ABSTRACT
General concepts 361 Precursor lymphoid cell neoplasms 362 The uterus as a site of leukemogenesis 362 Heterotopic gene expression in the thymus 362 Block of differentiation in precursor B cell neoplasms 364 Deregulated signal transduction in precursor lymphoid 365
cell neoplasia Mature lymphoid cell neoplasms 365 The tumor cell 365 The B cell receptor: antigen stimulation in mature 365
B cell neoplasms The germinal center reaction as a site of chromosomal 366
translocation and aberrant somatic hypermutation The origin of some mature lymphoid cell neoplasms may 371
be traced to precursor B cells
Disordered cell cycle as a primary alteration in 371 lymphomagenesis
The master role of the nuclear factor κB system 372 Foreign DNA material in the tumor clone 373 The microenvironment 373 The host 374 The host genetic background 374 Host infection with microorganisms associated with 374
lymphomagenesis The host immune system as a determinant of 375
lymphomagenesis Key points 376 References 376
Some general molecular features are shared by all lymphoid neoplasms: (1) molecular lesions predominantly affect genes regulating lymphoid maturation, cell cycle progression, and cell survival; (2) within a given clinico-pathological category, different genetic lesions in different patients may converge upon activation or disruption of the same molecular pathway; (3) many, though not all, genetic lesions are represented by recurrent and balanced chromosomal translocations; (4) the degree of generalized genomic instability is markedly lower than observed in solid cancers; and (5) a single genetic alteration is rarely, if ever, capable of driving the full development of a lymphoid neoplasm.
