Hansemann, Boveri, chromosomes and the gametogenesis-related theories of tumours.

Theodor Boveri (1862-1915) is often credited with suggesting (in 1914) the first chromosomal theory of cancer, especially in terms of abnormal numbers of chromosomes arising in cells by multipolar mitoses in adult cells. However, multipolar mitoses in animal cells had been described as early as 1875, and Hansemann (1858-1920), in publications between 1890 and 1919, included this mechanism among various ways by which abnormal chromosome numbers might arise in cells and cause tumour formation. Both theories were conceived in a period when gametogenic ideas of tumour formation were current.

Alkylating agents and DNA polymerases.

Alkylating agents, for example nitrogen "mustards", are variably toxic, mutagenic, carcinogenic and teratogenic, but by mechanisms which have not been clearly established. In particular, the mechanisms both of their delayed toxic effects (which are primarily against dividing cells, in association with retardation of the rate of cell division, disruption of mitoses, and breakages and other abnormalities of chromosomes) and of their carcinogenic actions are not understood. The literature on the testing of thousands of analogues has demonstrated great variability of effects on the various cell biological phenomena, and no aspect of chemical structure or biochemical reactivity of these agents has been established as especially related to any particular effect.

Cancer morphology, carcinogenesis and genetic instability: a background.

Morphological abnormalities of both the nuclei and the cell bodies of tumour cells were described by Müller in the late 1830s. Abnormalities of mitoses and chromosomes in tumour cells were described in the late 1880s. Von Hansemann, in the 1890s, suggested that tumour cells develop from normal cells because of a tendency to mal-distribution and other changes of chromosomes occurring during mitosis.

Embryonic reversions and lineage infidelities in tumour cells: genome-based models and role of genetic instability.

Reversions to "embryonic precursor"-type cells and infidelities of tumour cell lineage (including metaplasias) have been recognized as aspects of various tumour types since the 19th century. Since then, evidence of these phenomena has been obtained from numerous clinical, biochemical, immunological and molecular biological studies. In particular, microarray studies have suggested that "aberrant" expressions of relevant genes are common.

The cell-type-specificity of inherited predispositions to tumours: review and hypothesis.

Most hereditary predispositions to tumours affect only one particular cell type of the body but the genes bearing the relevant germ-line mutation are not cell-type-specific. Some predisposition syndromes include increased risks of lesions (developmental or tumourous) of unrelated cell types, in any individual predisposed to the main lesion (e.g.

Carcinogen-induced impairment of enzymes for replicative fidelity of DNA and the initiation of tumours.

Not all carcinogens are mutagens, and many mutagens are not carcinogens. Among related chemicals, small changes of structure can markedly influence carcinogenic potency. Many tumours are genetically unstable, but some, especially 'benign' types, rarely exhibit 'progression' or show other evidence of genetic instability.

Cardiac involvement in a case of acute lymphoblastic leukemia.

We present an extremely rare case of an immunocompromised patient with a T-cell acute lymphocytic leukemia relapse presenting as a right atrial tumor. Problems in diagnosis, vulnerability due to previous immunosuppression and bone marrow transplant, and successful surgical excision are highlighted. Cardiac involvement with hematologic neoplasms should be taken with more than academic interest, as it may be amenable to treatment.