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PubMed1975

Patterns of metastases in adenocarcinomas of man. An autopsy study of 4,728 cases.

This paper deals with 4,728 autopsy records collected at Roswell Park Memorial Institute, Department of Pathology. 1,436 adenocarcinomas provided the data to test whether certain adenocarcinomas had a higher propensity to seed metastatic organs than others. The data were subdiveded into four categories depending on the presence or absence of metastases at two keysites, i.e., lungs and liver. Metastatic keysites are defined as those organs whose chances of being seeded are the highest. Only adenocarcinomas were chosen to deal with the main theme discussed in the paper, i.e. soil specificity. "Soil specificity" is defined as a higher than expected occurrence of metastases at a particular organ, due to a primary adenocarcinoma, when compared to the overall group of adenocarcinomas. The location of the primary tumor and of the metastatic organ were taken into account to distinguish between a higher propensity to seed an organ either because of its anatomical proximity to the primary tumor or because of an affinity, possibly of biochemical nature. The presence or absence of metastases in lungs and liver clarifies the mode of spread of metastases, either by a direct spread, or by a cascade process which implies that no generalized metastases occur unless the lungs and liver are seeded.

Adenocarcinoma↗
PubMedDate not supplied

Splenic, thymic, bony and lymph node metastases from orthotopic human lung carcinomas in immunocompromised mice.

In orthotopic animal models of human lung cancer, bone and lymph node metastases have been observed with high frequency after periods of a few weeks, but metastases to other organs are rare. This study evaluated development of distant metastases over a six-month period in a model of orthotopic lung carcinoma in immunocompromised mice. Human A549 lung adenocarcinoma cells were stably transfected to express high levels of green fluorescent protein. Suspensions of 1 x 10(6) cells were instilled into the lungs of athymic and SCID mice to produce orthotopic human lung carcinomas. All animals had primary tumors at termination of the experiment six months later. Splenic metastases and lymph node metastases were present in 70% of the animals and two of the three SCID mice had thymic metastases. Three animals had bony metastases. Thus, a high percentage of immunocompromised mice with orthotopic lung carcinomas ultimately develop metastases.

Adenocarcinoma↗
PubMed1975

Carcinogenicity of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide, and its metabolites in rats.

Chronic oral administration of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388, DTIC), induced predominantly thymic and mammary tumors as demonstrated previously. Male and female Sprague-Dawley and female Buffalo rats were susceptible to the carcinogenicity of DTIC. A 50% incidence of mammary adenocarcinomas was induced in males within 18 weeks. Type of tumor and tumor incidence were dose dependent. Single and multiple intraperitoneal injections of DTIC did not alter organ specificity. DTIC-induced thymic lymphosarcomas and mammary adenocarcinomas were transplantable. Tissue distribution studies revealed no correlation between uptake of DTIC by a given tissue and its susceptibility to carcinogenicity. Metabolites of DTIC were tested for carcinogenic activity. Animals administered 5-diazoimidazole-4-carboxamide orally, intraperitoneally, or intragastrically developed low incidences of thymic, stomach, bladder, or mammary tumors. A low incidence of mammary tumors developed in rats fed 2-azahypoxanthine. A variety of tumors, including several ependymoblastomas, were induced in rats that received 5-aminoimidazole-4-carboxamide orally. 5-(3-Methyl-1-triazeno)imidazole-4-carboxamide (MTIC), when fed or given in single or multiple intraperitoneal injections, induced a high incidence of mammary adenofibromas and a low incidence of uterine leiomyosarcomas. Control rats had low incidences of mammary adenocarcinomas and adenofibromas after 52 weeks. These data show that the carcinogenic properties of DTIC resemble those of carcinogenic N-nitroso compounds, hydrazine, azo, and azoxy-alkanes and aryltriazenes and thus suggest similar mechanism(s) of action. These data also indicate that MTIC is involved in the induction of mammary adenofibromas and uterine leiomyosarcomas by DTIC.

Adenofibroma↗
PubMed1976

Large bowel carcinogenesis in mice and rats by several intrarectal doses of methylnitrosourea and negative effect of nitrite plus methylurea.

The carcinogenic effect of several dose levels and regimens of an aqueous solution of N-methyl-N-nitrosourea (MNU) administered intrarectally to mice and rats is reported. In Ha/ICR Swiss mice, a single dose of 1.8 mg MNU induces mainly lymphomas and pulmonary tumors in less than 20 weeks. Repeated doses of 1.5 mg MNU induces lymphomas, pulmonary tumors, and also large bowel tumors in less than 20 weeks. Doses of 0.3 mg decreased the yield of lymphomas and increased large bowel neoplasms over a period of 40 to 60 weeks. Repeated doses of 0.06 mg also gave a low yield of lymphomas and large bowel tumors over a 60-week period. Thus, a maximal yield of lymphomas is seen with a brief regimen of high doses, whereas large bowel tumors occur with a more frequent lower dose rate. Male Fischer strain rats given 1.0 or 2.5 mg MNU 3 times a week for 10 weeks had a multiplicity of large bowel tumors, proportional to dose, in 25 to 30 weeks. In fact, the high dose level led to a 100% yield in less than 20 weeks. Lymphomas were seen only at the higher dose when the animals were were young, at the beginning of the test. In mice and rats the carcinomas were polypoid or plaque shaped and were well differentiated with extensive invasion but no metastases. The adenomas were pedunculated or sessile. Intrarectal administration of a mixture of methylurea and nitrite for 20 weeks and further observation of the rats for an additional 35 weeks yielded no colon tumors. Thus, there is indirect evidence of a lack of the in situ formation of carcinogenic MNU in the large bowel under physiological conditions.

Adenocarcinoma↗
PubMed1992

[Surgical treatment of carcinoid tumors of the intestine].

Carcinoid tumours arise from the neuroendocrine system and present a characteristic morphological picture. They occur in almost every organ, predilected sites are the appendix and the small intestine. Prognosis depends on the primary localization and tumour size. Carcinoids of the appendix and rectum are mostly small and thus have a good prognosis. Growth of bronchial, stomach and small intestinal carcinoids is aggressive and implicates a high percentage of metastatic disease. First choice therapy is the surgical removal of the tumour. Depending on tumour size surgical treatment includes fulguration, local excision and oncologic radical resection up to extended organ extirpation. Reoperation and repeated surgery have good chances to be successful concerning tumour remission and improvement of the carcinoid syndrome. Additive treatment comprises in particular somatostatin therapy and, in some cases, chemotherapy.

Appendiceal Neoplasms↗