The major difference between these two groups of malignancies is that leukaemia is a defect in the growth and maturation of any of the blood forming cell lines of the bone marrow. Different leukaemias have different faults at different places in the growth and maturation cycle of blood forming cells. The result is infiltration of the bone marrow with lots of individual abnormal cells that are then released into the blood stream. This can not only involve both major types of white cells (myeloid or lymphoid) but also red blood cells and megakaryocytes (from which platelets derive). Leukaemia is often referred to as a liquid tumour. Lymphoma, however, is an abnormality of the lymphoid cells only and originates in lymphatic tissue, especially lymph glands, although it can also be found in gut, skin or indeed bone marrow tissue. These cells form structured lumps where the lymphoma cells' relationships with each other and supporting tissues are important. Lymphoma is therefore an example of a solid tumour. To confuse matters, lymphoma can ‘spill’ over into blood later in the disease in a leukaemic phase and leukaemia can infiltrate organs, typically the spleen, enlarging them and forming a lump. Leukaemia cells can occasionally form tumours as well, for example chloromas, in acute myeloid leukaemia.
Nonhodgkins Lymphoma, Mature Peripheral B cell CA, Follicular Lymphoma, poor Px 53 1-617+ 1218. +X 1418 or 8 14 -> BCL-2, > 6 Chromo breaks + Complex Karyotype, Burkitts Lymphoma, t(8;14), t(2;8), t(8;22)- chromo 2 has Myc, chemoRx --> 90% cure rate, MALT, H.Pylori Assoc MALT; Rx = Abx unless t(11;18)., Alot of t(14_) as well i.e., t(14;18), ALK+ Lg B cell Lymphoma, t(2;17) & t(2;5), Small Lymphocytic Lymphoma, aka - CLL, Highest genetic predisposition risk. FDR of CLL pt has 2-7 fold inc risk, Down Syndrome related MDS ~ GATA1 (X chromo) Px & GATA1 varies as a fx of child age, Trisomy 8, Mantle Cell, trisomy 12 = poor Px as well as .. rare t(8;14), p53, 3q+, 9q-, cyclin D1 genes, MM, risk of MM is 3.7 fold higher w/ FDR, 50% have 13q del & other remaining cytogenetic abnlties involve Translocations of chromo 14. > 90% older then 50yo, No cure, 3-4 yr survival, MGUS, 40-50% oinvolve 13q del, 40% hyperdiploidy, the rest scattered & involve chromo 14, Precursor B cell, B-ALL
HodgkinsLymphoma= Reed Sternberg Cells
Acute, ALL, Poor Px: t(9;22), 11q23, Hyperdiploidy. Good Px: 12;21, & hyperdiploidy. t(1;19) is another subtype, AML, Good Px w/ t(15;17), inv 16, t(8;21),, Poor Px = Inv 3, t(6;9), t(9;11)
5 q abnlty, MDS, 50% w/ cytogeneitc chnages, BM blasts @ < 20%, but somewhat hypercellular, Good Px = nl karyotype, Y-, 5q del, 20q del. Don't always have 5q-, Childhood MDS-Monosomy 7 worse Px then +8 or nl karyotype, 5q Syndrome, del of 5q as only abnlty, Females have good Px, hypo or nl marrow cellularity, blasts <5%
Chronic, CLL, -6, -11, -13 (inc freq), -17 (p53 on this chromo - worst Px), CML, Philidelphia Chromosome t(9;22)- ABL/BCR, Phili is also seen in 20% of adult ALL & some AML , childhood ALL, B cell lymphoblastic Leukemia, Extra skeletal myxoid, Chondrosarcoma, Gleevec
PNET/Ewing Sarcoma, Sarcoma = CA arising from Muscle, bone, fat, fibrous tissue, PNS, & Vessels, 85% of Ewing tunors w/ t(11;22)--> oncogenic chimera...
Rhabdomyosarcoma (RMS), Mesechymal tumor, varying degrees of striated muscle differentiation, E-RMS = Embryonal, hyperdiploid, A-RMS= Alveolar, Worse Px then E-RMS, t(2;13) Pax3 in translocation t(1;13) Pax7 in translocation
Synovial Sarcoma, t(X;18)& SSX1, SS18, SSX2, SSX4
Desmoplastic Small Round Cell Tumor, t(11;22)
Clear Cell Sarcoma, t(12;22)
Mixoid Round Cell Liposarcoma, t(12;16)
t(9;22)NR4A3 / EWSR1