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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three hundred and thirteen cases of human thyroid tissues, comprising 39 nodular goiters from 34 females and 5 males, 130 adenomas from 93 females and 37 males, and 144 carcinomas from 99 females and 45 males were used for the present immunohistochemical assessment of estrogen receptor (ER) expression. Thirty-three cases of follicular carcinoma, 115 cases of papillary carcinoma and 6 cases of anaplastic carcinoma were included in the malignant tumor group. Incidences of ER-positive cases were 23/39 (58.9%) for nodular goiter, 44/130 (33.8%) for adenoma and 26/144 (18.0%) for cancer. In the individual carcinoma categories, 7/23 (30.4%) follicular, 19/115 (16.5%) papillary and 0/6 (0%) anaplastic lesions were judged as positive cases. Thus, the incidence of ER-positive cases tended to decrease with the degree of malignancy; this trend being similar in both sexes. Moreover, the average ages of ER-positive cases were lower than those of ER-negative cases for all types of thyroid carcinoma except the follicular variety in males. It was thus suggested that ER expression may be related to prognosis and tumor growth at early stage. Since the incidence of ER does not significantly differ between females and males, the observed sex differences regarding thyroid tumor incidence may reflect the higher estrogen serum content in females.
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PMID:Immunohistochemical analysis of estrogen receptors in 313 paraffin section cases of human thyroid tissue. 845 Oct 35

The loss of HLA antigens by neoplastic cells is considered important for tumor growth and metastasis, inasmuch as it may allow tumors to escape immune surveillance. We have observed reduced expression of HLA antigens in sporadic colon cancer and adenomas from familial adenomatous polyposis patients. We now studied the expression of HLA class I antigens in patients with sporadic adenomas, which are precursors of colorectal cancer. Expression of HLA class I antigens was studied by immunohistochemistry in (a) sporadic colon adenomas, (b) histologically normal mucosa distant from the adenomas, (c) histologically normal colonic mucosa from patients with history of sporadic colon adenomas, and (d) colonic mucosa from normal subjects. HLA class I antigen expression was moderately reduced in 56% and severely reduced in 44% of the adenomas; this reduction was significant when compared to controls (P < 0.0001). The reduction of HLA class I expression in adenomas was related to the grade of dysplasia of the adenomas. HLA class I expression of normal appearing mucosa was decreased in 76% of patients with adenoma (P < 0.0001) and in 54% of patients with history of adenoma (P < 0.005) compared to normal controls. These changes were antigen specific, inasmuch as the expression of carcinoembryonic antigen, a surface antigen, was not affected. Our findings suggest that reduced HLA class I expression is an early event in the cell transformation process from normal to neoplastic state, preceding in many cases the onset of histological changes. HLA class I could be potentially used as a premalignant marker in the colon.
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PMID:Expression of HLA class I antigens in sporadic adenomas and histologically normal mucosa of the colon. 848 24

We analyzed the appearance of pericryptal fibroblasts (PCFs) identical to myofibroblasts in human colorectal epithelial tumors (adenomas, carcinomas) by an immunohistochemical method, with special reference to the histologic features and tumor growth patterns. The majority (61.5%) of adenomas contained well-developed PCFs. In contrast, carcinomas contained more poorly developed PCFs than adenomas. Approximately one third (35.4%) of the intramucosal and most (89.6%) of the submucosal carcinoma components had poorly developed PCFs. Pericryptal fibroblast development in pure carcinomas also was evaluated in association with two types of tumor growth patterns: polypoid growth carcinoma (PG-Ca) and nonpolypoid growth carcinoma (NPG-Ca). Polypoid growth carcinoma tended to contain well-developed PCFs, whereas NPG-Ca tended to lack PCFs. From the above findings, it is suggested that PCFs gradually decrease in the sequence of adenoma, intramucosal carcinoma, and submucosal invasive carcinoma. In addition, the two growth types (PG-Ca and NPG-Ca) are histologically different in PCF development, and the lack of a PCF network in NPG-Ca seems to be the reason why NPG-Ca can invade the submucosa more easily than PG-Ca, which has a consistent PCF network.
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PMID:Significance of pericryptal fibroblasts in colorectal epithelial tumors: a special reference to the histologic features and growth patterns. 849 92

To determine if apoptosis is involved in colorectal tumorigenesis and its progression, colorectal adenomas (n = 63), carcinomas (n = 49), and normal mucosa were investigated by using in situ end-labeling (TUNEL) method. The expression of Ki-67 was also analyzed immunohistochemically. TUNEL labeling index (TLI) and Ki-67 labeling index (KLI) were determined. TLI/KLI was significantly higher in the adenomas of small size and/or of low and middle grade atypia than those of large size and/or of high grade atypia. No difference was observed in the indices between adenomas and carcinomas and among the cancer groups classified on the basis of their clinicopathological features. The results indicate that the reduction of susceptibility to apoptosis plays an important role in the early stage of the adenoma-carcinoma sequence. Apoptosis can explain the enormous cell loss thought to exist in normal colorectal mucosa and in the tumor growth process.
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PMID:Significance of spontaneous apoptosis during colorectal tumorigenesis. 864 48

Integrins are heterodimeric transmembrane molecules that mediate cell-cell and cell-substratum adhesion. Because alterations in the adhesive properties of tumor cells influence tumor growth and progression, the distribution of different alpha and beta integrin subunits was studied in both the parenchyma and the connective tissue in 6 normal and 25 adenomatous human anterior pituitaries. All normal parenchymal cells expressed the alpha3beta1 and alpha6beta4 integrins. By contrast, in adenomatous parenchymal cells the expression of alpha3beta1 was down-regulated and that of alpha6beta4 abrogated. Neoexpression of alphavbeta3 Occurred in the parenchyma of a subset of adenomas. All normal connective tissue cells expressed the alpha1 and beta1 subunits, a third subunit (alpha5) being present in the normal endothelium. By comparison, all adenomatous stromal cells expressed many more integrin subunits (alpha1, alpha3, alpha5, alphav, beta1 and beta3), adenomatous endothelial cells bearing additional subunits (alpha6, beta4 and beta5). Vitronectin, absent from the normal connective tissue, was constantly observed in the adenomatous stroma. To conclude, compared with cells of the normal gland, adenomatous anterior pituitary cells display a decreased expression of integrins whereas the adenomatous stroma expresses a rich repertoire of integrins. These changes are not related to the secretory type, grade or invasiveness of the adenoma. The resulting alterations in the adhesive properties of adenomatous cells could facilitate their dissemination. Enrichment of the integrin repertoire expressed by the adenomatous vasculature is indicative of its dual nature, systemic and tumoral.
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PMID:Adenomatous transformation of the human anterior pituitary is associated with alterations in integrin expression. 869 May 24

We present mathematical analyses, experimental data, and clinical observations which support our novel hypothesis that tumor-induced alteration of microenvironmental pH may provide a simple but complete mechanism for cancer invasion. A reaction-diffusion model describing the spatial distribution and temporal development of tumor tissue, normal tissue, and excess H+ ion concentration is presented. The model predicts a pH gradient extending from the tumor-host interface, which is confirmed by reanalysis of existing experimental data. Investigation of the structure and dynamics of the tumor-host interaction within the context of the model demonstrates a transition from benign to malignant growth analogous to the adenoma-carcinoma sequence. The effect of biological parameters critical to controlling this transition are supported by experimental and clinical observations. Tumor wave front velocities determined via a marginal stability analysis of the model equations are consistent with in vivo tumor growth rates. The model predicts a previously unrecognized hypocellular interstitial gap at the tumor-host interface which we demonstrate both in vivo and in vitro. A direct correlation between the interfacial morphology and tumor wave front velocity provides an explicit, testable, clinically important prediction.
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PMID:A reaction-diffusion model of cancer invasion. 897 Nov 86

The purpose of the present study was to investigate the role of p53 in tumor progression of colorectal adenomas and early carcinomas, while especially focusing on flat tumors (depressed adenomas and non-polypoid carcinomas). Paraffin sections of 61 pure adenomas (33 polypoid, 28 depressed), 26 carcinomas in polypoid adenoma (CIA) and 63 pure carcinomas (36 polypoid, 27 non-polypoid) were examined for immunostaining using p53 monoclonal antibody (PAb 1801). All of the carcinomas were restricted to the mucosa. The number and distribution of the p53 positive tumor cells was evaluated, and then compared with tumor growth patterns and histological features. The incidence of p53 expression in carcinomas (58% in CIA and 51% in pure carcinomas) was significantly higher than that in polypoid adenoma (27% in CIA and 21% in pure adenomas). However, the same incidence in depressed adenomas (51%) was significantly higher than in polypoid adenomas. No correlation in carcinomas was observed between p53 expression and clinicopathologic data except for age. The distribution of p53 positive cells was different between adenomas and carcinomas. There tended to be fewer p53 positive cells in adenomas, even in depressed ones, than in carcinomas and they also tended to be confined to the superficial areas in adenomas, while they were diffusely distributed in carcinomas. Interestingly, the p53 positive cells were more frequently present in the deep mucosal areas than in the superficial areas of some non-polypoid carcinomas. In conclusion, the following hypotheses are suggested: (i) the increase of p53 expression from adenoma to carcinoma supports the hypothesis of an adenoma-carcinoma sequence in a polypoid tumor; (ii) the unique p53 expression in non-polypoid carcinoma suggests the existence of another type of carcinogenesis; and (iii) depressed adenomas are thus considered to have a high potential risk of carcinoma.
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PMID:p53 expression patterns in colorectal adenomas and early carcinomas: a special reference to depressed adenoma and non-polypoid carcinoma. 911 Mar 48

Forty-four adult acromegalic patients carrying growth hormone-producing pituitary macroadenomas were investigated with neuroradiological and endocrinological techniques. Plasma growth hormone and somatomedin-C levels were repeatedly measured before surgical removal of tumors and during the follow-up period. Twenty-five patients presented preoperatively with an invasive adenoma that involved the cavernous sinus (CS). Diagnosis of tumor invasivity was made according to distinct neuroradiological criteria and was confirmed or rejected during surgery Significantly higher basal growth hormone levels were found in patients with CS invasion than in cases without tumor growth in the CS. Evidence is presented that plasma growth hormone level in acromegalics is a more sensitive indicator for predicting tumor invasiveness than somatomedin-C. Growth hormone basal values before surgery and the extent of their decrease after removal of tumor correlate with adenoma growth in the parasellar compartments and should be used as a prognostic factor to aid in planing adjuvant tumor treatment.
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PMID:Factors predicting pituitary adenoma invasiveness in acromegalic patients. 929 20

The purpose of this study was to determine whether chronic, low-level exposure of mammary-tumor-prone mice to 2450 MHz radiofrequency radiation (RFR) promotes an earlier onset (decreased latency), a greater total incidence, or a faster growth rate of mammary tumors. One hundred C3H/ HeJ mice were exposed in circularly polarized waveguides (CWG) for 18 months (20 h/day, 7 days/wk) to continuous-wave, 2450 MHz RFR at a whole body average specific absorption rate (SAR) of 0.3 W/kg; 100 mice were sham exposed. Before exposure, SARs were determined calorimetrically; during experimentation, SARs were monitored by differential power measurement. All animals were visually inspected twice daily and were removed from the CWG cages for a weekly inspection, palpation, and weighing. From the time of detection, tumor size was measured weekly. Animals that died spontaneously, became moribund, or were killed after 18 months of exposure were completely necropsied; tissues were fixed and subjected to histopathological evaluations. Results showed no significant difference in weight profiles between sham-irradiated and irradiated mice. Concerning mammary carcinomas, there was no significant difference between groups with respect to palpated tumor incidence (sham = 52%; irradiated = 44%), latency to tumor onset (sham = 62.3 +/- 1.2 wk; irradiated = 64.0 +/- 1.6 wk), and rate of tumor growth. In general, histopathological examination revealed no significant differences in numbers of malignant, metastatic, or benign neoplasms between the two groups; a significantly greater incidence of alveolar-bronchiolar adenoma in the sham-irradiated mice was the only exception. In addition, survival analysis showed no significant difference in cumulative percent survival between sham and irradiated animals. Thus, results indicate that under the conditions of this study, long-term, low-level exposure of mammary-tumor-prone mice to 2450 MHz RFR did not affect mammary tumor incidence, latency to tumor onset, tumor growth rate, or animal longevity when compared with sham-irradiated controls.
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PMID:Chronic exposure of cancer-prone mice to low-level 2450 MHz radiofrequency radiation. 945 3

In previous studies, the birth rate of new cells in parathyroid adenomas measured at the time of surgical excision was shown to be much too low to account for growth of the tumors from a single cell in the time available, but comparison with normal rates was not possible. We measured the prevalence of cells expressing the Ki-67 antigen, a cell cycle marker, in 55 parathyroid adenomas using the MIB-1 antibody and microwave antigen retrieval; in 22 cases, separate measurements were made in nonadenomatous tissue from the same glands. In 10 cases complete maps of the gland profile were reconstructed to study the distribution of labeled cells. The proportion of Ki-67-positive cells, estimated by systematic random sampling, was used to calculate cell birth rate assuming a duration of Ki-67 expression of 24 h; the results were compared to rates previously determined in normal parathyroid glands by the same method. The geometric mean cell birth rate was 9.97%/yr, about double the normal rate of 5.4%/yr, but less than a third of the cases had values above the normal range. The corresponding value in nonadenomatous tissue was 2.58%/yr, about half the normal rate. In 10 cases studied in more detail, the cell birth rate was 12.3%/yr in the peripheral regions and 6.2%/yr in the central regions, a value not significantly different from normal. The results in adenomas are in reasonable agreement with previous estimates of cell birth rate of 13.7%/yr using [3H]thymidine labeling and 6.4%/yr using prevalence of the mitotic karyotype. The proportion of Ki-67-positive cells using unbiased sampling was about 50 times smaller than that in previous studies using selective sampling. Cell birth rates at the time of excision were about 20-25 times lower than initial rates estimated from modeling tumor growth by the Gompertz function. We conclude that 1) cell birth rate in parathyroid adenomas has fallen substantially during the growth of the tumors and is only modestly greater than normal; 2) the fall in cell birth rate had been greater in the central and presumably older regions of the adenoma than in the peripheral and presumably younger regions; 3) nonadenomatous tissue was suppressed with respect to its proliferative as well as its secretory function, presumably as a result of hypercalcemia; and 4) the progressive fall in cell birth rate, despite the accumulation of mutations that are supposed to increase cell birth rate, is most readily explained by the set-point hypothesis.
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PMID:Rates of cell proliferation in adenomatous, suppressed, and normal parathyroid tissue: implications for pathogenesis. 950 41


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