Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective study of cellular DNA content was made by means of flow cytometry in a nonconsecutive series of 100 patients undergoing surgery for primary colorectal adenocarcinoma. DNA-aneuploidy was present in 80% of cases (80/100); 39% of these were multiclonal (31/80). There was no significant correlation between DNA-ploidy and the clinical and pathological features examined, except for the primary tumor site (right colon vs. left colon vs. rectum: P less than 0.001). After a minimum follow-up of 30 months, out of 40 patients with no local invasion and/or distant metastases, 100% (9/9) of those with DNA-diploid neoplasias showed no signs of disease relapse, vs. 55% (17/31) of the DNA-aneuploid cases (P less than 0.05). Furthermore, in 45 cases with a minimum follow-up of 30 months, overall survival was 90% in patients with DNA-diploid carcinomas and 43% in the DNA-aneuploid cases (P less than 0.05).
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PMID:Patterns of DNA-ploidy in operable colorectal carcinoma: a prospective study of 100 cases. 189 Aug 38

The carcinogen-treated cockerel is a model for studying the early stages of arteriosclerotic plaque development. Carcinogen administration accelerates arteriosclerotic plaque development in cockerels, and transforming elements are present in DNA from advanced human plaques. In this study, we asked whether transforming elements could also be detected at early stages of plaque development in cockerels. NIH3T3 cells were transfected with DNA from plaques isolated from carcinogen-treated cockerels and from the healthy arterial wall underlying the plaques. Approximately 5 x 10(6) cells from each group were injected into nude mice. Tumors appeared in five of five mice in the plaque DNA group; no tumors appeared in mice from the healthy arterial wall group. All five plaque DNA-associated tumors hybridized to a cockerel genomic probe. Eight cockerel-specific bands were identified in EcoRI digests of first-round (primary) tumors. DNA from a primary tumor was tested in a second round of transfection. Five of five mice developed tumors after injection with these secondary transformants. All second-round tumors contained cockerel DNA, and a prominent cockerel-specific band (greater than 28 kb) was seen in EcoRI digests of all second-round tumors. In addition, a 5.2-kb band appeared prominently in one of five second-round tumors. No evidence was found for activation of the oncogenes Ha-ras, Ki-ras, src, or myc in the plaque-associated tumors. Similarly, DNA from plaque-associated tumors did not hybridize to probes for Marek disease virus, herpes simplex virus 1, or reverse transcriptase, suggesting that neither herpesviruses nor retroviruses are involved in the transforming activity of plaque DNA. These results indicate that transforming elements are a general property of arteriosclerotic plaques and are detectable in plaques of young animals.
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PMID:Transforming potential is detectable in arteriosclerotic plaques of young animals. 190 51

The cellular DNA content of 90 primary squamous cell carcinomas of the floor of mouth was determined by flow cytometry. Aneuploid cell lines were detected in 86% of the cases. The proportion of diploid carcinomas decreased with size (T1: 63%, T2: 11%, T3: 7%) and histologic grade (G1: 17%, G2: 16%, G3: 9%). Only 15% of the diploid, but 61% of the aneuploid tumors showed evidence of lymph node involvement. A 96% sensitivity of the test and a negative predictive value of 85% emphasize the prognostic importance of DNA ploidy in the primary tumor to evaluate the risk of subclinical dissemination.
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PMID:[The DNA ploidy in squamous cell carcinomas of the mouth floor determined by flow cytometry]. 193 36

The nuclear DNA ploidy pattern and c-erbB-2 oncoprotein expression in primary and metastatic lesions were investigated using paraffin-embedded materials from 44 cases of colorectal carcinoma with hepatic metastases and 45 cases without hepatic metastases. The frequency of aneuploidy and positive staining of c-erbB-2 in primary tumor with hepatic metastases were significantly higher compared with those without hepatic metastases (p less than 0.05). There were significant correlations between diameter of metastases and DNA ploidy pattern of the metastases and between metachronous metastases, degree of metastases, vessel involvement and DNA ploidy pattern of the primary tumor. Positive staining of c-erbB-2 was detected more frequently with the advancement of depth of tumor invasion. There was no significant correlation between DNA ploidy pattern and c-erbB-2 expression. In the survival of patients whose primary tumor and hepatic metastases were resected, it was shown that DNA ploidy pattern of metastases was the most important independent prognostic factor. Expression of c-erbB-2 in primary tumor predicted the hepatic metastases.
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PMID:[DNA content and c-erbB-2 oncoprotein expression in hepatic metastases from colorectal carcinoma--in relation to clinicopathologic findings and prognosis]. 196 Nov 85

The DNA ploidy pattern and amplification of ERBB and ERBB2 genes were examined in paraffin-embedded tissue from gastric carcinomas using flow cytometry and a slot-blot hybridization technique. The incidence of aneuploidy in well differentiated adenocarcinomas (56%) was significantly higher (p less than 0.05) than that in poorly differentiated adenocarcinomas (21%). The DNA ploidy pattern was not remarkably different between the primary tumors and metastatic deposits in lymph nodes. Of the nine specimens having an aneuploid stem cell line in the primary tumor and/or in metastases, three showed ERBB2 gene amplification and one showed ERBB gene amplification. The incidence of epidermal growth factor (EGF) immunoreactivity in tumor cells showed no difference between diploid and aneuploid tumors. These findings indicate that aneuploidy is frequently associated with amplification of ERBB and ERBB2 genes.
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PMID:DNA ploidy pattern and amplification of ERBB and ERBB2 genes in human gastric carcinomas. 197 Jun 90

We have previously shown, using tumor cell populations genetically tagged by random integrations of plasmid DNA, that metastatically-competent clonal cell variants have a strong growth advantage within primary tumors over their non-metastatic counterparts. As a result, primary tumors can become overgrown by the progeny of such cells, a process referred to as "clonal dominance" of primary tumors by metastatically-competent cells. Because of the well-known "metastatic inefficiency" of the multi-step cascade process of spread and growth, clonal dominance within primary tumors may be necessary for distant metastatic spread or increase the probability of its occurrence. To examine this hypothesis mice were inoculated s.c. with mixture of non-metastatic and genetically tagged, metastatically-competent mouse mammary carcinoma cells in defined ratios, but always containing an excess of the unmarked non-metastatic population. Progressive overgrowth of the metastatic subpopulation was monitored as a function of time by Southern analysis of DNA obtained from mixed primary tumors. This allowed us to evaluate the effects that surgical removal of the primary tumor had before, during and after effective clonal dominance, and what influence this had on the subsequent formation of distant metastases. Surgical removal of primary tumors before metastatic clonal dominance resulted in a low (0.25%) frequency of lung metastases, whereas removal just 1 or 2 weeks later during or after clonal dominance was achieved resulted in a high (75-100%) frequency of such metastases. Our results support the hypothesis that dominance of primary tumors by metastatically competent cells may be necessary for distant metastatic spread, and also suggest that clonal interactions play a significant role in modulating the metastatic ability of tumor cells in vivo.
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PMID:Dominance of metastatically competent cells in primary murine breast neoplasms is necessary for distant metastatic spread. 198 66

Two cases of the so-called ovarian myxoma are reported. One was from a 13-year-old girl who had a 31-year follow-up and no evidence of recurrence. The second case, from a 65-year-old woman, recurred intraperitoneally, 19 years after the surgery. Both tumors were myxoid, with round to stellate cells. Immunohistochemical, electron microscopic (EM), and DNA flow cytometric (FCM) studies were performed on formalin-fixed, paraffin-embedded tissue of the second patient on both the primary tumor and the recurrence. Tumor cells expressed vimentin and were focally positive for desmin and myoglobin. EM findings suggested a fibroblastic differentiation. An aneuploid cell population was present in the recurrent tumor by DNA-FCM studies. Only four other cases of so-called ovarian myxoma were reported to date, and the follow-up does not exceed 18 months. The authors conclude that the presence of aneuploidy and the late recurrence of one of their cases suggest that certain ovarian myxomas might behave like low-grade sarcomas. The histogenesis of this tumor remains unsettled, but similarities were found with myxomas in other locations.
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PMID:Ovarian myxoma. A study of two cases with long-term follow-up. 199 43

Little is known about the prevalence and significance of ras gene activation in neural crest tumors such as neuroblastomas, pheochromocytomas, and medullary thyroid cancers (MTCs). Therefore, we analyzed DNA from 10 human neuroblastoma cell lines and 10 primary human pheochromocytomas for activating mutations in N-ras, H-ras, and K-ras. We also studied DNA from 24 primary neuroblastomas and 10 MTCs for N-ras mutations. ras genes were analyzed by direct sequencing of specific DNA fragments amplified by the polymerase chain reaction. With the exception of the SK-N-SH cell line, the examined ras gene sequences were normal in all the neuroblastomas, pheochromocytomas, and MTCs tested. A single point mutation was identified at codon 59 (GCT(ala)----ACT(thr)) in one N-ras allele in an SK-N-SH subline. Interestingly, this mutation is different from the activating codon 61 mutation which resulted in the initial identification of N-ras from SK-N-SH DNA. Therefore, we analyzed the sequences of earlier passages and sublines of the SK-N-SH cell line, but mutations at codon 59 or 61 were not detected, suggesting that neither mutation was present in the primary tumor. Our results indicate that N-ras mutations may occur spontaneously during in vitro passage of cell lines but rarely, if ever, occur in primary neuroblastomas, pheochromocytomas, and MTCs. In addition, we have not found H-ras or K-ras mutations in any neuroblastoma cell line or primary pheochromocytoma.
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PMID:Low frequency of ras gene mutations in neuroblastomas, pheochromocytomas, and medullary thyroid cancers. 199 49

Our previous studies using randomly integrated plasmid DNA as unique clonotypic markers of SPI mouse mammary tumor cells transplanted into syngeneic CBA/J or nude mice demonstrated reproducible selection and eventual overgrowth of the primary transplant tumors by genotypically distinct metastatic subclones. Two independent metastatic SPI clones, neo5 and ras1, were shown to exhibit "clonal dominance" relative to the non-metastatic SPI tumor-cell population. These results suggested that the capacity for preferential growth within the tumors may be related to cellular properties associated with metastatic ability. To investigate the clonal interactions of metastatic SPI clones present within the same tumor mass, we have analyzed tumors composed of paired mixtures of neo5 and ras1. The tumors were monitored for the relative proportion of each clone by Southern blot analysis. The ras1 clone was found to dominate over the neo5 clone in the majority of tumors examined, even when present as 1% of the mixed inoculum. This represents a 20- to 50-fold enrichment of ras1, while the proportion of neo5 within the tumors was reduced at least 5-fold. No evidence for selection of either clone was seen during co-culture in vitro. Neo5 and ras1 are indistinguishable with respect to tumorigenic and metastatic potential when inoculated separately into different mice, suggesting that clonal dominance is independent of metastatic ability. Analysis of the metastases resulting from mixed inocula indicates that it is possible for a subpopulation representing less than 1% of the primary tumor mass to give rise to metastases. This also suggests that the process of metastasis within metastatic tumors is independent of clonal dominance.
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PMID:Clonal selection within metastatic SP1 mouse mammary tumors is independent of metastatic potential. 200 57

To investigate tumor cell heterogeneity and subpopulations with metastatic ability in differentiated adenocarcinoma of the lung, the primary and metastatic lesions in 20 cases of differentiated adenocarcinoma were examined by histologic and cytofluorometric DNA analyses. The primary tumor was divided histologically into three compartments: tumor area of type 1, papillary adenocarcinoma with thin stroma; tumor area of type 2, papillary adenocarcinoma with thickened fibrovascular stroma: tumor area of type 3; solid carcinoma with scant gland formation. The nuclear DNA content (NDC) was higher in type 2 than in type 1 tumor in terms of mean NDC and DNA histogram pattern (p less than 0.01). Metastatic tumors in distant organs often resembled the type 2 of primary tumors histologically and also in their DNA histogram patterns, and their mean NDC values were significantly correlated with each other (p less than 0.01). Metastatic tumors in regional lymph nodes had a significantly lower mean NDC than those in distant organs (p less than 0.01). These results suggest that (1) type 2 tumors originate from type 1 tumors by malignant progression and metastasize hematogenously, and (2) hematogenous metastases are composed of tumor subclones different from those of lymphatic metastases.
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PMID:Tumor cell heterogeneity and subpopulations with metastatic ability in differentiated adenocarcinoma of the lung. Histologic and cytofluorometric DNA analyses. 200 98


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