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At least 19 recordsLinked to original sources
PubMed1975

The relationship of histology to the spread of cancer.

This paper investigates the question of whether different types of histology at the same site can affect the spread of metastases - that is, producing a greater or fewer number of metastases depending on the histological diagnosis. Autopsy records were the source of the data analyzed in this paper. The metastases were subdivided into four categories - central nervous metastases, endocrine metastases, metastases at various lymphatic areas, and a miscellaneous group of metastases called the "remainder" group. It was found that adenocarcinoma and oat-cell carcinoma of the lungs are more aggressive in their metastatic spread than squamous cell carcinoma at the same site. Adenocarcinoma of the cervix uteri had more widespread metastases than squamous cell carcinoma at the same site. No difference at all was detectable in the number of metastases, in men or in women, between transitional cell carcinoma and adenocarcinoma of the bladder and kidney. Cystadenocarcinoma of the ovaries appeared to be less widespread than adenocarcinoma (not otherwise specified) of the same site.

Adenocarcinoma↗
PubMed1977

Acute dermatomyositis-polymyositis and malignancy.

A partial review of selected published case reports of AD-P associated with malignancy has been enhanced by the presentation of pertinent data on 15 unreported examples of the association. It is noteworthy that the first case in current literature of AD-P associated with a malignancy was described in 1916. The brief clinical report of a patient with proximal muscle weakness and skin lesions, with the obvious association with a malignancy (adenocarcinoma of the stomach), describes an example that has been repeated many times with different types of tumors but with essentially no variations in the clinical findings. In 1959 Williams identified 590 cases of AD with an overall tumor rate of 15%, and recently Barnes identified 258 cases of AD associated with a malignancy. The original designation, dermatomyositis or AD, has now been expanded to include proximal muscle polymyositis with systemic involvement, which syndrome at the current state of the art is indistinguishable clinically and pathologically from AD except for the lack of skin lesions. It may be that at some future time one or more immunologic features may differnetiate the clinical entity polymyositis from AD and further subdivide each of these entitites from similar clinical syndromes associated with a malignancy. However, the problem in management in either AD or polymyositis is similar. A number of patients with a malignancy and muscle weakness or neuropathy have been reported. These associations have been mentioned briefly, but insufficient data are available to determine whether these should be considered as a variant of AD-P or only casually related conditions with certain clinical features in common. Most of the patients described in the literature of AD-P with an associated malignancy have had skin lesions; a minority only have lacked this feature. However, unless a patient is followed carefully, it is possible for a transient or evanescent erythema or insignificant skin lesions to be present and not recorded in the case record.

Acute Disease↗
PubMed1975

Teratomas in childhood.

Of 107 teratomas in children, 86 were benign and 21 malignant. Sacrococcygeal and pelvic teratomas predominated (51 cases) and these fell into 3 groups: post sacral, dumb-bell and presacral. The 34 purely posterior tumours were always congenital and benign, whilst the incidence of malignancy in dumb-bell and presacral teratomas increased as the tumour became more internal. Malignant teratomas were carcinomas, usually containing glandular, papillary and clear-cell areas, and metastases were similar. Immature tissues in benign teratomas were usually neural or connective tissue. They did not give rise to neuroblastomas or sarcomas, and did not indicate a worse prognosis. Only 2 originally benign teratomas later developed malignancy.

Adolescent↗
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↗
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↗
PubMed1992

Changes in frequency, morphology, and behavior of tumors induced in mice by a polyoma virus mutant with a specifically altered oncogene.

Alterations in the tumor-inducing ability of a polyoma virus mutant encoding a partially defective middle T oncogene have been investigated. The mutant middle T associates with and activates the tyrosine protein kinase pp60c-src normally but does not promote binding of a second enzyme, phosphatidyl-inositol 3-kinase. Compared with the wild type virus, this mutant shows an altered and reduced ability to induce tumors after inoculation into newborn mice, as judged by the following criteria: lower frequency of tumors, reduced morbidity and increased survival times of host mice, changes in the spectrum of tumor types, and altered morphologic properties of tumors at several target organ sites. These results indicate an important role of changes in 3-phosphoinositide metabolism in induction of a variety of tumors in this experimental system.

Animals↗