gene
VELOCARDIOFACIAL SYNDROME
116
Usually diagnosed in newborns because of:
○ feeding difficulties due to palatal
abnormalities (cleft palate)
○ cardiac defects (75%)
○ characteristics with facial dysmorphisms
with prominent nose and retrognathia
velocardiofacial syndrome
117
● del22q11.2, 10p, 1q, 6q involving GCSL gene
DIGEORGE SYNDROME
118
➢ Cleft palate
➢ Heart defect
➢ Hypoplasia of the thymus with resultant T-cell
immunodeficiency
➢ Parathyroid hypoplasia giving rise to severe
hypocalcemia, and seizures
are Clinical manifestations of
digeorge syndrome
119
● del Xp22.32, involving the STS gene
ICHTHYOSIS
120
Clinical manifestations of?
➢ Scaly skin
➢ Short stature
➢ Hypogonadism
➢ Mental retardation
itchthyosis
121
● del Xp22.3, involving the KAL1 gene
Clinical manifestations:
➢ Hypogonadism
➢ Inability to smell
kallman syndrome
122
● Mutation in single gene with large effects
MENDELIAN DISORDERS
123
expressed in mathematical
terms
penetrance
124
If a trait is seen in all individuals carrying
the mutant gene but is expressed
differently among individuals, the
phenomenon is called ?
variable expressivity
125
_____________ SYNDROME
● 600 mutations, mostly missense
● Fibrillin-I or FBNI gene → Fibrillin I protein
● FBNI on 15q21.1; FBN2 on 5q23.31
AD - MARFAN
126
Fibrillin I protein
○ Component of microfibrils
○ Provides skeleton on which tropoelastin is
deposited to form elastic fibers (aorta,
ligaments and ciliary zonules)
what syndrome
ad- marfan
127
➢ Mitral valve prolapse (MVP) → mitral regurgitation
(MR)
➢ Aneurysm of the ascending aorta → valve
incompetence → left ventricular hypertrophy (LVH)
→ heart failure (HF)
are manifestations of what syndrome?
ad-marfan
128
● Defect in synthesis of fibrillar collagen
● Encompasses the 3 patterns of transmutants:
○ May be transmitted through autosomal
recessive
○ As a sex-linked disorder
● Group of clinically and genetically heterogeneous
disorders
AD (AR, X-LINKED) - EHLERS-DANLOS SYNDROME (EDS)
129
________ may be caused by mutations involving
structural proteins or enzymes
EDS
130
Common manifestations 0f ________________ involve the:
➢ Skin (hyperextensibility)
➢ Ligaments
➢ Joints (hypermobility)
AD (AR, X-LINKED) - EHLERS-DANLOS SYNDROME (EDS)
131
● 1:2,500 live births, carrier rate of 1:20
● Most common lethal genetic diseases affecting
Caucasians CFTR gene, 7q31.2
AR - CYSTIC FIBROSIS
132
Disorder of ion transport in epithelial cells of
exocrine glands and lining epithelial cell of the
respiratory, GI and reproductive tracts
ar-cystic fibrosis
133
● Hereditary deficiency of one of the enzymes
involved in glycogen synthesis or degradation.
● Enzymatic defects dictate the organ of involvement
(distribution)
AR - GLYCOGENOSIS
134
________ Forms
➔ Von Gierke/Type I
◆ Glucose-6-phosphate deficiency
➔ Liver phosphorylase and Debranching enzymes
➔ Hepatomegaly and hypoglycemia
Hepatic
135
________ Forms
➔ McArdle disease/Type V
◆ Muscle phosphorylase deficiency
➔ Type VII
◆ Muscle phosphofructokinase deficiency
➔ Failure of ATP production → muscle cramps and
lactate level fail to rise
Myopathic
136
● Deletion, Xp21
● May result from frameshift mutation, point mutation
● 2/3 familial, 1/3 de novo
SLD - DUCHENNE MUSCULAR DYSTROPHY
137
● Females are carriers, asymptomatic, increased
creatine kinase
● Males manifest at 5 y/o, wheelchair-dependent at
10-12
SLD - DUCHENNE MUSCULAR DYSTROPHY
138
● Normal at birth
● Delayed walking due to muscle weakness
● Pelvic girdle muscles are the first to weaken
● Pseudohypertrophy of leg muscles
SLD - DUCHENNE MUSCULAR DYSTROPHY
139
● Pseudohypertrophy of leg muscles
○ Increase fiber size then replacement by
connective tissue, fat
● Heart involvement → failure and arrhythmia →
death
SLD- DUCHENNE MUSCULAR DYSTROPHY
140
● Diminished dystrophin
● Mutation causes synthesis of abnormal, smaller
protein
BECKER MUSCULAR DYSTROPHY
141
● Onset during late childhood or adolescence (later
than Duchenne)
● Heart disease
● Normal lifespan
BECKER MUSCULAR DYSTROPHY
142
● Second leading cause of mental retardation
and is the primary cause of inherited mental
retardation
● 1:1550 for affected males and 1:8000 for affected
females
SLD - FRAGILE X SYNDROME
143
● Break or gap in the structure of the X
chromosome that can be detected cytogenetically
SLD - FRAGILE X SYNDROME
144
In SLD-FRAGILE X SYNDROME, A normal transmitting male and carrier female have _________ repeats (premutations) whereas affected individuals, 200 – 4000 repeats (full
mutation)
55 – 200
145
Clinical manifestations of WHAT SYNDROME in affected males:
➢ Mentally retardation
➢ Long face with macrognathia
➢ Large everted ears
➢ Macroorchidism (90% of postpubertal males)
SLD-FRAGILE X SYNDROME
146
Clinical features of fragile X syndrome worsen with
each generation (anticipation).
T OR F
TRUE! Padagdag ng padagdag ang clinical
manifestations per generation
cytogenetics
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