Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

Metabolism and possible health effects of aluminum.

The genetic characterization of chronic lymphocytic leukemia (CLL) has made significant progress over the past few years. While conventional cytogenetic analyses only detected chromosome aberrations in 40-50% of cases, new molecular cytogenetic methods, such as fluorescence in situ hybridization (FISH), have greatly enhanced our ability to detect chromosomal abnormalities in CLL. Today, genomic aberrations are detected in over 80% of CLL cases. Genes potentially involved in the pathogenesis were identified with ATM in a subset of cases with 11q deletion and p53 in cases with 17p13 deletion. For the most frequent aberration, the deletion 13q14, candidate genes have been isolated. Genetic subgroups with distinct clinical features have been identified. 11q deletion is associated with marked lymphadenopathy and rapid disease progression. 17p deletion predicts for treatment failure with alkylating agents, as well as fludarabine and short survival times. In multivariate analysis 11q and 17p deletions provided independent prognostic information. Recently, another important issue of genetic risk classification in CLL was identified with the mutation status of the immunoglobulin variable heavy chain genes (V(H)). CLL cases with unmutated V(H) show more rapid disease progression and shorter survival times. Whether CD38 expression can serve as a surrogate marker for V(H) mutation status is currently discussed controversially. V(H) mutation status and genomic abnormalities, such as 17p and 11q deletion, have recently been shown to be related to each other, but were of independent prognostic information in multivariate analysis. Moreover, genomic aberrations and V(H) mutation status appear to give prognostic information irrespective of the clinical stage and may therefore allow a risk assessment for individual patients early in the course of their disease.

Genetics of chronic lymphocytic leukemia: genomic aberrations and V H gene mutation status in pathogenesis and clinical course

Clustering of aberrations to specific chromosomes in human neoplasms. IV. A survey of 1,871 cases.

This survey of chromosomal aberrations in human neoplasms comprises 1,871 cases distributed on 15 groups of malignant disease, viz. 4 groups of myeloproliferative disorders with 1,328 cases, 5 groups of lymphoproliferative disorders with 369 cases and 6 groups of solid tumors with 174 cases. The material is presented in 17 tables, in which the variation of each chromosome is listed separately for each geographic region. In the discussion part a number of special problems are looked into. The difference in variation between the individual chromosomes was highly signifcant statistically. Within each tumor, all chromosomes which exceeded the average variation with more than 1 standard deviation were considered selectively involved. In all neoplasms taken together, the chromosomes selectively involved clustered to 15 of the 24 human chromosome types. Other topics taken up for discussion were the following: possible differences in chromosome variation between geographic regions; the specificity of certain marker chromosomes; the hypothesis of 2 essentially different kinds of chromosome aberration in cancer. The phenomena of genic amplification and recurrent translocation often found in cancer require the assumption of unorthodox cytogenetic mechanisms. One main conclusion of the paper is that the aberrations of the selectively involved chromosomes influence cancer development because of the genes they carry.

Clustering of aberrations to specific chromosomes in human neoplasms

Nonrandom chromosomal aberrations in chronic lymphocytic leukemia revealed by polyclonal B-cell-mitogen stimulation.

Chromosome analyses have revealed abnormalities in many cases of lymphoma, non-lymphocytic leukaemia and acute lymphoblastic leukaemia. Most studies on chronic lymphocytic leukaemia (CCL), however, have shown normal karyotypes1–4 although chromosomal abnormalities have been reported5,6 . In most of these studies specific surface marker analyses on leukaemic lymphocytes have not been carried out. It has been difficult to establish whether the metaphases seen in the majority of the CLL studies were from normal or from leukaemic cells. Recently, in one of our laboratories special interest has centred on cases of CLL with monoclonal serum protein bands; in two such cases with immunoglobulin M (IgM) bands, it was demonstrated with idiotypic antisera against the serum IgM band that the leukaemic lymphocytes were the precursors of plasma cells responsible for the monoclonal serum IgM7,8. In addition, the leukaemic lymphocytes of these patients could be stimulated in vitro to divide and to differentiate to plasma cells8. Epstein–Barr virus (EBV)-transformed lymphoblastoid cell lines were obtained from the two patients. With the idiotypic determinants as leukaemia specific markers, certain of these lines were shown to be derived from leukaemic cells9. Thus, rapidly proliferating populations of cells, which could be identified with certainty as being of CLL origin, were available for chromosome analysis. In the present study, conventional G- and Q-banding techniques for karyotypic analysis were carried out on the leukaemic lymphocytes induced to divide in vitro and on the cells of the leukaemic lymphoblastoid lines. Aneuploid karyotypes were found in the leukaemic B cells of both patients.

Chromosome abnormalities of leukaemic B lymphocytes in chronic lymphocytic leukaemia

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Chromosome abnormalities of leukaemic B lymphocytes in chronic lymphocytic leukaemia