1. GENETIC DISORDERS IMPOSSIBLE!!!!! HORROR!!!!! ANXIETY!!!!!! DREAD!!!!!
INADEQUACY!!!!!

2. DISEASES GENETIC ENVIRONMENTAL BOTH Are ALL diseases “genetic”?
Are all diseases “environmental”?
How does “congenital” fit in? How does “immune” fit in?
How does this fit in with DEG-INF-NEO?

3. Base pair triplet gene chromosome segment whole chromosome genome
MUTATIONS
PERMANENT change in DNA
GENE MUTATION: (may, and often, result in a single base error)
CHROMOSOME MUTATION: (visible chromosome change)
GENOME MUTATION: (whole chromosome)
The chapter is organized in order of increasing size of the chromosomal molecular anatomic defect.
Base pair triplet gene chromosome segment whole chromosome genome

4. GENE MUTATION
DELETION OF A SINGLE BASE
SUBSTITUTION OF A SINGLE BASE

5. Classical ideal concept of a point mutation, which also happens to be the REAL defect in sickle cell anemia.Why would this NOT cause a frameshift?
POINT MUTATION

6. GENE MUTATION POINT MUTATION within a coding sequence: VAL-GLU
MUTATIONS in NON-coding sequences defective transcription, regulation, apop.
DELETIONS/INSERTIONS “frameshift” mutation, involvement is NOT a multiple of 3
Tri-nucleotide REPEATS, e.g., CGG repeats many times in fragile X syndrome, CAG in others
In a “frameshift mutaton”, NON-multiple of three mutations “shift” the whole DNA “frame”!
A frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides in a DNA sequence that is NOT divisible by three!

7. GENE MUTATIONS INTERFERE with protein synthesis
SUPPRESS transcription, DNARNA
PRODUCE abnormal mRNA
DEFECTS carried over into TRANSLATION
ABNORMAL proteins WITHOUT impairing syntheses
In the classical one-gene, one-protein model, abnormal (i.e., mutated) genes mean abnormal proteins.

8. GENETIC DISORDERS
SINGLE gene mutations, following classical MENDELIAN inheritance patterns the most
MULTIFACTORIAL inheritance
CHROMOSOMAL disorders
NON-MENDELIAN disorders
The chapter is organized in order of increasing size of the chromosomal molecular anatomic defect, from single base pair to entire chromosome!

9. MENDELIAN inheritance patterns
AUTOSOMAL DOMINANT
AUTOSOMAL RECESSIVE
SEX-LINKED (recessive), involving “X” chromosome
Each has it’s own characteristics, each has its own list of common diseases, and each has its own pedigree or pattern of inheritance

10. AUTOSOMAL DOMINANT REDUCED PENETRANCE (environment?, other genes?)
Disease is in HETEROZYGOTES
NEITHER parent may have the disease (NEW mut.)
REDUCED PENETRANCE (environment?, other genes?)
VARIABLE EXPRESSIVITY (environment?, other genes?)
May have a DELAYED ONSET
Usually result in a REDUCED PRODUCTION or INACTIVE protein
Heterozygous ~ “less aggressive”? Single trouble?

11. AUTOSOMAL DOMINANT MARFAN SYNDROME EHLERS-DANLOS SYNDROMES (some)
HUNTINGTON DISEASE
NEUROFIBROMATOSIS
MYOTONIC DYSTROPHY
TUBEROUS SCLEROSIS
POLYCYSTIC KIDNEY
HEREDITARY SPHEROCYTOSIS
VON WILLEBRAND DISEASE
MARFAN SYNDROME
EHLERS-DANLOS SYNDROMES (some)
OSTEOGENESIS IMPERFECTA
ACHONDROPLASIA
FAMILIAL HYPERCHOLESTEROLEMIA
ACUTE INTERMITTENT PORPHYRIA
NOT to memorize, but be familiar with, but it would be nice to memorize, because just about every other classic genetic disease is autosomal recessive! AR>>>AD

12. AUTOSOMAL DOMINANT PEDIGREE
1) BOTH SEXES INVOLVED
2) GENERATIONS NOT SKIPPED

13. AUTOSOMAL RECESSIVE Disease is in HOMOZYGOTES
More UNIFORM expression than AD
Often COMPLETE PENETRANCE
Onset usually EARLY in life
NEW mutations rarely detected clinically
Proteins show LOSS of FUNCTION
Include ALL inborn errors of metabolism
MUCH more common that autosomal dominant
Homozygous ~ “more aggressive”? Double trouble?
This SHOULD make sense too?

14. AUTOSOMAL RECESSIVE CF PKU GALACTOSEMIA HOMOCYSTINURIA
LYSOSOMAL STORAGE
Α-1 ANTITRYPSIN
WILSON DISEASE
HEMOCHROMATOSIS
GLYCOGEN STORAGE DISEASES
Hgb S
THALASSEMIAS
CONG. ADRENAL HYPERPLASIA
EHLERS-DANLOS (some)
ALKAPTONURIA
NEUROGENIC MUSC. ATROPHIES
FRIEDREICH ATAXIA
SPINAL MUSCULAR ATROPHY
Most of the classical “genetic” diseases are autosomal RECESSIVE, rather than autosomal DOMINANT, by far.
NOT to memorize, but be familiar with.

15. AUTOSOMAL RECESSIVE PEDIGREE
1) BOTH SEXES INVOLVED
2) GENERATIONS SKIPPED
Why generations skipped in AR, but not AD?
Because you need defects (mutations) in BOTH alleles!

16. SEX (“X”) LINKED MALES ONLY HIS SONS are OK, right?
ALL his DAUGHTERS are CARRIERS
The “Y” chromosome is NOT homologous to the “X”, i.e., the classic concept of dominant/recessive has no meaning here
HETEROZYGOUS FEMALES have no phenotypic expression (carriers)….usually, this means autosomal “recessive”, right?

17. SEX (“X”) LINKED DUCHENNE MUSCULAR DYSTROPHY HEMOPHILIA , A and B
G6PD DEFICIENCY
AGAMMAGLOBULINEMIA
WISKOTT-ALDRICH SYNDROME
DIABETES INSIPIDUS
LESCH-NYHAN SYNDROME
FRAGILE-X SYNDROME
You should know reflexively that ALL these diseases are sex linked.
We will soon see a map of the X-chromosome.

18. SEX LINKED PEDIGREE 1) MALES ONLY, sons of affected males are OK
2) GENERATION SKIPPING DOESN’T MATTER

19. SINGLE GENE DISORDERS ENZYME DEFECT (Most of them, e.g., PKU)
Accumulation of substrate
Lack of product
Failure to inactivate a protein which causes damage
RECEPTOR/TRANSPORT PROTEIN DEFECT (Familial Hypercholesterolemia)
STRUCTURAL PROTEIN DEFECT (Marfan, Ehl-Dan)
Structure
Function
Quantity
ENZYME DEFECT WHICH INCREASES DRUG SUSCEPTIBILITY: G6PDPrimaquine

20. STRUCTURAL PROTEIN DEFECTS
Marfan Syndrome
Fibrillin-1 defect (not -2 or -3)
Tall, dislocated lens, aortic arch aneurysms, etc.
Abraham Lincoln?, Osama bin-Laden?
Ehlers-Danlos Syndromes (AD, AR)
Multiple (6?) different types
Classical, Hypermob., Vasc., KyphoSc., ArthChal., Derm
Various collagen defects
Hyperelastic skin, hyperextensible joints
Fibrillin-1 is a major component of the microfibrils that form a sheath surrounding the amorphous elastin. It is believed that the microfibrils are composed of end-to-end polymers of fibrillin.

21. RECEPTOR PROTEIN DEFECTS
FAMILIAL HYPERCHOLESTEROLEMIA
LDL RECEPTOR defect
Cholesterol TRANSPORT across liver cell impaired
ergo, CHOLESTEROL BUILDUP IN BLOOD
“Scavenger System” for CHOL kicks in, i.e., MACROPHAGES
YOU NOW KNOW THE REST OF THE STORY
YOU NOW KNOW WHY MACROPHAGES are “FOAMY”

22. ENZYME DEFICIENCIES LYSOSOMAL STORAGE DISEASES comprise MOST of them
BY FAR, THE LARGEST KNOWN CATEGORY
SUBSTRATE BUILDUP
PRODUCT LACK
SUBSTRATE could be HARMFUL
LYSOSOMAL STORAGE DISEASES comprise MOST of them
The concept is extremely simple: If an enzyme cannot convert A  B, then A builds up abnormally.

23. LYSOSOMAL STORAGE DISEASES
GLYCOGEN STORAGE DISEASES
SPHINGOLIPIDOSES (Gangliosides)
SULFATIDOSES
MUCOPOLYSACCHARIDOSES
MUCOLIPIDOSES
OTHER
Fucosidosis, Mannosidosis, Aspartylglycosaminuria
WOLMAN, Acid phosphate deficiency
You will probably never see any of these disorders personally, but nevertheless, you should have familiarity with the process behind each disease. You should already know from biochemistry what these substances are already.
We will define and differentiate these groups of chemicals as we progress.

24. GLYCOGEN STORAGE DISEASES
MANY TYPES (at least 13)
Type 2 Pompe (acid-α-glucosidase) , von Gierke (Glu-6P-ase), McArdle (phosphorylase), most studied and discussed, and referred to
Storage sites: Liver, Striated Muscle (Skel + Ht)
Generic description, for more info :

25. SPHINGOLIPIDOSES MANY types, Tay-Sachs most often referred to
GANGLIOSIDES are ACCUMULATED
Ashkenazi Jews (1/30 are carriers)
CNS neurons a site of accumulation
CHERRY RED spot in Macula
Usually fatal by age 4
Sphingolipids are a class of lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine. “Sphingo” comes from Sphinx, because of their original enigmatic nature!
Tay-Sachs disease (abbreviated TSD, also known as GM2 gangliosidosis or Hexosaminidase A deficiency) is an autosomal recessive genetic disorder. In its most common variant known as infantile Tay-Sachs disease it presents with a relentless deterioration of mental and physical abilities which commences at 6 months of age and usually results in death by the age of four.

26. SULFATIDOSES
MANY types, but the metachromatic leukodystrophies (CNS), Krabbe, Fabry, Gaucher, and Niemann-Pick (A and B) are most commonly referred to
SULFATIDES, CEREBROSIDES, SPHINGOMYELIN are the accumulations
Sulfatides are a class of sulfated galactosylceramides synthesized primarily in the oligodendrocytes in the central nervous system. Sulfatides are a type of sulfolipid.

27. NIEMANN-PICK TYPES A, B, C SPHINGOMYELIN BUILDUP
Sphingomyelinase (ASM), is the missing enzyme
MASSIVE SPLENOMEGALY
ALSO in ASHKANAZI JEWS
OFTEN FATAL in EARLY LIFE, CNS, ORGANOMEGALY
Sphingomyelin (SPH), (sphin-go-my-e-lin (sfi ng gōˈmīəlin)), is a type of sphingolipid found in animal cell membranes, especially in the membranous myelin sheath which surrounds some nerve cell axons. It usually consists of phosphorylcholine and ceramide. In humans SPH represents ~85% of all sphingolipids.

28. GAUCHER DISEASE ALL MACROPHAGES, liv, spl, nodes, marrow
GLUCOCEREBROSIDE BUILDUP
99% are type I, NO CNS involvement
ALL MACROPHAGES, liv, spl, nodes, marrow
Cerebrosides are glycosphingolipids which are important components in animal muscle and nerve cell membranes. Myelin is the most well known cerebroside. Glucocerebroside (also called glucosylceramide) is any of the cerebrosides in which the monosaccharide head group is glucose.
Gaucher's disease is the most common of the lysosomal storage diseases. It is caused by a hereditary deficiency of the enzyme glucocerebrosidase (also known as acid β-glucosidase). The enzyme acts on a fatty substance glucocerebroside (also known as glucosylceramide). When the enzyme is defective, the substance accumulates, particularly in cells of the mononuclear cell lineage.

29. MUCOPOLYSACCHARIDOSES
HURLER/HUNTER, for I and II, respectively, 14 types
DERMATAN sulfate, HEPARAN sulfate buildup, respectively
coarse facial features
clouding of the cornea
joint stiffness
mental retardation
URINARY EXCRETION of SULFATES COMMON
Note this is heparAn, NOT heparIn.
Mucopolysaccharides
Mucopolysaccharides are long chains of sugar molecules that are found throughout the body, often in mucus and in fluid around the joints. They are more commonly called glycosaminoglycans.

30. OTHER LYSOSOMAL STORAGE DIS.
FUCOSIDOSIS
MANNOSIDOSIS
ASPARTYLGLYCOSAMINURIA
WOLMAN (CHOL., TRIGLYCERIDES)
ACID PHOSPHATE DEFICIENCY (PHOS. ESTERS)
Fucosidosis, also called alpha-l-fucosidase deficiency, is a rare autosomal recessive lysosomal storage disease in which the enzymefucosidase is not properly used in the cells to break down fucose.
Mannosidosis is a deficiency in mannosidase, an enzyme.
Aspartylglucosaminuria (AGU), also called aspartylglycosaminuria, is a rare, autosomal recessive lysosomal storage disorder caused by deficient activity of the enzyme N-aspartyl-beta-glucosaminidase (aspartylglucosaminidase). This enzyme normally cleaves long sugar chains known as oligosaccharides in the lysosome.
Wolman disease (also known as Wolman's disease, Wolman's syndrome, and acid lipase deficiency) is a rare autosomal recessive lipid storage disease that is usually fatal at a very young age. It is in the family of lysosomal storage diseases. 
Acid Phosphate Deficiency is caused by mutations in the ACP2 (beta subunit) and ACP3 (alpha subunit) genes.

31. ALCAPTONURIA BLACK URINE BLACK NAILS (OCHRONOSIS), SKIN
NOT a LYSOSOMAL ENZYME DISEASE
FIRST ONE TO BE DESCRIBED
HOMOGENTISIC ACID
HOMOGENTISIC ACID OXIDASE
BLACK URINE
BLACK NAILS (OCHRONOSIS), SKIN
BLACK JOINT CARTILAGE (SEVERE ARTHRITIS)
Alkaptonuria (black urine disease or alcaptonuria) is a rare inherited genetic disorder of phenylalanine and tyrosine metabolism. This is an autosomal recessive condition that is due to a defect in the enzyme homogentisate 1,2-dioxygenase (EC  ), which participates in the degradation of tyrosine.

33. Endogenous pigment looking like ANY other endogenous pigment, e. g
Endogenous pigment looking like ANY other endogenous pigment, e.g., hemosiderin, melanin, bile, lipofucsin

34. NEUROFIBROMATOSIS 1 and 2 1 1-von Recklinghausen
2- “acoustic” neurofibromatosis 1
Neurofibromas, café-au-lait, Lisch nodules
Neurofibromatosis (commonly abbreviated NF) is a genetically-inherited autosomal dominant disease in which the nerve tissue grows tumors (i.e., neurofibromas) that may be harmless or may cause serious damage by compressing nerves and other tissues. The disorder affects all neural crest cells (Schwann cells, melanocytes, endoneurial fibroblasts). Cellular elements from these cell types proliferate excessively throughout the body forming tumors and the melanocytes function abnormally resulting in disordered skin pigmentation.The tumors may cause bumps under the skin, colored spots, skeletal problems, pressure on spinal nerve roots, and other neurological problems.

35. NEUROFIBROMATOSIS 1 and 2 1-von Recklinghausen
2- “acoustic” neurofibromatosis 2
Bilateral acoustic neuromas and multiple meningiomas

36. MULTIFACTORIAL INHERITANCE
Multi-”FACTORIAL”, not just multi-GENIC
“SOIL” theory
Common phenotypic expressions governed by “multifactorial” inheritance
Hair color
Eye color
Skin color
Height
Intelligence
Diabetes, type II
We are now moving the discussion up from ONE gene MULTI-genes Parts of chromosomes WHOLE chromosomes.

37. FEATURES of multifactorial inheritance
Expression determined by NUMBER of genes
Overall 5% chance of 1st degree relatives having it
Identical twins >>>5%, but WAY less than 100%
This 5% is increased if more children have it
Expression of CONTINUOUS traits (e.g., height) vs. DISCONTINUOUS traits (e.g., diabetes)
If a disease or condition is scalable, rather than on or off, it is probably multigenic, or multifactorial, just part of the spectrum of HOMO-zygous diseases being HOMO-geneous, and HETERO-zygous diseases being VARIABLE.

38. “MULTIFACTORIAL” DISORDERS
Cleft lip, palate
Congenital heart disease
Coronary heart disease
Hypertension
Gout
Diabetes
Pyloric stenosis
MANY, MANY, MANY, MANY MORE…..
You might imagine that the list of “multifactorial” disorders blends in with the entire list of human diseases. Hence are “all” diseases “genetic”? This is almost an UNFAIR list, therefore
NO single gene mutation can be indicted as being the cause of any of these diseases..

39. KARYOTYPING Defined as the study of CHROMOSOMES 46 = (22x2) + X + Y
Conventional notation is “46,XY” or “46,XX”
G(iemsa)-banding, 500 bands per haploid recognizable
Short (“p”-etit) arm = p, other (long) arm = q
The Giemsa stain, named after Gustav Giemsa, is a VERY common stain in pathology, often used to identify organisms in cells such as malaria and helicobacter, and MANY other things such as parts of cells and connective tissue. It is a VERY simple stain to do.

40. The “official” notation for the normal male pattern is: “46, XY”
Please be able to recognize the 3 most common ABNORMAL karyotypes: Down, Turner, Klinefelter

41. More KARYOTYPING info
A,B,C,D,E,F,G depends on chromosome length
A longest
G shortest
Groups within these letters depend on the p/q ratio
ARMREGIONBANDSub-BAND, numbering from the centromere progressing distad

42. Is it surprising that the “regions” of the “X” chromosome are the same as the list of sex-linked diseases? Ans: NO
Have you see this list before? Ans: YES

43. F.I.S.H. (gene “probes”) greatly enhances G-banding
Fluorescent In-Situ Hybridization
Uses fluorescent labelled DNA fragments, ~10,000 base pairs, to bind (or not bind) to its complement
Awesome research technique, used often in everyday pathology too, fluorescently “labels” pieces of DNA which connect to the corresponding strand during DNA replication. In situ hybridization (ISH) is a type of hybridization that uses a labeled complementary DNA or RNA strand (i.e., probe) to localize a specific DNA or RNA sequence in a portion or section of tissue (in situ)

44. FISH SUBTLE MICRODELETIONS COMPLEX TRANSLOCATIONS
AND TELOMERE ALTERATIONS
FISH is POWERFULLY more sensitive, accurate, and specific, than G-banding.

45. TRIPLE CHROMOSOME #20 A DELETION in CHROMOSOME #22
Common applications for FISH. Examples of diseases that are diagnosed using FISH include Prader-Willi syndrome, Angelman syndrome, 22q13 deletion syndrome, chronic myelogenous leukemia, acute lymphoblastic leukemia,Cri-du-chat, Velocardiofacial syndrome, and Down syndrome, but, IN GENERAL, diseases with partial or whole chromosome abnormalities.
TRIPLE CHROMOSOME #20
A DELETION in
CHROMOSOME #22

46. SPECTRAL KARYOTYPING
This technique is used to identify structural chromosome aberrations in cancer cells and other disease conditions when Giemsa banding or other techniques are not accurate enough. Each chromosome has a different color, sort of, although some of this is digital false color techniques, much in the same way, electron microscopy can generate “false” colors.
This was our spectacular title page, and you have probably figured out why.

47. CYTOGENETIC DISORDERS
DEFINITIONS:
EUPLOID (46XX or 46XY)
ANEUPLOID (NOT AN EXACT MULTIPLE OF 23)
MONOSOMY, AUTOSOME OR SEX
TRISOMY, AUTOSOME OR SEX
DELETION
BREAKAGE

48. MORE DEFINITIONS
Just about everything you can imagine geometrically which can happen to that piece of string------does!

49. COMMON CYTOGENETIC DISEASES
AUTOSOMES
TRISOMY-21 (DOWN SYNDROME)
8, 9, 13 (Patau), 18 (Edwards), 22
22q.11.2 deletion
SEX CHROMOSOMES
KLINEFELTER: XXY, XXXY, etc.
TURNER: XO

50. TRISOMY-21
Maternal “nondisjunction” is the classical explanation of Trisomy 21.

51. TRISOMY-21 #1 cause of mental retardation
Most trisomies (monosomies, aneuploidy) are from maternal non-disjunction
(non-disjunction or anaphase lag are BOTH possible)
#1 cause of mental retardation
Maternal age related
Congenital Heart Defects, risk for acute leukemias, GI atresias
Most LOVABLE of all God’s children

52. You do not have to see many trisomy-21 patients until you can recognize them very quickly and easily. There is NO way you can learn from a textbook how to recognize these patients quickly. If you KNOW one or are RELATED to one, or loved one, you NEVER fail to recognize the face without having to describe the details, i.e., pattern-recognition.
MEMORIZE THIS PIC!

53. Chromosome 22q11.2 Deletion Syndrome
Because of a DELETION, this cannot be detected by standard karyotyping and needs FISH
Cardiac defects, DiGeorge syndrome, velocardiofacial, CATCH*
22q11.2 deletion syndrome, also known as DiGeorge Syndrome, Velo(soft palate)Cardio(heart)Facial(face) Syndrome, conotruncal anomaly face syndrome, Congenital Thymic Aplasia, Strong Syndrome, Thymic hypoplasia, and DiGeorge anomaly. It also has the mnemonic C-A-T-C-H, for :
Cardiac Abnormality (especially Fallot's Tetralogy) Abnormal facies Thymic aplasia Cleft palate Hypocalcemia

54. Cute smiles?

55. SEX CHROMOSOME DISORDERS
Problems related to sexual development and fertility
Discovered at time of puberty
Retardation related to the number of X chromosomes
If you have at least ONE “Y” chromosome, you are male
Sexuality can be defined in many ways, having at least ONE “Y” chromosome is a good definition of being male.

56. KLINEFELTER (XXY, XXXY, etc.)
Hypogonadism found at puberty
#1 cause of male infertility
NO retardation unless more X’s
47, XXY 82% of the time
L----O----N----G legs, atrophic testes, small penis

58. TURNER (XO) NECK “WEBBING” 45, X is the “proper” designation
Mosaics common
Often, the WHOLE chromosome is not missing, but just part
NECK “WEBBING”
EDEMA of HAND DORSUM
CONGENITAL HEART DEFECTS most FEARED
“STREAK” OVARIES

59. “STREAK” ovaries are the rule, neck webbing and cardiac structural abnormalities are also at the top of the list.

60. HERMAPHRODITES ♀ ♂
GENETIC SEX is determined by the PRESENCE or ABSENCE of a “Y” chromosome, but there is also, GONADAL (phenotypic), and DUCTAL sex
TRUE HERMAPHRODITE: OVARIES AND TESTES, often on opposite sides (VERY RARE)
PSEUDO-HERMAPHRODITE:
MALE: TESTES with female characteristics (Y-)
FEMALE: OVARIES with male characteristics (XX)
“Pseudo”-hermaphrodites are MUCH more common that TRUE hermaphrodites.

61. SINGLE GENE, NON-Mendelian
Triplet repeats
Fragile X (CGG)
Others: ataxias, myotonic dystrophy
Mitochondrial Mutations: (maternal)
(LEBER HEREDITARY OPTIC NEUROPATHY)
Genomic “IMPRINTING”: (Inactivation of maternal or paternal allele, contradicts Mendel)
Gonadal “MOSAICISM”: (only gametes have mutated cells)
The fragile X syndrome is a learning disability genetic disorder caused by a mutation of the FMR-1 gene on the X chromosome. Mutation at that site is found in 1 out of about every 2000 males and 1 out of about every 259 females. (Incidence of the disease itself is about 1 in every 4000 females.) The number of trinucleotide repeat diseases is growing every year:
Leber’s Hereditary Optic Neuropathy (LHON) or Leber optic atrophy is a mitochondrially inherited (mother to all offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision; this affects predominantly young adult males. However, LHON is only transmitted through the mother as it is primarily due to mutations in the mitochondrial (not nuclear) DNA and only the egg contributes mitochondria to the embryo.
Genomic imprinting is a genetic phenomenon by which certain genes are expressed in a PARENT-OF-ORIGIN specific manner.

62. MOLECULAR DX by DNA PROBES
BIRTH DEFECTS, PRE- or POST- NATAL
TUMOR CELLS
CLASSIFICATIONS of TUMORS
IDENTIFICATION of PATHOGENS
DONOR COMPATIBILITY
PATERNITY
FORENSIC
My #1 peeve, is people who identify pathology with forensic pathology. It shows they have been watching WAY too much TV.

63. Immuno- Antigen Proteins
H&E tissue structures
Immuno- Antigen Proteins
GENES that
MAKE those
PROTEINS
Evolution of tumor classifications: 1) Histology 2) Immunochemistry 3) Gene micro-arrays