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M Pollard

Publications and source records attributed to M Pollard.

184 records · Page 11Linked to original sources

Immunotherapy by BCG against prostate adenocarcinomas in anatomical compartments.

The prostate adenocarcinoma-III (PA-III) cell line manifests a high rate of metastasis from the SC tumor site through lymphatic channels to the lungs in which they produce visible focal tumors. i.v. inoculation of BCG interfered with the passage of PA-III cells to the lungs; but not if the BCG was inoculated IP. IP inoculation of BCG suppressed propagation of PA-III cells in the peritoneal cavity, but there was no effect on metastasis of PA-III cells from a SC PA-III tumor to the lungs. Inoculation of BCG did not induce a systemic anticancer effect unless PA-III cells and BCG occupied the same anatomical compartment. Two compartments are described: intravascular and intraperitoneal.

Adenocarcinoma↗

The antimetastatic effect of IV-inoculated BCG on adenocarcinomas in the prostate-seminal vesicle complex of L-W rats.

Adenocarcinomas were induced in the prostate-seminal vesicle complex of Lobund-Wister (L-W) rats by a single IV inoculation of N-methyl-N-nitrosourea. This was followed by three slow-release S.C. implants of testosterone propionate, each at intervals of 2 months. Small (0.5 cm diameter) palpable tumors developed which enlarged during the following month to 3-4 cm diameter. At the latter stage, tumor cells spread via lymphatics to the lungs and/or by direct extension into the peritoneal cavity. Rats with small palpable tumors were inoculated IV with viable Bacillus Calmette-Guerin (BCG). One month later, the rats were killed and examined. Untreated rats with large tumors served as controls. Comparison of the two groups revealed that body weights and tumor sizes were similar and most of them had developed metastatic tumors in the peritoneal cavity. However, lung metastases were rare in the BCG-inoculated rats compared to controls. Spleen and liver weights were significantly heavier in the BCG-treated rats. It is speculated that an intra-vascular mechanism(s), engendered by BCG, immobilized the circulating tumor cells, but not those tumor cells that spread by direct extension from the primary tumor into the peritoneal cavity.

Adenocarcinoma↗

The anti-metastatic effect of intravenously-inoculated BCG on prostate tumor cells.

The complication of metastasis from the primary tumor site to the distant organ is difficult to control. Tumor cells usually spread through the vascular system: lymphatics and/or blood; or by direct extension into adjacent sites. Transplantable prostate adenocarcinoma (PA-III) cells in L-W rats produces a tumor in the implant site and then spreads via the ipsilateral lymphatic route to the lungs in which new visible tumors develop. Viable bacillus Calmette-Guerin (BCG) was inoculated SC or IV into rats which were then inoculated either SC or IV with PA-III cells. They were examined thereafter for primary and for lung tumors. IV-inoculated BCG generated a strong intravascular intervention mechanism on metastatic PA-III cells in L-W rats. This immobilization mechanism was not demonstrable in rats that had been inoculated SC with BCG.

Adenocarcinoma↗

Phenobarbital promotes multistage pulmonary carcinogenesis in MNU-inoculated L-W rats.

Lobund-Wistar (L-W) rats develop adenocarcinomas spontaneously in the accessory sex glands (prostate-seminal vesicles) (P-SV) in the livers and in the lungs-all after long periods of latency. This report addresses (a) the multistage pattern of induced lung carcinomas in L-W rats and (b) the role(s) of two putative promotional agents (testosterone propionate (TP) and phenobarbital (PB) in the development of carcinomas in the lungs of L-W rats. Lung cancer is a rare slow-growing spontaneous neoplasm in L-W rats. Their incidence increased from 4.4% in avg 25.6 months (spontaneously) to 23.8% in avg 19 months following a single IV inoculation of methylnitrosourea (MNU), and further increased to 57% in avg 15 months by adding phenobarbital to the diet of MNU-inoculated rats. Three stages of lung tumorigenesis were manifested in L-W rats following treatments with MNU, or MNU + PB: hyperplasia, adenoma, and carcinoma.

Adenocarcinoma↗