Intravascular lymphomatosis presenting as adult respiratory distress syndrome.

An unusual case of intravascular lymphomatosis caused by small noncleaved, non-Burkitt's lymphoma, which presented with adult respiratory distress syndrome, is described. Extensive invasion of the small- and medium-size blood vessels of the lung, liver, spleen, kidneys, heart, esophagus, stomach, small and large intestines, bladder, and brain-but not the bone marrow or peripheral blood-is documented. The possible mechanism and the unusual features of this case are discussed in comparison with previously reported cases. The pertinent literature is reviewed. The problem of diagnosing this pathological entity is emphasized.

Expression of a methotrexate-resistant dihydrofolate reductase gene by transformed hematopoietic cells of mice.

DNA-mediated gene transfer was used to introduce DNA from a methotrexate-resistant mouse fibroblast cell line into mouse bone marrow cells. This cell line contained a methotrexate-resistant dihydrofolate reductase, active at 10(-4) M methotrexate, which was electrophoretically separable from the wild-type mouse enzyme. Transformed hematopoietic cells were returned to irradiated mice and selected in vivo by methotrexate administration. Some recipients of transformed marrow cells expressed the electrophoretically distinct, methotrexate-resistant dihydrofolate reductase in hematopoietic cells. These observations suggest that successful transformation of marrow stem cells to methotrexate resistance is accomplished by insertion of a dihydrofolate reductase gene coding for a mutant enzyme that is highly resistant to methotrexate.

Insertion of new genetic information into bone marrow cells of mice: comparison of two selectable genes.

A system for insertion of new genetic information into mouse hematopoietic cells is described. Two selectable genes were examined: herpesvirus thymidine kinase and a mutant mouse dihydrofolate reductase. The DHFR system appears to be superior in terms of the frequency and stability of gene insertion and expression in hematopoietic tissues. About 70% of mice had indirect (karyotypic) evidence of gene insertion; of these, about 60% (three of five) had stable expression of the inserted mutant DHFR. In contrast, only 13% of mice demonstrated stable karyotypic transformation by HSVtk, and of those with stable transformation five of seven showed persistent viral gene sequences in hematopoietic tissues.

Growth hormone stimulation of normal and leukemic human T-lymphocyte proliferation in vitro.

In order to investigate the effect of human growth hormone on T lymphocytes, we utilized a clonogenic assay for mitogen-responsive human peripheral blood T lymphocytes. Lymphocytes were purified by density gradient centrifugation and incubated in the presence of phytohemagglutinin using a two-layer agar technique for CFU- T-lymphocyte culture. Nanogram concentrations of human growth hormone, ovine prolactin, human chorionic somatomammotropin, or growth hormone fragment were added to cell cultures. Growth hormone potentiated normal T-cell colony formation in a species-specific manner. Cells from a homogeneous T-lymphoblast line derived from a patient with a T-cell variant of hairy cell leukemia also showed augmentation of colony growth in the presence of human growth hormone. These studies provide evidence for a direct effect of growth hormone on normal and some neoplastic human T cells.

Insertion of a new gene of viral origin into bone marrow cells of mice.

DNA containing the herpes simplex virus thymidine kinase (HSVtk) gene was used to transform wild-type tk+ mouse L cells to a tk++ status in vitro using methotrexate as a selective agent. HSVtk DNA was also used to transform mouse bone marrow cells in vitro. Transformed marrow cells injected into irradiated and methotrexate-treated recipient mice gave rise to proliferating cells which in some cases dominated the marrow population and which contained HSVtk gene sequences.