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Biomedical subjects

A Telerman

Publications and source records attributed to A Telerman.

25 records · Page 2Linked to original sources
PubMed1987

The cDNA sequence and gene analysis of the human pim oncogene.

The putative oncogene pim-1 is frequently activated by provirus insertion in MuLV-induced T cell lymphomas in mice. By analogy with other cellular oncogenes that are similarly activated (e.g., myc, myb, erbB) it is possible that pim-1 may also be involved in some human tumors. To study human pim-1 we cloned and sequenced human pim-1 cDNA clones. The human pim-1 codes for a protein of 313 amino acids (aa) which is highly homologous (94%) to the deduced amino acid sequence of mouse pim-1. All the mouse pim-1 residues which are homologous to protein kinases are conserved in the human pim-1. We also isolated the human pim-1 gene and mapped it relative to the cDNA. The RNA transcript of human pim-1 is approx. 3.0 kb and it is highly expressed in the erythroleukemia cell line K562.

Animals↗
PubMed1985

Gastrointestinal metastases from extra-abdominal tumors.

Over a period of 4 years, metastatic lesions to the gastrointestinal tract were analysed in postmortem and clinical series. Melanoma, breast and lung cancers were the most common primary lesions. The topography of parietal involvement shows that all patients evidenced tumor involvement of the submucosa, but not all of them revealed invasion of the mucosa and serosa, suggesting a hematogenous route of dissemination. Although almost all cases had widespread disease at the time of referral for diagnosis, patients who were submitted to surgery had a median survival of 8 months (range 1-48). In selected cases, surgery offers good palliation and may permit resumption of otherwise active chemotherapeutic treatments.

Adult↗
PubMed1984

Lactoferrin: no evidence for its role in regulation of CSA production by human lymphocytes and monocytes.

Lactoferrin (LF) has been recently proposed as a physiologic regulator of the granulocyte monocyte progenitor (CFU-GM). This glycoprotein, when saturated with iron, has been said to limit CFU-GM growth by decreasing production and release of colony stimulating activity (CSA) by monocytes and macrophages. Human milk LF saturated with iron, at concentrations ranging from 10(-18) to 10(-8) M was added either to endogenously stimulated bone marrow cells or to mononucleated cells used as feeder layers for adherent cell-depleted marrow. Irrespective of the concentration of LF within the culture system used, no significant inhibition of CFU-GM growth was observed. Moreover, the CFU-GM stimulating activity of medium conditioned by a 4-day incubation of 1 X 10(6) mononucleated blood cells in the presence or in the absence of LF was the same. Various possible explanations for not confirming the reported inhibiting activity of iron saturated LF were explored: 1) masking inhibition of the system by prostaglandin E2 (PGE2), 2) masking inhibition of the system by bovine LF still detectable in the fetal calf serum after heating, 3) preinhibition of the system by leukemic-associated inhibitory activity (LIA) possibly present in the culture system, 4) the iron and calcium content of the culture medium used, 5) the fixation of LF to plastic compounds, 6) the source of the human LF used, 7) the marrow cell separation methods used. None of these factors was shown to play a role in vitro in the activity of LF and thus no evidence was found for a significant role of LF in the regulation of CSA production by monocytes. Peripheral blood human monocytes isolated by elutriation and incubated in albumin free medium in the presence of either 125I-LF or colloidal gold-labeled LF showed no LF binding.

Animals↗
PubMed1982

A case of chronic aneosinocytosis.

A 59-year-old woman, after complete recovery from an episode of drug-induced agranulocytosis, was found to sustain a chronic absence of recognizable mature and immature eosinophils in blood and bone marrow during a follow-up period of 8 years. Her bone marrow and peripheral blood cells cultured in vitro were able to produce normal numbers of eosinophil colonies. The present disorder was thus not caused by a lack of EO-CFU-C, nor by a defect in EO-CSA, nor by an immunologically mediated mechanism acting on mature or immature eosinophils or on EO-CSA producing cells. It is suggested that the marrow was not able to differentiate normally along the eosinophil pathway, possibly owing to a microenvironmental defect or, less likely, an intrinsic stem cell defect.

Agranulocytosis↗