Pulmonary Adenomata Research Articles

Characterization of a neoplastic epithelial cell strain derived by dexamethasone treatment of cultured normal mouse type 2 pneumocytes

The epithelial cell strain NAL1A cultured from normal adult mouse lung has been transformed by culturing in dexamethasone into an invasive neoplastic cell strain. The criteria for neoplastic transformation include the capacity for anchorage independent growth in soft agar as well as the formation of invasive neoplastic nodules after subcutaneous transplantation in thymectomized irradiated newborn mice. The cells of the invasive neoplastic nodules induced by dexamethasone culturing of NAL1A were indistinguishable histopathologically and by electron microscopy from invasive nodules evoked by the subcutaneous inoculation of CMT64, a cell line cultured from a metastasizing mouse lung tumour and cell strain NUL1 derived from mouse pulmonary adenomata induced by urethane. Cells of the nodules derived from all three cultured strains possessed desmosomes, surface microvilli and phospholipid lamellar bodies characteristic of the type 2 pneumocyte. It is concluded that cultured cell strains NAL1A, cultured in dexamethasone, NUL1 and CMT64 evoke invasive subcutaneous neoplasms derived from a common ancestor, presumably a type 2 pneumocyte related stem cell.

The multipotential carcinogenic action of N-ethyl-N-nitrosourea administered neonatally to mice.

Newborn A, C57BL, DBAf and IF mice were injected s.c. with a range of doses of N-ethyl-N-nitrosourea (ENU). A high proportion of treated mice developed tumours, particularly hepatomata, pulmonary adenomata and carcinomata, and malignant lymphomata of thymus and spleen. Liver tumours occurred most frequently in C57BL and DBAf mice, lung tumours in A mice, and lymphomata in A and DBAf mice. A small proportion of C57BL, DBAf and IF mice developed tumours of the nervous system. The results are discussed with reference to the ready induction of nervous system tumours in similarly treated rats, and their relevance for human cancer.

Cell kinetics of urethane-induced murine pulmonary adenomata: II, the growth fraction and cell loss factor.

Continuous labelling of urethane induced pulmonary adenomata in adult male A2G mice at intervals up to 20 weeks showed that the growth fraction fell progressively from 18% at 7 weeks to 7% at 20 weeks. This fall appears to be wholly responsible for the decrease in production of adenoma cells with age. A fraction labelled mitoses curve was constructed for pulmonary adenomata at 14 weeks post urethane. Only the first peak was apparent, giving median t2 and ts values of 2 and 9 h respectively. The cell cycle time was calculated at 45 h and the growth fraction at 6-2%, whilst the cell loss factor was estimated at 31%. Other cell loss values were calculated from data on the rate of entry into DNA synthesis obtained previously by double labelling. These values remained constant with time at 83-95%, suggesting that cell loss is in some way linked to cell production. However, the development of polyploidy in adenoma cells could not be eliminated. No areas of necrosis were seen in the adenomata at any time although karyorrhexis occurred in isolated cells. The labelling characteristics of alveolar wall cells in the same lung sections as the adenomata did not vary with time and the continuous labelling curve gave a growth fraction of 1-8%, a DNA synthetic time of 10 h and a cell cycle time of 30 h.

Cell kinetics of urethane induced murine pulmonary adenomata: I. The growth rate.

A single injection of urethane into adult male A2G mice produced an increase in the proliferative rate of alveolar wall cells, reaching a peak at 2 weeks post urethan (PU) and declining to control levels by 2 months PU. During this urethane induced proliferative response the single and double labelling indices and the native metaphase index were all elevated although there was no corresponding alteration in the arrested metaphase index. This proliferative response may not be restricted to hyperplasia of potentially neoplastic cells, such as type II epithelium, but may also include type I epithelial cells and alveolar macrophage precursors. However, it was impossible to identify individual cell populations by methods used. The growth rate of adenomata decrease with time and cell kinetic techniques showed that the rates of entry of adenoma cells into DNA synthesis and into metaphase were decreasing concurrently with the growth rate. Thus the rate of cell production falls as adenomata age but how much cell loss contributes to the decrease in growth rate is not yet known. Decreasing cell production could be due to an increased cell cycle time and/or a decreased growth fraction. The duration of DNA synthesis in adenomata increased markedly as the mice survived, suggesting that the cell cycle time might be increased, but further experiments are required to determine whether the growth fraction changes. Attention is drawn to a complication that Colcemid introduces into kinetic studies on alveolar wall cells.

Demonstration of virus particles in ovine pulmonary adenomata.

Elektronenmikroskopischer Nachweis bei Lungen-Adenokarzinomen von Schafen, dass diese jeweils zusammen mit Viruspartikeln auftreten, die morphologisch solchen aus verschiedenen spontanen und ubertragbaren Neoplasmen von Geflugel, Nagetieren und Katzen ahnlich sind.

Pulmonary adenomata induced by carcinogen treatment in organ culture. Influence of increasing amounts of carcinogen.

Explants of lung from 1 month old inbred BALB/c mice were cultured in vitro for 4 days with 3-methylcholanthrene added to the culture medium at various dose levels. They were subsequently implanted subcutaneously into 6-week-old mice of the same strain.Lung adenomata appeared in a high proportion of explants.

Pulmonary Adenomata Induced by Carcinogen Treatment in Organ Culture. Influence of Duration of Treatment

Pulmonary Adenomata Induced by Carcinogen Treatment in Organ Culture. Influence of Duration of Treatment

Evaluation of Primary Carcinoma of the Lung and Survival Rate after Curative Resection in a Large City Hospital

Los autores exponemos nuestra experiencia en el diagnóstico de la hidatidosis pulmonar, presentando 76 quistes hidatídicos en 72 pacientes estudiados.Destacan la importancia de la epidemiología, una exhaustiva historia clínica y el escaso valor de la exploración física, así como los datos de laboratorio general. Consideramos la intradermorreacción de Cassoni como la prueba biológica más eficaz, preponderando sobre todo el estudio radiológico simple y tomográfico, así como la tomografía axial computarizada (TAC) y ecografía, encontrando poco valor a la broncoscopia, broncografía, gammagrafía pulmonar, citología del esputo y arteriografia pulmonar.Al final exponemos el exacto valor de la toracotomía exploradora a veces como el único medio diagnóstico para esta afección.We describe our experience in the diagnosis of pulmonary hydatidosis with seventy-two patients in whom seventy-six hydatid cysts were seen.Factors of importance were: epidemiology, exhaustive clinical history, low valué of physical examination and general laboratory findigns.We consider Cassoni’s intradermal reaction as the most significant biological test. Simple radiologic and tomographic studies together with computed axial tomography (TAC) and echography are more valuable diagnostic procedures than are bronchoscopy, bronchography, pulmonary gammagraphy, pulmonary arteriography and sputum cytology.The valué of thoracotomy which at times may be the only exploratory procedure possible for the diagnosis of hydatidosis, is also discussed.

Pulmonary adenomata induced by carcinogen treatment in organ culture.

Pulmonary adenomata induced by carcinogen treatment in organ culture.

A study of the effects of zinc and tin administered orally to mice over a prolonged period

Mice which received 1000 or 5000 ppm tin as sodium chlorostannate in drinking water or 5000 ppm tin as stannous oleate in their diet experienced a lower incidence of malignant lymphoma, hepatoma and pulmonary adenoma than untreated controls, and showed no other untoward effects. Mice which received 5000 ppm zinc as zinc oleate in the diet developed severe anaemia. Accordingly the level of zinc oleate was reduced to 1250 ppm. Prolonged feeding at this level failed to increase the incidence of malignant lymphoma or pulmonary adenomata above control levels. A slight but probably insignificant increase of hepatomata was recorded. The inclusion of 1000 or 5000 ppm zinc as zinc sulphate in the drinking water did not lead to an increased incidence of tumours at any site.

The Induction of Pulmonary Adenomata in Mice by Urethane

The Induction of Pulmonary Adenomata in Mice by Urethane

The Histology and Histogenesis of Pulmonary Adenomata of Mice

The Histology and Histogenesis of Pulmonary Adenomata of Mice