Biomedical subjects
Publications and source records attributed to I Seidman.
Chondrosarcoma arising in the nasal septum has been previously described only 11 times. In this report, another case occurring in an 89-year-old man is discussed. The rarity of such a tumor arising in previously normal cartilage is emphasized. Prognostic factors and surgical treatment are discussed.
A case of gastric duplication in an adult is reported with review of the English literature concerning the clinical aspects of this rare anomaly including age, sex, location, clinical presentation, associated anomalies, and treatment. The most popular embryological theories as to the origin of gastric duplication are discussed.
Six epoxides of structurally related chloroalkenes were examined for their carcinogenicity by chronic testing in female ICR/Ha Swiss mice, 30/group. Repeated skin application three times weekly or s.c. injection once weekly were used for the life spans of the mice. The epoxides were: cis-1-chloropropene oxide, trans-1-chloropropene oxide, cis-1,3-dichloropropene oxide, trans-1,3-dichloropropene oxide, trichloroethylene oxide (TCEO), and tetrachloroethylene oxide (PCEO). In mouse skin, cis-1-chloropropene oxide, trans-1-chloropropene oxide, cis-1-,3-dichloropropene oxide, and trans-1,3-dichloropropene oxide induced statistically significant incidences of squamous carcinomas of the skin; TCEO did not cause any skin tumors; and PCEO resulted in three mice with benign skin tumors and one with a squamous carcinoma of the skin. Repeated s.c. injection of the four propene oxides induced statistically significant incidences of local tumors, mostly fibrosarcomas. This was not the case with TCEO and PCEO. The data are consistent with the carcinogenicity findings on the parent chloropropenes and suggest that the epoxides function as their activated carcinogenic intermediates. The essentially negative findings with TCEO and PCEO suggest further studies on the carcinogenicity of trichloroethylene and tetrachloroethylene.
4a alpha-Phorbol-9,9a-didecanoate, 4a alpha-phorbol-9-myristate-9a-acetate, and phorbol-9-myristate-9a-acetate-3-aldehyde were tested for skin tumor-promoting activity by using 7,12-dimethylbenz(a)anthracene as the initiating agent. There were 30 female ICR/Ha mice/group, and tests were continued for 434 to 461 days. 4a alpha-Phorbol-9,9a-didecanoate and 4a alpha-phorbol-9-myristate-9a-acetate were devoid of tumor-promoting activity. Phorbol-9-myristate-9a-acetate-3-aldehyde resulted in 10 mice with papillomas, 2 of which also bore squamous carcinomas of the skin. The positive control group, in which phorbol myristate acetate was used as promoting agent, resulted in 30 mice bearing multiple papillomas and 15 bearing squamous carcinomas of the skin. The effects of structural and stereochemical changes on tumor-promoting activity suggest that a primary interaction of the phorbol ester series is binding at specific sites on the plasma membrane.
Seventeen analogues of the tumor-promoting agent anthralin were tested for the same biological property by repeated skin application on mouse skin using female ICR/Ha Swiss mice, after a single application of a subcarcinogenic dose of 7,12-dimethylbenz[a]anthracene. Seven of the compounds tested are new compounds. They are 1,8-diacetoxy-9-anthrone, 1,8-dimyristoyloxy-9-anthrone, 1,8-dihydroxy-10-acetyl-9-anthrone, 1,8-dihydroxy-10-myristoyl-9-anthrone, 1,8,10-trihydroxy-9-anthrone, 1,8-dihydroxy-9,10-dihydroanthracene, and myristoyljuglone. All compounds were used in pure form for the bioassays. Of the 17 test compounds four showed notable tumor-promoting activity. They are 1,8-dihydroxy-10-acetyl-9-anthrone, 1,8-dihydroxy-10-myristoyl-9-anthrone, 1-hydroxy-9-anthrone, and juglone. In order to determine whether there is any relationship between tumor-promoting activity and metal chelation in this series, the chelating abilities of anthralin and of its inactive analogue 1,8-dihydroxyanthraquinone were examined using the bivalent metal ions Cu(II), Zn(II), Mn(II), Mg(II), and Ca(II). No relationship between chelation and tumor-promoting ability was found.
Phorbolol myristate acetate (PHMA) had been previously prepared from the potent mouse skin tumor promoter phorbol myristate acetate (PMA) by sodium borohydride reduction of the C-5 carbonyl group in PMA to a secondary alcohol. PHMA was shown to have an inflammatory effect in mouse skin equal to that of PMA. 2,3-Dihydrophorbol myristate acetate (DPMA), a new compound, was prepared from the 3-aldehyde of PMA by catalytic hydrogenation. DPMA exhibited no detectable inflammatory effect in mouse skin. Both DPMA and PHMA were tested on the dorsal skins of female ICR/Ha Swiss mice (30/group) for 433 and 380 days, respectively, in separate experiments. The tumor-promoting activity of both compounds was reduced significantly, compared with that of equimolar doses of PMA. For each treatment the number of mice with tumors per total number of tumors was: DPMA, 9/17; PMA, 29/553 at 10 microgram/mouse; PMA, 30/317; PHMA, 24/69 at 2.5 microgram/mouse. The results suggest that specific binding requirements influence the tumor-promoting and hyperplastic activity of PMA and its closely related derivatives in mouse skin.
The flame retardants tris(2,3-dibromopropyl)phosphate, tetrakis(hydroxymethyl)phosphonium chloride, and polyvinyl bromide were tested for carcinogenic activity by skin application 3 times weekly in random-bred female ICR/Ha Swiss mice for 420 to 496 days. Tris(2,3-dibromopropyl)phosphate at two dose levels (30 mg and 10 mg/application) induced benign and malignant tumors of the skin, forestomach, and oral cavity (tongue and gingiva) in a statistically significant number of mice (30/group). A statistically significant incidence of papillary tumors of the lung was observed at both dosages, and the higher dose also resulted in one mouse with a tubular adenoma of the kidney. Tetrakis(hydroxymethyl)phosphonium chloride (2 mg/application, 60 mice) and polyvinyl bromide (0.1 ml latex suspension/application, 30 mice) were inactive. Polyvinyl bromide was also injected s.c. into another group of female ICR/Ha Swiss mice once weekly for 48 weeks, and the mice were observed for a total of 60 weeks. Liposarcomas were induced in 19 of 30 mice, which was ascribed to physical carcinogenesis. Appropriate solvent and no-treatment control groups were included.
Primary carcinoma of breast was treated in 967 patients from 1962 through 1972. Thirty-five of these patients had a second primary tumor of which 50% were discovered simultaneously. A family history for cancer was recorded in 26% of the patients with bilateral cancer. Patients found their tumor more often than the physician except in the simultaneous cases where the physician was more successful. Pathological examination showed 10% of the tumors were comedo, lobular carcinoma in situ, papillary, or tubular cancers. In the metachronous group, 50% of the axillae were involved on both sides. In the simultaneous cases the axilla was less frequently involved. Mammography, biopsies of the second breast, and prophylactic mastectomy in certain high-risk patients should improve survival rates.
Rat mammary gland explants placed in organ culture underwent intraductal hyperplasia in the presence of insulin. The hyperplasia reached its maximum at about 2 weeks of culture and exhibited several morphologic variations. By ultrastructural criteria, it was shown that the proliferating cell was derived from the epithelial rather than the myoepithelial component of the ductal lining cells. Testosterone, added at the beginning of the experiment, partially inhibited the hyperplastic process.
Two-stage carcinogenesis experiments on mouse skin (female ICR/Ha Swiss mice) were done by initiating mice at three age levels (6, 44, and 56 weeks) and promoting after a 2-week interval. In another series, mice were initiated at age 6 weeks, and three time intervals (2, 36, and 56 weeks) were used between initiation and promotion. The initiating agent was 7, 12-dimethylbenz(a)anthracene and the promoting agent was phorbol myristate acetate in all experiments. The results showed a general decrease in tumor production with increasing age at the time of promotion. However, the initiating effect persisted even when the interval between initiation and promotion was 56 weeks.
Four bifunctional and one trifunctional alpha-chloro ethers were tested for carcinogenicity. These compounds were bis-1,2-(chloromethoxy)ethane (Compound I), bis-1,4-(chloromethoxy)butane (Compound II), bis-1,6-(chloromethoxy) hexane (Compound III), bis-1,4-(chloromethoxy)-p-xylene (Compound IV), and tris-1,2,3-(chloromethoxy)propane (Compound V). trans-1,4-Dichlorobutene-2 (Compound VI) was tested along with the five alpha-chloro ethers. All six compounds were tested in female ICR/Ha Swiss mice for 502 to 569 days, depending on survival, by skin application or s.c. and i.p. injection. There were 30 or 50 mice/group. The i.p. and s.c. injections were given once weekly at 0.1 or 0.3 mg of compound dissolved in 0.05 ml tricaprylin for Compounds I to V and 0.05 mg/0.05 ml tricaprylin for Compound VI for the duration of the tests. The skin applications, three times weekly, were at doses of 0.3 or 1.0 mg/0.1 ml cyclohexane for the alpha-chloro ethers and 1.0 mg/0.1 ml acetone for Compound VI. Vehicle and no treatment controls were carried out together with the test compounds. Significance values (p) were calculated for all the compounds tested. Three compounds, I, IV and V, gave notable tumor incidences by all three routes of administration. Compounds II, III, and VI were either inactive by one or more routes of administration or gave low tumor yields.
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