Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the years 1975-1988, twenty lung cancer patients with symptomatic pericardial effusion were treated conservatively at our center. Echocardiography demonstrated small pericardial effusion in 2 patients, medium size effusion in 3 patients and large amount of fluid in 15 patients. Fifteen patients developed cardiac tamponade; in three of these patients, this was the presenting manifestation of lung cancer. Pericardiocentesis resulted in prompt, though temporary, symptomatic relief in all patients. Fluid cytology demonstrated suspected malignant cells in 2 patients and malignant cells in 13 patients. Based on cytology, the diagnosis of adenocarcinoma was established in six patients, small cell carcinoma in three patients, and epidermoid carcinoma in one patient. All patients were dead within 9 months from the time of diagnosis of pericardial effusion; 17 died within less than 3 months. It is concluded that pericardial effusion in lung cancer is indicative of rapid tumor progression and short survival. Fluid cytology provides an immediate and accurate means of diagnosis.
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PMID:Symptomatic pericardial effusion in lung cancer patients: the role of fluid cytology. 221 90

The implications of cytologic atypia, patterns of growth, stromal refractoriness, and immune responses in actinic keratoacanthoma are examined here in a speculative manner with the following conclusion: keratoacanthoma is a generic designation for a spectrum of invasive, keratinocytic hyperplasias. In this context, hyperplasia may affect both genomically normal and abnormal keratinocytes. In keratoacanthoma, it does so indiscriminately. The universality of the process in which both benign and neoplastic clones are affected qualifies as immunostimulation. The affected keratinocytes, regardless of genomic characteristics, extend beyond their sustaining stroma into retinaculum and the basement membrane, as an immunologic barrier, is disrupted. Following a period in which the stroma and the immune response are refractory, one or more clones of keratinocytes are exposed to an immune response. For the adnexal contributions, the eventual encounter with the immune response is brief and short-lived. The fate of these genomically intact cells is predictable: complete regression is the inviolate pathway. For the genomically deranged populace, the results of the encounter are unpredictable and potentially manifold. The options, variably expressed, include regression, spatial progression (expansion in space), and neoplastic progression (expansion in the number and types of neoplastic clones). In some actinic keratoacanthomas, neoplastic clones are represented in either focal or extensive carcinomalike patterns from the inception of the hyperplasia. In them, a potential for neoplastic progressions is inherent. If autonomous, aggressive clones are selected in the progressions, the transition from universal hyperplasia (keratoacanthoma) to malignancy (carcinoma) is effected. In the transition, hyperplastic, genomically intact, follicular keratinocytes are not affected; actinically deranged keratinocytes are. The final pathway for an individual evolving lesion is unpredictable, but in some cases it leads to biologic carcinoma (carcinoma ex-keratoacanthoma).
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PMID:Actinic keratoacanthoma. Speculations on the nature of the lesion and the role of cellular immunity in its evolution. 224 66

Recent studies have shown that orthotopic (transurethral) transplantation of human bladder cancer cell lines into nude mice permits tumor growth that accurately reflects their clinical malignant status in the original host. Thus, such a system allows a unique opportunity to analyze the genetic events involved in the conversion of low-grade bladder cancer, the vast majority of which are curable, to the high-grade life-threatening form of the disease. Since 5-10% of transitional cell carcinomas (TCCs) have been shown to contain a mutated HRAS gene, and protein expression levels of all forms of HRAS have been correlated with TCC progression, we chose to study the contribution of the HRAS oncogene in bladder tumor progression. We evaluated the effects of transfection of normal or mutated HRAS genes into a human TCC, called RT-4, that behaves as a superficial noninvasive papillary tumor after transurethral orthotopic inoculation into athymic nude mice. We found that overexpression of either transfected normal or mutated HRAS genes converted RT-4 cells to express an invasive phenotype remarkably similar in nature to the clinical behavior of high-grade bladder carcinomas. These results suggest a role for overexpressed normal or mutated RAS genes in human bladder carcinoma progression, and highlight the importance of using orthotopic inoculation systems for evaluation of the contribution of oncogenes to malignant tumor progression.
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PMID:Overexpression of normal and mutated forms of HRAS induces orthotopic bladder invasion in a human transitional cell carcinoma. 224 80

Although neoplastic changes in canine hepatoid perianal glands (HPG) are quite common, the biological behaviour is sometimes difficult to assess on the basis of the histopathological examination. In an attempt to detect differences in the glycoconjugate expression between normal and neoplastic HPG, and to verify their relation to the degree of neoplastic progression, normal and neoplastic HPG were studied in 13 dogs, using 11 biotinylated lectins. In HPG adenomas the majority of the cells did not stain or stained weakly after incubation with pokeweed mitogen, LCA and UEA-I. In HPG carcinoma the basal cells lost the specific binding for WGA while heterogeneous distribution of conconavalin-A staining was observed.
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PMID:Glycoconjugate expression in normal hepatoid glands and hepatoid gland adenomas and carcinomas in dogs. 226 15

We examined 35 cases of stomach carcinoma and 40 cases of colonic carcinoma with PNA associated with peroxidase (peanut agglutinin, lectin which binds to the terminal disaccharide galactose beta (1,3)-N-acetil-galacto-samine). In this way evaluation of the functional aspects of the normal-neoplastic sequence was undertaken. This method was carried out for histological and ultrastructural investigations. The results obtained in both cases showed a different reactivity in the evolution of neoplastic disease: in fact, positivity in dysplasia is finely granular intracytoplasmic, whereas in well-differentiated neoplastic transformation such a reactivity is preferentially localized along the cellular membranes, with restoration of gross positivity in the cytoplasm for the poorly-differentiated neoplasm. We therefore believe PNA to be a marker not only of neoplastic progression but of differentiation as well: we also hypothesize it to reveal glycoprotein groups with possible antigenic power, involved in immunologic interactions between tumor and host.
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PMID:PNA: a marker of neoplastic progression and differentiation in the gastro-intestinal tract. 228 82

The ploidy, DNA heterogeneity and the phases of the cell cycle of the tumor were analyzed, by means of single-cell DNA cytophotometry, in 329 patients with locally advanced prostatic carcinoma to find out and establish prognostic factors apart from those already known (stage, grade). Follow-up periods ranged from 1 to 9 years. 253 (76.8%) of the 329 patients had carcinoma stage T3 Nx M0, and 76 of them (23.1%) had carcinoma stage T3/T4 N2-4 M1. 11.8% of the patients showed a cytological grade of malignancy I, while 64.3% had grade II carcinoma and 23.8% had grade III carcinoma. Single-cell DNA cytophotometry demonstrated aneuploidy rates of up to 71% and diploidy rates of up to 23.8% for the higher grades of malignancy, i.e. grades II and III, whereas the diploidy rate established for grade I was 68% and the respective aneuploidy rate was 21%. These differences are significant (p less than 0.001). There was a significant correlation between the results of DNA cytophotometry and the clinical course of the disease. Only 3 (3.7%) of the patients with diploid tumor cell nuclei developed metastases and local tumor progression within 8 years, whereas patients with aneuploid tumor cell nuclei showed metastases and local tumor progression within 8-22 months. These patients died of carcinoma after an average 18 months following primary diagnosis.
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PMID:Nuclear DNA analysis: the relevance of ploidy, DNA heterogeneity and phases of the cell cycle in 329 patients with prostatic carcinoma. A study on a follow-up of eight years. 228 53

Serum concentrations were determined serially in two groups of patients with colorectal carcinoma: in 123 after curative resection and in 34 with residual cancer. Of the first group, in 98 serum CEA fluctuated within the normal range or with a 2-fold larger amplitude evidencing effective surgery because only 9 had recurrence; in 25 serum CEA rose persistently from a postoperative nadir indicating relapse, mostly liver metastases. Of the 34 patients with relapse, 3 had clinically and 7 CEA-directed second-look laparotomy; although 7 had operation with curative intent, only 3 remained disease-free. In the second group, there were 26 patients after palliative surgery and 8 during nonsurgical treatment. Serum CEA fluctuated within the normal range in 2 patients in remission and in 3 with progressive cancer, and rose in parallel to cancer progression in 29. Thus, serum CEA within or slightly above the normal range was 88% predictive that the patient might be free of disease or in remission; whereas elevated or rising level indicated disease progression. Accordance between serum CEA and clinical status occurred in 145 of 157 (92%) patients.
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PMID:Serial determinations of serum CEA in monitoring management of patients with colorectal carcinoma. 236 57

The purpose of this study was to establish an in vitro model for tumor progression in colorectal carcinogenesis, by transforming the premalignant human colonic PC/AA adenoma cell line to the malignant phenotype. A rare clonogenic variant AA/C1 [colony-forming efficiency (CFE) on plastic of 1.05%] was isolated from the diploid PC/AA adenoma cell line (C. Paraskeva, S. Finerty, and S. Powell, Int. J. Cancer, 41: 908-912, 1988). AA/C1 was aneuploid and when treated with 1 mM sodium butyrate for 14 days gave rise to the AA/C1/SB cell line which had an increased CFE on plastic (6.13%) although the cells remained anchorage dependent and nontumorigenic. After exposure of these AA/C1/SB cells to the carcinogen N-methyl-N'-nitro-N'-nitrosoguanidine an anchorage-independent cell line was isolated (AA/C1/SB10). On continuous in vitro passage, the CFE in agarose of AA/C1/SB10 has increased to 17.3% and the cells have become tumorigenic producing adenocarcinomas in athymic nude mice. AA/C1, AA/C1/SB, and AA/C1/SB10 cell lines have common chromosomal abnormalities including a pericentric inversion of chromosome 1 with deletion of part of the short arm and monosomy for chromosome 18. This in vitro progression provides the first reported experimental evidence for the adenoma to carcinoma sequence in the human colon, and the cytogenetic evidence suggests that it is relevant to in vivo carcinogenesis.
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PMID:Neoplastic transformation of a human colonic epithelial cell line: in vitro evidence for the adenoma to carcinoma sequence. 236 46

DNA content of prostatic adenocarcinoma was determined by flow cytometry on formalin-fixed, paraffin-embedded tissue from 57 radical prostatectomies. This was done to define the relationship of aneuploidy to prostatic adenocarcinoma grade, volume, and pathologic stage and to examine its utility in candidates for surgical treatment. Aneuploidy was found in 26 (46%) cases. With one exception, all of the aneuploid cases were found in tumors larger than 4 cc. The percentage of aneuploid cases increased with advancing pathologic stage, and it was highest in those cases with lymph node metastases. This percentage was also higher among more poorly differentiated tumors. However, diploid tumors were also found among these groups, and the relationship between aneuploidy versus pathologic stage and grade did not achieve statistical significance. Except for a 91% specificity for tumor volume greater than 4 cc, the sensitivity and specificity of DNA content analysis to predict these groups was low (50% to 72%). It is concluded that aneuploidy is a later event linked to tumor progression, but it is not a requirement for progression to occur. The overlap in aneuploid and diploid tumor behavior precludes the use of DNA content analysis as an independent predictor to direct preoperative treatment of prostatic carcinoma.
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PMID:DNA content in prostatic adenocarcinoma. A flow cytometry study of the predictive value of aneuploidy for tumor volume, percentage Gleason grade 4 and 5, and lymph node metastases. 238 3

The extent of tumor in prostatectomy specimens was determined by a grid method in 117 patients with prostatic adenocarcinoma. A plastic strip or ruler with squares of 3.0 mm was used, and the ratio of squares overlying carcinoma to the total number of squares overlying prostate tissue was calculated. This grid ratio, which represents an estimate of the percentage of the prostate involved by tumor, was a significant prognosticator closely tied to the likelihood of tumor progression and to survival time, as assessed by logistic regression analysis and a proportional hazard model. The grid ratio was better than histologic grade in predicting tumor progression and patient survival; also, the ratio was more objective than histologic grade as judged by interobserver agreement values. Only slight improvement in prognostication was obtained with concurrent use of both extent and grade. The grid ratio method was slightly better in predicting tumor progression and patient survival than a second method of assessing the percentage of prostatic tissue involved by tumor, the pathologist's percentage estimate. These results indicate that it is important to quantitate tumor extent within prostatectomy specimens; such quantitation need not require step-sectioning of the entire prostate and an expensive and time-consuming method such as computerized morphometrics but rather may be performed by a simple estimate of the percentage of the prostate involved by tumor. Reporting of histologic grade and tumor extent in the prostate gland is recommended as both appear to be important in identifying those patients at risk for a poor outcome after prostatectomy for prostatic carcinoma.
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PMID:Intraglandular tumor extent and prognosis in prostatic carcinoma: application of a grid method to prostatectomy specimens. 238 73


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