Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human uterine cervix offers a unique opportunity to study the early lesions of squamous cell carcinoma, i.e., carcinoma in situ and dysplasia [combined as cervical intraepithelial neoplasia (CIN)]. In vivo, the patients with CIN have the epidemiological common denominators or "markers" of early onset of coitus, multiple sexual partners, 1st delivery before age 20, and antibodies to herpes simplex virus type 2 more frequently than do controls. The lesions themselves have specific epithelial and vascular changes observable with the colposcope in addition to the usual histological markers from biopsy specimens. The chromosomes and DNA content of cells in these lesions are abnormal. In vitro, the cells from CIN have characteristics somewhat between normal and invasive carcinoma. They lack contact inhibition and may be transferred for several generations, in contrast to normal cervical epithelial cells. The fibroblasts from areas adjacent to DIN are different from normal fibroblasts. The mitotic mechanism in cells cultured from CIN has a significantly prolonged prophase and telophase when compared to similar normal cells. The surface of CIN cells, unlike normal cells, has numerous microvilli when examined by scanning electron microscopy and has characteristic differences from normal cells with numerous elongated, irregular microvilli. With the transmission electron microscope, an increase in microvilli and a decrease in desmosomes and tonofibrils are seen in CIN cells. Some of these markers are being used clinically to manage patients with CIN. Other markers are the basis for further investigation of human carcinogenesis.
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PMID:In vivo and in vitro "markers" of human cervical intraepithelial neoplasia. 5 20

Prophylactic effect of repeated intravenous administrations of oil-attached BCG cell-wall skeleton (BCG-CWS) on the induction of tumor by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in various strains of mice. The subcutaneous injection of DMBA emulsified in oil induced squamous cell carcinoma in almost all of the strains of mice. Treatment of C57BL/6, BALB/c, and ddO strains with BCG-CWS with appropriate route and timing resulted in the retardation of DMBA-induced tumor development manifested by a prolonged latent period of tumor outgrowth. In contrast, the same BCG-CWS treatment of C3H/He and BTK mice was incapable in preventing such DMBA-induced carcinogenesis. Thus, the treatment with BCG-CWS was effective for preventing the DMBA-induced carcinogenesis in certain strains of mice, but the effectiveness varied depending on the strain. The implication of such a strain variationof the BCG-CWS effect on the prophylaxis of chemical carcinogenesis was discussed in the context of differences in the magnitude of immunopotentiation of the host by BCG-CWS.
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PMID:Prophylactic effect of BCG cell-wall skeleton on the tumor induction by 7,12-dimethylbenz[a]anthracene in mice: strain difference. 10 42

The effects of splenectomy on carcinogenesis by a single 10-mg dose of 7,12-dimethylbenz[alpha]anthracene (DMBA) given in olive oil by gavage was tested on BTOs, C57BL/60s, C3H/HeOs, and BALB/cOs mice. The splenectomy, performed a week before the DMBA was given, did not affect physical status or the incidence of acute toxic death of animals. DMBA-treated animals developed neoplasms at a significantly higher rate than did untreated mice. Splenectomy did not influence the overall incidence of neoplasms. Observed tumors in DMBA-treated groups were those of skin, forestomach, colon, liver, lung, adrenal, ovary, breast, hematopoietic-lymphoreticular system, and vascular system, depending on the strain. Types of DMBA-treated neoplasms were affected by prior splenectomy, depending on the strain: Splenectomy inhibited lung adenomas in BALB/cOs females and hepatomas in C57BL/60s females; splenectomy enhanced skin neoplasms in C57BL/60s and squamous cell carcinoma of the forestomach in BTOs males. The most significant change was in the incidence of the group of lymphomas. Myelogenous leukemia was increased in DMBA-treated groups of all strains, but splenectomy inhibited the development of this type of lymphoma.
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PMID:Neoplasms in strains of splenectomized mice after a single 7,12-dimethylbenz[alpha]anthracene treatment. 17 27

Previous studies with agar diffusion technique demonstrated that antibodies produced in rabbits by injection of urea extractable proteins of rat cornfied cells cross react with proteins extracted from normal epidermis of hairless mice using the same technique. In the present study we investigated by indirect immunofluorescence microscopy the immunoreactivity of epidermal proteins in normal and ultraviolet light (UVB) induced hyperplasia and malignant transformation. Reactivity to the antibody was seen over the entire epidermis of nontreated skin and hypertrophied epidermis which occurred at 6-8 weeks after initiation of UVB irradiation. However, the reactivity diminished when malignant changes took place in the epidermal cells. Almost complete disappearance of the immunoresponse was observed in squamous cell carcinoma produced by further UVB radiation. These results suggest that the reactivity of this urea extractable protein serves as an additional immunologic marker for normal epidermal cells. Alterations in the immunoreactivity parallels UVB induced carcinogenesis.
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PMID:Immunofluorescent studies of epidermal protein during UV induced carcinogenesis. 40 10

Epidermoid carcinoma of the lateral border of the tongue can be induced in a standard strain of hamsters, applying DMBA in acetone after traumatizing the area with a root canal broach. Employing the same technique in an inbred strain of hamsters resulted in the more rapid development of carcinomas. The inbred strain should be a useful model for experimental carcinogenesis of tongue.
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PMID:Lingual carcinogenesis in an inbred strain of hamsters. 41 62

Carcinogenicity of phenacetin was tested using Sprague-Dawley rats. Two groups of animals containing 50 males and 50 females per group were fed respectively with 2.5% and 1.25% phenacetin diet for 18 months and fed thereafter with basal diet for 6 months. Control animals containing 65 males and 65 females were fed with basal diet for 24 months. Animals surviving more than 24 months were regarded as effective animals and killed. Rats that died of tumor development within 24 months were also regarded effective animals. Every organ from the killed and dead animals was fixed in 10% formaldehyde solution and examined histopathologically. Effective number of rats was 27 males and 27 females in 2.5% phenacetin feeding group, and 22 males and 25 females in 1.25% phenacetin feeding group. In control group, 19 males and 25 females were effective. Neoplasms including spontaneous tumors were detected in 26 out of 27 males (96.3%) and 21 out of 27 females (77.8%) of 2.5% phenacetin feeding group, and in 20 out of 22 males (90.9%) and 19 out of 25 females (76.0%) of 1.25% phenacetin feeding group. In control group, 1 out of 19 males (5.3%) and 6 out of 25 females (24.0%) showed spontaneous tumor development. Histopathologically, carcinomas of the nasal cavity, such as adenocarcinoma, squamous cell carcinoma, and transitional cell carcinoma, and the urinary passage, as renal cell carcinoma of the kidney pelvis, and transitional cell carcinoma of the urinary bladder, were most conspicuous, suggesting the target organs of phenacetin carcinogenesis. Males showed higher tumor incidence compared to females. The higher the concentration of phenacetin given, higher incidence of tumors was observed.
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PMID:Tumors of Sprague-Dawley rats induced by long-term feeding of phenacetin. 44 75

The present communication is a report of a case where histological changes, identical to those described recently to be of condylomatous nature in the genital tract, were found in the bronchial epithelium adjacent to an invasive squamous cell carcinoma. The significance of this finding in the light of squamous cell carcinogenesis is discussed, and the conclusion is drawn that these lesions are worth recording until proved to be unrelated to the carcinogenesis, or to be involved in it.
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PMID:Condylomatous changes in neoplastic bronchial epithelium. Report of a case. 53 37

Approximately 8000 cigarette-smoking men over the age of 45 have entered into a lung cancer detection program in New York City. Cytologic examinations of sputum were carried out on 4000 subjects and lung cancer was found by this technique in nine men with normal chest x-rays. Seven had in situ or incipient invasive epidermoid carcinoma confined to the bronchus. These seven cases were studied by detailed histologic examinations of the bronchial tree in the resected specimens through sixth generation subsegmental bronchi. It was concluded that: 1) invasive epidermoid carcinoma arises from carcinoma in situ of bronchial surface epithelium or an extension of that neoplastic epithelium in bronchial glands; 2) the site of origin is a segmental bronchus in most instances; and 3) each carcinoma should be considered as unifocal in origin even though there is a continuing risk of another primary lung cancer. It seems unlikely that squamous metaplasia or basal hyperplasia is an essential step in carcinogenesis; rather, we believe that carcinoma may arise in bronchial epithelium without regard to the presence or absence of basal hyperplasia or squamous metaplasia, which should be considered nonspecific reactions to injury that may or may not accompany carcinogenesis.
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PMID:Radiologically occult in situ and incipient invasive epidermoid lung cancer: detection by sputum cytology in a survey of asymptomatic cigarette smokers. 60 71

Subserial examinations of the noncancerous esophagus from 86 autopsy materials (male 47, female 39) in Kagoshima Prefecture revealed epithelial dysplasia in 54 instances (63%); 32 males (68%) and 22 females (57%). Higher grades of dysplasia were shown in 17 males (36%) and 3 females (8%). Histologically a formation of the rete ridge-like elongation of basal epithelium was characteristically conspicuous in these materials. Tabacco and alcohol intakes were regarded as promoting factors of dysplasia. Distribution and severity of dysplasia around carcinoma were histologically examined on semiserial blocks in 100 surgical materials under the consideration of preoperative treatment. A coexistence of carcinoma with extensive dysplasia was found in 24 instances and that with multifocal dysplasia in 46. Multicentric in situ carcinoma was found in 19 patients. These in situ carcinomas were frequently surrounded by severe dysplasia and occasionally showed gradual transition to the latter. The lesion of invasive carcinoma sometimes did not show sharp demarcation from the surrounding mucosa, especially in cases of well differentiated squamous cell carcinoma. The results indicate that dysplasia plays a significant role on carcinogenesis of the esophagus as a precursor lesion.
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PMID:Epithelial dysplasia in cancerous and noncancerous esophagi. 64 89

In an attempt to shorten tumor induction time and alter tumor anaplasticity, ductal metaplasia was induced in the submandibular gland of 30 rats by ligation of the duct and artery followed by the implanation of 4-mg pellets of pure DMBA. Control groups consisted of 19-ligated and 15-DMBA implanted rats. The ligate controls showed degeneration and atrophy of the affected gland and replacement of glandular tissue by scar tissue. The DMBA controls followed the expected pattern, with all rats eventually developing well-differentiated squamous cell carcinoma. The CMBA-ligated rats showed a combination of the two processes, each acting separately from the other. There was no difference either in induction time or tumor anaplasticity between the DMBA control rats and the DMBA-ligated rats. It seems that only factors relating to a change in the immunologic response of the host affect the latent period of tumor induction time in submandibular gland carcinogenesis.
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PMID:Experimental carcinogenesis in duct-artery ligated rat submandibular gland. 106 21


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