The document discusses different types of leukemia, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). It describes the signs, symptoms, diagnosis, and classification of leukemias. The most common type of childhood leukemia is acute lymphoblastic leukemia (ALL), which accounts for approximately 80% of cases in children.
WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues : 2016 U...Ankit Raiyani
This is a complilation of expected changes in the myeloid neoplasms in the upcoming 2016 update of the "WHO classification of tumours of haematopoietic and lymphoid tissues".
Some of the changes may not be incorporated in the actual published book.
This compilation has been prepared from presentations from persons actually concerned with revision of the book. All credits goes to them.
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues : 2016 U...Ankit Raiyani
This is a complilation of expected changes in the myeloid neoplasms in the upcoming 2016 update of the "WHO classification of tumours of haematopoietic and lymphoid tissues".
Some of the changes may not be incorporated in the actual published book.
This compilation has been prepared from presentations from persons actually concerned with revision of the book. All credits goes to them.
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
AML:ACUTE MYELOID LEUKAEMIA
for medical colleges teaching faculty and students as well. it includes AML causes , histopathological slides of subclasses of Acute myeloid leukemia, classification , diagnosis, management modalities, complications .Acute leukemias are stem cell disorders characterized by malignant neoplastic proliferation and accumulation of immature and non functional hematopoietic cells in the bone marrow.
The neoplastic cells show increased proliferation and/or decreased apoptosis.
If the defect primarily affects the common myeloid progenitor (CMP) then it is called Acute myeloid leukemia.
Acute myeloid leukemia (AML) is a neoplastic disease characterized by infiltration of the blood, bone marrow, and other tissues by proliferative, clonal undifferentiated cells of the hematopoietic system.
AML is the result of a sequence of somatic mutations in a multipotential primitive hematopoietic cell or, in some cases, a more differentiated progenitor cell.
It can be slow growing or rapidly fatal.
AML is the predominant form of leukemia during the neonatal period
Incidence : 1.5/100,000/year in infants decreases to approximately 0.4 per 100,000 children ages 5 to 9 years, increases gradually to 1.0 persons per 100,000 until age 25 years, and thereafter increases exponentially until the rate reaches approximately 25/100,000 persons.
AML accounts for 15 to 20 percent of the acute leukemias in children and 80 percent of the acute leukemias in adults.
Men > Women (4.5 : 3)
HEREDITY
1) Chromosomal aneuploidy like Trisomy 21 noted in Down syndrome
2) Defective DNA repair, e.g., Fanconi anemia, Bloom syndrome, and Ataxia telangiectasia
3) Congenital neutropenia ie Kostmann syndrome
4) Germline mutations of CCAAT/enhancer-binding protein α (CEBPA), runt-related transcription factor 1 (RUNX1), and tumor protein p53 (TP53) have also been associated with a higher predisposition to AML
RADIATION
Peaks after 5 to 7 yrs of exposure.
Therapeutic radiation alone seems to add little risk of AML but can increase the risk in people also exposed to alkylating agents.
CHEMICAL AND OTHER EXPOSURES
Exposure to benzene, plastic, rubber, petroleum products, paint, ethylene oxide, herbicides and pesticides can increase the risk.
Smoking can also increase the risk
DRUGS
Anticancer drugs are the leading cause of therapy-associated AML.
Alkylating agent–associated leukemias occur on average 4–6 years after exposure, and affected individuals have aberrations in chromosomes 5 and 7.
Topoisomerase II inhibitor–associated leukemias occur 1–3 years after exposure, and affected individuals often have aberrations involving chromosome 11q23.
Other agents like Chloramphenicol, phenylbutazone, and, less commonly, chloroquine and methoxypsoralen.
SYMPTOMS :
Present with nonspecific symptoms initially.
Fatigue is the first symptom
Fever with or without infection will be present in approximately 10% patients
Bleeding, easy bruising
occasional
ACUTE MYELOID LEUKEMIA is a neoplastic disease characterized by
infiltration of the blood,
bone marrow, and
proliferative, clonal undifferentiated cells of the hematopoietic system.
acute leukemia
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2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
We all have good and bad thoughts from time to time and situation to situation. We are bombarded daily with spiraling thoughts(both negative and positive) creating all-consuming feel , making us difficult to manage with associated suffering. Good thoughts are like our Mob Signal (Positive thought) amidst noise(negative thought) in the atmosphere. Negative thoughts like noise outweigh positive thoughts. These thoughts often create unwanted confusion, trouble, stress and frustration in our mind as well as chaos in our physical world. Negative thoughts are also known as “distorted thinking”.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
The Art Pastor's Guide to Sabbath | Steve ThomasonSteve Thomason
What is the purpose of the Sabbath Law in the Torah. It is interesting to compare how the context of the law shifts from Exodus to Deuteronomy. Who gets to rest, and why?
The Indian economy is classified into different sectors to simplify the analysis and understanding of economic activities. For Class 10, it's essential to grasp the sectors of the Indian economy, understand their characteristics, and recognize their importance. This guide will provide detailed notes on the Sectors of the Indian Economy Class 10, using specific long-tail keywords to enhance comprehension.
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Model Attribute Check Company Auto PropertyCeline George
In Odoo, the multi-company feature allows you to manage multiple companies within a single Odoo database instance. Each company can have its own configurations while still sharing common resources such as products, customers, and suppliers.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
Unit 8 - Information and Communication Technology (Paper I).pdfThiyagu K
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3. Leukemia: is characterized by abnormal
proliferation of blood cells,usually
WBCs(Leukocytes).
Acute leukemia: rapid increase of immature
blood cells.
Chronic leukemia: excessive build up of
relatively mature, but still abnormal blood cells.
4. Leukemia results
- From somatic mutations in the DNA.
- By activating oncogenes or deactivating
tumor suppressor genes.
FACTORS:
Ionizing radiation
Viruses: HumanT-lymphotropic virus (HTLV-1)
Chemicals: Benzene,chemotherapy.
Smoking: slight increase in leukemia incidence.
Genetic predisposition: Down syn.,Fanconi anemia
5.
6. Normal hemopoiesis is finely tuned by hemostatic
feedback mechanisms involving cytokines and
growth factors that modulate the marrow output of
red cells, granulocytes and platelets.
These mechanisms are deranged in marrows involved
by myeloid neoplasms.
Loss of control on growth & survival and suppressor
fuctions.
CSBRP-SDUMC-Oct-2014
12. The most common malignant
neoplasms of childhood are Leukemias
Which one is the commonest type of
childhood Leukemias?
AML 10%
ALL 80%
CML 2-3%
JCML 1-2%
13. Myeloblast Promyelocyte Myelocyte Metamyelocyte Band Neutrophil
MATURATION
Adapted and modified from U Va website
Myeloid maturation:
14. Two types of classifications:
1- FAB classification
- degree of maturation & lineage of blasts
- usage of cytochemistry & IHC
2-WHO classification
- degree of maturation & lineage of blasts
- Immunophenotyping
- cytogenetic & molecular features
- clinical outcome
CSBRP-SDUMC-Oct-2014
16. 1. AML with recurrent genetic abnormalities
2. AML and MDS
3. AML -Tx related
4. AML not otherwise categorised
5. Myeloid Sarcoma
6. Myeloid proliferation related to Down
Syndrome
17. Most of the signs and symptoms are due to:
1-Anemia.
2-Leukopenia.
3-Thrombocytopenia.
Bicytopenia, Pancytopenia.
All symptoms associated with leukemia
can be attributed to other diseases,
consequently, leukemia is always
diagnosed by laboratory investigations.
24. AML M0, M1, M2 : Chloromas
AML M3 : DIC
AML M4, M5 : Gum hypertrophy
AML M7 : Mediastinal mass
(germ cell tumors)
CSBRP-SDUMC-Oct-2014
25.
26. 1. CBC a. Anemia
b. Trombocytopenia
c. WBC
High Normal Low
2. Coagulation Studies (M3-DIC)
3. Biochemical Studies
27. Bone marrow (>20% blasts)
- Morphology
- Cytochemistry
- Immunophenotyping
- Cytogenetics
Peripheral blood examination
blasts in almost all cases
Molecular Genetic Analysis
28. The diagnostic requisite of 20 percent type I and II
myeloblasts in the peripheral blood or bone marrow.
BLAST Equivalents:
1. In AML (M3), the predominant leukemic cell is
promyelocyte
2. In AML (M5A), the predominant proliferating cell is the
monoblast
3. In AML (M5B), the predominant cell is the
promonocyte.
4. The megakaryoblasts of acute megakaryoblastic
leukemia vary in morphology but uniformly lack the
cytochemical properties of myeloblasts.CSBRP-SDUMC-Oct-2014
29. < 1% of the normal bone marrow, not observed in
normal blood
Vary in size, but are usually large
Nucleus is delicate, large, round or oval, with
prominent nucleoli. Stain purplish red with
Wright stain. Chromatin stains evenly
Small to moderate amount of bluish nongranular
cytoplasm
Three major types:Type I, II, and III
30. Fine nuclear chromatin
2 to 4 distinct nucleoli
Moderate rim of pale to basophilic
cytoplasm
Without azurophilic granules
Type II
Delicate azurophilic granules in
the cytoplasm (up to 20)
Type III
Numerous azurophilic granules
in the cytoplasm
32. CYTOLOGIC FEATURES OF BLASTS IN AML & ALL
AML ALL
Blast size Medium to large, uniform Variable Small to medium
Cytoplasm
Fine granules may be
present
Usually scant, a few coarse
granules may be seen
Auer rods
Present in 60-70% of
cases
absent
Nuclear
chromatin
Finely dispersed Fine to coarse
Nucleoli 2-4, prominent 1-3, indistinct
33. Is an azurophilic linear structure (Single or multiple)
present in numerous blasts or in rare cells
• Present approximately 60 to 70 % of cases of AML.
• MPO, SBB, and CAE positive
The presence of an Auer rod in one or more blasts is
definitive evidence of AML.
(The finding is not specific for any one type of AML.)
34. CYTOCHEMICAL PROFILES OF ACUTE LEUKEMIAS
MPO
/ SBB
CAE NSE PAS AP
ALL _ _ + / -
Focally
+
75%
+ / -
Focal in T-
ALL
AML + +
+
Monocytic-
diffuse
- / + +
MPO-myeloperoxidase, SBB-Sudan balck B, CAE-chloracetate esterase, NSE-
non specific esterase, PAS-periodic acid schiff, AP-acid phosphataseCSBRP-SDUMC-Oct-2014
cvcv
39. FAB Immunological marker
AML with minimally differentiated CD13,CD34, HLA-DR,
CD33,CD117,CD2,CD7,TdT
AML without maturation CD13,CD14,CD33, CD34
AML with maturation and with
t(8;21)
CD34,CD56
Acute promyelocytic leukemia CD13,CD33, HLA-DR absent, CD34
negative
Acute myelomonocytic leukemia
with abnormal eosinophils and
inversion 16
CD13,CD34,CD11b,CD11c,CD14,CD33
Acute monocytic leukemia and 11q23
abnormalties
CD14,CD4,CD36,CD64
Erythroleukemia Glycophorin 7,Transferrin receptor CD71
Acute Megakaryocytic leukemia cCD41,cCD42b,cCD61
41. 5% of AML cases
No definite evidence of myeloid differentiation can be given by
morphology & cytochemistry.
Blasts resembles M1 blast and L2 Lymphoblast
PS: Large cells with pale grey blue CYTOPLASM
NUCLEUS has opened fine chromatin with >= 1 nucleoli
Cytochemistry:
< 3% blasts reactive for MPO, SBB or NSE
Immunophenotyping:
20% blasts express one or more myeloid antigens: CD13,
CD14, CD33
may beTdT positive;
44. 15-20% of all AML cases
M1 is differentiated from M2 by the fact that
>90% blasts of non erythroid cells
<10% of marrow nucleated cells are promyelocytes or more
mature neutrophils
PS: Blasts have variable N/C ratio with pale basophilic CYTOPLASM
NUCLEUS has 1-4 nucleoli
Cytochemistry:>3% blasts reactive for MPO or SBB.
Immunophenotyping: Blasts express myeloid antigens: CD13, CD14,
CD33.
45. BLOOD SMEAR BONE MARROW SMEAR
BLAST WITH PALE TO BASOPHILIC AGRANULAR CYTOPLASM ,
NUCLEI WITH FINE CHROMATIN & PROMINENT NUCLEOLI
46. Commonest (30%) of all AML
Evidence of maturation to promyelocytes and more mature
neutrophils in 10 percent or more of the cells.
PS: Blasts are large with pale basophilic CYTOPLASM
NUCLEUS: oval to indented with 2-3 nucleoli
Cytochemistry: MPO, SBB, CEA +ve
Immunophenotyping: CD15, CD13, CD33 +ve
In t(8,21) associated cells: Pathognomonic
40-80% are positive for CD19
20% areTdT positive
48. A form of AML characterized primarily by a
proliferation of abnormal promyelocytes.
It is usually accompanied by
• DIC
• t(15;17)
The disease presents in two morphologic types:
1) hypergranular APL
predominant cell is an abnormal promyelocyte with
markedly increased and coarse azurophilic granules
2) microgranular or hypogranular APL
predominant cell is an abnormal promyelocyte with
diminished or small azurophilic granules.
49. The most common presenting symptoms, occurring in
90 % of patients, relate to hemorrhagic manifestations
and include
easy bruisability,
bleeding gums,
hemoptysis,
epistaxis, petechiae,
symptoms of gastrointestinal &
intracranial hemorrhage.
Basic pathology is DIC.
50. BONE MARROW SMEAR
HYPERGRANULAR
Nucleus : Folded, lobulated, granular
obscure border.
Cytoplasm: Prominent Azurophilic
granules.
Auer rods: Frequent, FAGGOT cells
( cells with bundles of auer rods)
56. >80% of leukemic cells are monocytic lineage
• Neutrophil component may constitute <20%
• Acute monoblastic M5a Vs monocytic leukemias M5b:
PS: Monoblasts >80% in monoblastic leukemia
Promonocytes are predominant in monocytic leukemias
Cytochemistry :SBB – Fine scattered granules in monoblast
NSE – Diagnostic
IFT: CD14, CD11b, CD11c, CD64, CD68
57. BLOOD SMEAR BONE MARROW SMEAR
MONOBLAST
80% or more are MONOBLAST
Abundant cytoplasm
Round nuclei with nucleoli
MONOBLAST WITH ABUNDANT
CYTOPLASM WITH FINE GRANULES
58. BLOOD SMEAR
BONE MARROW SMEAR
PROMONOCYTES
<80% Monoblast
Mature monocytes or
promonocytes predominate
59.
60. Def: Erythroleukemia by definition involves both the
granulocytes and erythroid cells
TYPES:
M6a Erythroleukemia
M6b PURE erythroleukemia
Erythroblast:
Relatively high nuclear/cytoplasmic ratio
Nucleus round with slightly condensed chromatin;
Nucleoli variably prominent
Deeply basophilic cytoplasm that may be vacuolated
61. 5% of AML cases
More COMMONTHAN pure erythroid leukemia.
Bimodal distribution- <20 yrs and >60yrs.
CRITERIA FOR DIAGNOSIS
>50% of nucleated marrow cells are erythroid lineage
>20% of nonerythroid cells are myeloblast
Dyserythropoiesis is prominent
Cytochemistry:
MPO +ve, PAS +ve
IFT: Glycophorin A +, CD13, CD33, CD117
63. Very rare
Also called ERYTHEMIC MYELOSIS ,
ACUTE Di GUGLIELMO SYNDROME
>80% of marrow cells are erythroblast
No significant myeloblastic component
65. AML M6 Case-3 Bone marrow smear, May-Giemsa stain, x1000
66. History: 47year old man with a
history of renal transplant as
well as refractory anemia with
ringed sideroblasts diagnosed 1
year back.
Now he has fatigue and loss of
weight. He is on cyclosporin
and prednisolone.
Source:CAP
AML M6b case-5
67. Investigations:
Blood count revealed anemia and thrombocytopenia and rare
blasts.
BM revealed 81% erythroid precursors, marked dysplastic
changes and “block-and-blush” PAS positivity of erythroid
lineage. There were 12% myeloblasts and minimal dysplasia of
granulocytic cell line.
Diagnosis:
Acute erythroleukemia-M6b (pure erythroleukemia).
AML M6b case-5
Source:CAP
68. 10% ofAML in children & 5% of adult AML
Bimodal distribution- Infancy and elderly
Most common leukemia seen in Down’s Syndrome.
May be associated with mediastinal germ cell tumors
CRITERIA FOR DIAGNOSIS
Megakaryoblast 20% or more in BM
Bone marrow fibrosis
MK blast:
12-18µm
Round nucleus with reticular
chromatin
1-3 nucleoli
Cytoplasm is basophilic and agranular
Cytoplasmic blebs
May resemble Lymphoblast
69. Morphologically confused with
- L2 subtype ofALL
- AML M1.
Diagnosis depends on
Elevated serum Lactate Dehydrogenase level.
Marked leucocytosis
Cytochemistry : MPO, SBB,TdT are negative
Some scattered PAS positivity
Immunophenotyping : CD41, CD61, Gp IIb/IIIa
70. Blast show distinct cytoplasmic blebs or psedopods formation
Peripheral blood – fragments of megakaryoblast
micromegakaryocytesOr dysplastic large platelets seen
73. Favorable:
younger age (<50)
WBC <30,000
t(8;21) – seen in >50% with AML M2
inv(16) – seen in AML M4 eos
t(15;17) – seen in >80% AML M3
Unfavorable:
older age (>60)
Poor performance status
WBC >100,000
Elevated LDH
prior MDS or hematogic malignancy
CD34 positive phenotype, MRD1 postive phenotype
del (5), del (7)
trisomy 8
t(6;9), t(9;22)
t(9;11) – seen in AML M5
FLT3 gene mutation (seen in 30% of patients)
75. CML is a clonal stem cell disorder characterised
by increased proliferation of myeloid elements at
all stages of differentiation.
15% of leukaemias.
It occurs most often between 40–60yrs
Incidence increases with age, M > F.
76. Philadelphia chromosome
Present in >80% of those with CML. It is a
hybrid chromosome comprising reciprocal
translocation between the long arm of
chromosome 9 and the long arm of
chromosome 22—t(9;22) forming a fusion gene
BCR/ABLon chromosome 22, which has
tyrosine kinase activity
77.
78. CML is characterised by 3 distinct phases
Chronic Phase:
Proliferation of myeloid cells, which show a full range
of maturation.
Accelerated Phase: decrease in myeloid differentiation
occurs.
Blast crisis: (acute leukemia)
79. 1) Chronic granulocytic leukemia
Classical CML with Ph chromosome +ve/ -ve
But bcr/abl 1 +ve
2) Atypical CML or Ph –ve CML
Monocytosis is intermediate b/w Classical CML & CMML
( 3-10%)
bcr/abl 1 –ve
3) Chronic myelomonocytic leukemia (CMML)
Ph –ve CML with predominance of monocytes in blood
( >10%)
80. Symptoms
Asymptomatic (50% of patients)
Fatigue
Weight loss
Abdominal fullness and anorexia
Abdominal pain, esp splenic area
Increased sweating
Easy bruising or bleeding
Signs
Splenomegaly (95%)
(50% of patients have a palpable spleen ≥ 10 cm BCM, Usually firm and non
tender)
Hepatomegaly (50%)
81. Approximately 85%of patients are diagnosed in the chronic
phase and then progress to the accelerated and blast phases
after 3-5 years.
The diagnosis of CML is based on
Histopathologic findings in the peripheral blood
&
Philadelphia chromosome in bone marrow cells
Investigation
CBC with differential
peripheral blood smear
bone marrow analysis
US using for liver/spleen
82. Peripheral blood – neutrophils 20,000 - >500, 000/ L
- basphilia
- LAP score
- blasts < 5%
- Nucleated RBCs
- Thrombocytosis
- Anaemia
Neutrophils and Myelocytes are PREDOMINANT
cells with blasts being < 3%.
83. PS shows increased Myelocytes and Mature
Polymorphs
85. Leukemoid
reaction
CML
WBC High High
Anemia (-) (+)
PBS Shift to the Left
Toxic granulation
Dohle bodies
Shift to the left (blast)
Eosinophilia,
basophilia
LAP score High Low
Philadelphia
chromosome
(-) (+)
86. Leukemias are clonal disorders
Mutations in oncogenes is the most common
underlying pathology
Present with: Anemia, Petichiae, infections,
hepatosplenomegaly, Lymphadenopathy
There may be normal, low or elevated total white
count.
87. AML is a heterogeneous disease
Blast count should be 20% in BM
There are blast equivalents
The presence of an Auer rod is definitive
evidence of AML
WHO classification is well accepted
Detection of genetic abnormalities dictates
Tx and Prognosis
