-Philadelphia Chromosome

-9q-22q Translaocation

-ABL-BCR chimeric gene

-Myeloproliferative disorder 

-Drives Proliferation of granulocytic and megakaryocytic progenitors and release of immature granulocytic forms into the blood

-Blast Crisis can be of any myeloid cell type

-Mainly a disease of adults 

-8q-14q Translocation causing c-MYC Gene Mutation that leads to increased activity

-Starry Sky pattern of cells

-Occurs in Germinal Center B-Cells

-Found in children and young adult

-Manifest at extra nodal sites

-Sporadic- Abdominal and pelvis viscera

-Endemic- EBV associated: Jaw, Skull

-CD10, 19, 20, TdT-, Slg+, BCL6+

14-18 translocation

BCL2 gene mutation

antiapoptosis of B-Cells

Comes From germianl center B cells

Cells express CD 19, 20, 10, surface Ig, and BCL6

Normal Follicular center B cells are BCL 2 (-), but BCL 2 is expressed in 90% of cases.

Affiliated with dendritic cells

Usually in adults and low grade

-Excess Lymphocytes in Bone Marrow

-1-19 Translocation and 12-21 Translocation

-TCF3-PBX1 Gene Mutation

-Neoplasm Composed of Immature B-Cells (85%) or T-Cells (TdT+)

-Most Common Cancer of Children

-B-Cell-CD19 and CD10, MLL gene mutation(9,22)

-T-Cell-CD3, CD7

15-17 Translocation

RAMA-PML Gene Mutation

-11-14 translocation (rare)

-Usually Caused by a deletion

-BCL1 gene mutation

-Most Common Leukemia for adults

-Peripheral B-Cell Neoplasm

-Express CD19, CD20, CD23, CD5

-Disrupts normal immune function through -unknown reasons

-Can undergo Richter Syndrome and transform into DLBCL. 

-Diffuse Pattern of Growth

-Low Grade

-Germinal Center or post germinal center B cells

-Most Common Form of NHL in older adults

-Peripheral B cell neoplasm

-Cells express CD19 and 20 and most have surface Ig.

-Generally have an over expression of BCL6

-Less frequently has a 14-18 trans of BCL2 if developed from lymphoma

-Subtypes can be caused by EBV or AIDS

-High Grade

c-MYC

BCL2

BCL6

p53

NOTCH1

Cyclin D

BCL10

MALT1

-Plasma Cell Neoplasm involving the skeleton

-Punched out lesions in bone

-Somatic Hypermutation of post germinal cells

-Net increase in osteoclast and bone reabsorption promoted by IL-6 (leads to high calcium)

-Many Different Translocations (Robbins pg.609)

-Disease of the elderly

-Production of Monoclonal antibodies by plasma cells

-Bence Jones Proteins

-B-Cell Neoplasm of Older adults

-Plasma cells secrete IgM, and cause Walden-Strom

-No Bone destruction observed

-Markers are CD20 and surface Ig

-Usually a deletion in Chrom 6q

-Tumor cells resemble the normal mantle zone b cells that surround the germinal center.

-Express high levels of Cyclin D- t(11:14) 

-Most express CD 19, 20, and surface Ig

-Usually CD5+ and CD23-

-Diffuse pattern with small wrinkled lymphocytes

-Marginal zone B-cell neoplasm of older males

-Express's pan B-cell markers (19,20) and CD11c, CD25, CD103

-Post Germinal Center memory B-Cell origin

-Indolent with peripheral pancytopenia, dry tap, and splenomegaly.

-Cells appear hairy and Contain acid phosphatase

-NOS: Mature peripheral T-Cells

-Diffuse with a mixture of large and small cells

-Poor Prognosis

-Mature peripheral T-Cells

-ALK gene mutation- Active Tyrosine Kinase

-Effects younger population

-Will respond to aggressive chemotherapy

-Diffuse with a mixture of large and small cells

-Poor Prognosis

-HTLV+, CD4+

-Large pick cells w/ wright stain

-Cytotoxic (CD3) or NK cell (CD56)

-Indolent CD8+

-Neutropenia and Anemia

-Peripheral Blood

-Can lead to Sinonasal NK cell Lymphoma

-EBV associated but Unknown infection route

-Poor prognosis in advanced cancers

-Occurs at just one node or chain of nodes

-Contains Reed-Sternberg Cells (eye-ball)

    -Release facotrs that cause accumulation of            Immune Cells

    -Derived from germinal center B cells

-32 AAO, common among children and young adults

-Curable in most cases

-Lymphocyte Predominant (Pop Corn Cells)

     -CD45, CD 20

-Classical (RS cells)

     -CD 15(leu M1), CD 30 

-Progenitor Cell Tumor- Impedes differentiation

-Leads to immature myeloid blast in the marrow

-2 Theories of how they proliferate- See Notes

-Effects all ages but increases with age

-Clinical:Anemia, Neutropenia, Thrombocytopenia

-Symptoms: Fatigue, Fever, Spontaneous Bleeding

1. Nodular Sclerosis 

2. Mixed Cellularity 

3. Lymphocyte Rich

4. Lymphocyte Deletion

5. Lymphocyte predominance

M0-TdT (-), and early Myeloid antigens

M1-Nothing defining, some MPO(+)

M2-t(8,21)

M3-t(15,17) Retinoic Acid Receptor Mutation

M4-inv16- MPO+

M5-MPO(-), heterogeneous

M6-50% of BM is neoplastic erythroblast

M7-Megakaryoblastic Features (vWF and Gp2)

1)AML w/Genetic Aberrations 

    -t(18,21), t(15,17), inv(16)- favorable

    -t(11q23,v)- poor

2)Associated w/ MDS

    -poor prognosis

3)Following Chemotherapy

    -Very poor prognosis

4)Not otherwise specified

   -All have intermediate prognosis

-T-Cell neoplasm involving the skin

-CD4+ 

-Effects elderly

-Sezary Syndrome- Leukemic cell phase"bright red"