SEARCH · PubMed Health

Results for “Metastatic patterns”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources

PubMed2004

Nephroblastoma arising in a germ cell tumor of testicular origin.

We report a nephroblastoma arising in a germ cell tumor of testicular origin occurring in a 22-year-old man. Orchiectomy demonstrated a malignant mixed germ cell tumor composed of mature and immature teratoma with nephroblastoma and rhabdomyosarcoma. Following chemotherapy, the patient developed supraclavicular and retroperitoneal lymphadenopathy. Excision demonstrated metastatic teratoma at both sites. No recurrence was noted with 21 months of additional follow-up. Using tissue microdissection and loss of heterozygosity analysis, we investigated the clonality of the mature teratoma, immature teratoma, nephroblastoma, and rhabdomyosarcoma components of the primary tumor and of the metastatic mature teratoma at the two separate distant sites. Nine microsatellite polymorphic makers were used to examine the pattern of allelic loss in both primary and metastatic tumors. Loss of heterozygosity was found in 4 DNA loci, and the same pattern of allelic loss was demonstrated at all 4 loci in all of the different components of the primary tumor and the metastatic mature teratomas, supporting the germ cell tumor origin of the nephroblastoma component. Loss of heterozygosity on chromosome 17p13 (TP53) was detected in metastatic mature teratoma, but not in the primary tumor. Loss of heterozygosity was observed at 11p13, the locus of WT1 inactivation in patients genetically predisposed to nephroblastoma, and this loss may be an important genetic mechanism in nephroblastomatous differentiation of germ cell tumors. These data support a common clonal origin for nephroblastoma and the other germ cell tumor components.

Adult↗

PubMed2000

Cytokeratin 7 and 20 expression in choroid plexus tumors: utility in differentiating these neoplasms from metastatic carcinomas.

Tumors derived from choroid plexus epithelium are uncommon and may exhibit a wide variety of histologic patterns. They often are difficult to distinguish from metastatic carcinomas. Previous studies that addressed this issue yielded conflicting results. Recent reports have demonstrated that evaluation of coordinate expression of cytokeratin (CK) 7 and CK20 aids in distinguishing primary from metastatic lesions in a number of anatomic sites and that tumors that commonly are metastatic to the brain retain their CK7/CK20 immunophenotype in this location. We examined 35 choroid plexus tumors with a panel of antibodies to determine their CK7/CK20 immunophenotype. Tumors from 35 patients (7 male, 28 female; mean age, 25 years), including 31 choroid plexus papillomas and 4 atypical papillomas, were evaluated. All tumors were intraventricular or within the cerebellopontine angle and composed predominantly of orderly columnar epithelial cells resting on distinct fibrovascular cores. Atypical papillomas contained combinations of focal loss of architectural pattern, increased mitotic activity, necrosis, and brain parenchymal invasion. No lesion was unequivocally malignant. Twenty-six tumors (74%), including all atypical papillomas, were CK7 positive and CK20 negative. Two tumors stained with both markers, one stained with CK20 only, and six stained with neither marker. Other findings included expression of glial fibrillary acidic protein in 24 tumors, S-100 protein in 19 tumors, transthyretin in 31 tumors, Ber EP4 in 1 tumor, CAM5.2 in 33 tumors, epithelial membrane antigen in 4 tumors, and pancytokeratin in 27 tumors. Our results indicate that the majority of choroid plexus tumors have a CK7-positive/CK20-negative immunophenotype. This finding may be useful in differentiating these lesions from metastatic carcinomas that have differing CK7/CK20 profiles.

Adolescent↗

PubMed1994

Primary brain tumors differ in their expression of octamer deoxyribonucleic acid-binding transcription factors from long-term cultured glioma cell lines.

Nervous system-specific transcription factors that bind to the octameric deoxyribonucleic acid sequence motif ATGCAAAT (or ATTTGCAT) are known as N-Oct proteins. Neurons and glia contain the ubiquitous Oct-1 protein and four polypeptide complexes termed N-Oct-2, N-Oct-3, N-Oct-4, and N-Oct-5. Previously, we showed that N-Oct proteins are differentially expressed by human neuroblastoma and glioblastoma cell lines in vitro. We have now extended this work to freshly isolated human primary and metastatic brain tumors. Contrary to brain tumor cell lines, of the five astrocytomas and three glioblastomas analyzed, all but two tumors displayed the complete N-Oct protein profile, irrespective of histopathological tumor grade. Two astrocytomas were negative for N-Oct-4. Ten of 13 ependymomas exhibited N-Oct-2, N-Oct-3, and N-Oct-4 but lacked the N-Oct-5 complex. In contrast, brain metastases of two patients with extracerebral carcinomas contained only Oct-1, and cerebral metastases from two cases of B cell lymphomas showed Oct-1 and Oct-2 complexes, the characteristic Oct protein pattern of B lymphocytes. Thus, metastatic carcinoma and lymphoma expressed a non-nervous system phenotype of Oct proteins.

Astrocytoma↗

PubMed2001

Analysis of expressions of components in the plasminogen activator system in high- and low-metastatic human lung cancer cells.

PURPOSE: To determine the expressive patterns of the components of the plasminogen activator system in human large-cell lung carcinoma strains and to analyze the effects of the patterns on tumor invasion and metastasis. METHODS: The in vitro and in vivo invasive and metastatic potential of two human large-cell lung carcinoma strains with high (strain 95D) and low (strain 95C) metastatic potential was further confirmed by the Boyden chamber model and nude mice model. After this, the expressions of the components of the plasminogen activator system--including urokinase-type and tissue-type plasminogen activator (uPA and tPA), urokinase receptor (uPAR), and type-1 and type-2 plasminogen activator inhibitor (PAI-1 and PAI-2) in strain 95D and 95C cells--were determined by RT-PCR and immunohistochemical staining. The effects of monoclonal antibodies of uPA, uPAR, and PAI-1 on the invasive potential of strain 95D cell line were also evaluated. RESULTS: Strain 95D cells were found to have a stronger in vitro and in vivo invasive and metastatic potential than strain 95C cells. In the former, the average number of infiltrating cells in the in vitro model in one field of vision (40055) was 73.75 +/- 7.42, while in the latter, it was 56.33 +/- 6.28 (P < 0.001). Lung metastatic loci were observed in all six nude mice inoculated with 95D cells (6/6), but not in any of the nude mice inoculated with 95C cells (0/6). The high-metastatic strain 95D cells expressed higher uPA and uPAR and lower tPA and PAI-2 than the low-metastatic strain 95C cells. The PAI-1 expressions in both 95D and 95C cells were almost the same. Monoclonal antibodies of uPA and uPAR greatly reduced the invasive potential of strain 95D cells in vitro. CONCLUSIONS: These data suggest that the invasive and metastatic potential of human large-cell lung carcinoma cell lines is associated with differential expressions of the components of the plasminogen activator system and that the determination of these components may be used as a marker for judging clinically the possibility of tumor metastasis as well as the prognoses of patients.

Carcinoma, Large Cell↗

PubMed1986

[The role of intra-operative biopsy in the diagnosis of regional metastases of lung cancer].

The paper discusses the results of a histologic study of intrathoracic lymph nodes removed during surgery for lung cancer in 621 cases at different stages of metastatic spread. The gross appearance of some lymph nodes did not match their real histologic pattern: about 36% of grossly-identifiable metastatic nodes were microscopically shown to be intact whereas about 12% of grossly normal lymph nodes proved to be involved, particularly in cases of adenocarcinoma. Most of the enlarged and compact lymph nodes in cases of low-differentiated lung carcinoma revealed metastases. Intraoperative biopsy of intrathoracic lymph nodes followed by microscopy serves as a highly-predictive procedure in assessing the extent of regional dissemination of lung cancer.

Biopsy↗

PubMed1990

Role of glycolipids in the metastatic process: characteristics of neutral glycolipids in clones with different metastatic potentials isolated from a murine fibrosarcoma cell line.

We investigated whether metastatic phenotype is associated with a characteristic glycolipid pattern. For this study, we developed a system of variants with different metastatic potentials that we isolated from the highly metastatic T3 murine fibrosarcoma line by culture in 0.3% agar or on plastic. The glycolipid profiles of T3 cells and of their highly metastatic isolates were characterized by a high level of globotriaosylceramide (Gb3ose). On the other hand, Gb3ose was reduced in a weakly metastatic clone isolated from T3 cells. A reduced level of Gb3ose was also found in a weakly metastatic subclone isolated from a highly metastatic T3 clone. Propagation of this subclone led to the emergence of a series of variants which expressed a high metastatic potential together with a high Gb3ose level. We also observed that Gb3ose was 10 times more prevalent on the cell surface in T3 cells than in a weakly metastatic clone. On the whole, these findings indicate that, in our system of metastatic cells, a high Gb3ose level correlates with metastatic phenotype. It is possible that the highly exposed Gb3ose in metastatic cells is relevant to the metastatic process in view of the role played by the unique molecular structure of this glycolipid in other models of cell-to-cell interaction.

Animals↗

PubMed1993

An immunohistochemical study of c-erbB-2 protein in gastric carcinomas and lymph-node metastases: is the c-erbB-2 protein really a prognostic indicator?

An immunohistochemical study of the c-erbB-2 protein was conducted on formalin-fixed paraffin-embedded tissue sections from 136 primary gastric carcinomas and 50 metastatic lymph-node tumors obtained at gastrectomy. Expression of the protein was detected in 35 of 136 primary gastric carcinomas (25.7%) and 22 of 50 metastatic lymph nodes (44%). The staining pattern of tumor cells was classified as membranous or cytoplasmic. An immunohistochemical study using serially diluted antibody demonstrated that 82.6% of positive cases in metastatic lymph nodes showed c-erbB-2 immunoreactivity stronger than that in the primary tumors. Membranous staining was stronger than cytoplasmic staining. c-erbB-2 protein of the cytoplasmic as well as membranous types was confirmed to be a 185-kDa whole molecule by immunoblotting. Correlation between the expression of c-erbB-2 protein and clinical and histological parameters was investigated. No significant correlation between 5-year survival rate of patients and expression of c-erbB-2 protein was found. In the poorly differentiated carcinoma group possessing c-erbB-2 protein, overall survival was significantly shorter than in cases without protein expression (p < 0.01). We conclude that c-erbB-2 protein is not a useful prognostic indicator in gastric carcinomas.

Female↗

PubMed1993

Serum CA-15.3 and CEA patterns in postsurgical follow-up, and in monitoring clinical course of metastatic cancer in patients with breast carcinoma.

Serum CA-15.3 and CEA levels were longitudinally determined in 307 patients with breast carcinoma during postsurgical follow-up and/or therapy. Of 120 patients with no apparent disease, the specificity of marker levels fluctuating within the normal range (true-negative) was 98% for CA-15.3 alone (P = 0.004) and about 88% for CEA alone or for the tests combined. However, the false-negative levels in patients with progressive cancer reduced the predictive value of the tandem to around 76%, i.e. normal levels of both markers correctly predicted uneventful postsurgical course in only three fourths of the patients. Of 187 patients with active disease, the sensitivity of raised or increasing marker levels was around 70% for CA-15.3 alone or CEA alone, and 82% for the tests combined (P = 0.006). The 11% false-positive rate of CEA in patients with no apparent disease decreased the predictive value of a positive test from 98% for CA-15.3 alone (P = 0.006) to 91% for CEA alone or the tandem. Serum CA-15.3 or CEA paralleled the site of relapse: at least one marker was found elevated in 60% of patients with locoregional disease or with metastases to the lungs or bones exclusively, and in 90% of those with metastases to the lungs and bones or to the liver. A concurrent decrease of both marker levels reflected response to therapy while an increase of at least one marker level reflected treatment failure. It may be concluded that the marker tandem was better than either marker alone for follow-up aimed at detection of relapse, and that the tests were approximately 80% accurate for follow-up and/or monitoring therapy.

Adult↗

PubMed1990

[Flow cytometric analysis in colorectal cancer with hepatic metastases and its relationship to metastatic characteristics and prognosis].

Nuclear DNA ploidy studies were performed by flow cytometry on extracted nuclei from 65 heptic metastases from colorectal cancer. In 25 patients, both primary and metastatic lesions were available for analysis. Primary carcinomas were DNA diploid pattern in 48.1%, DNA aneuploid in 51.9%. Of 31 hepatic metastases, 11 (35.5%) metastases showed a DNA diploid pattern, and 25 (64.5%) showed a DNA aneuploid pattern. Ploidy pattern was constant between primary and metastases in 80% of tumors. No significant relationship between metastatic characteristics and DNA ploidy pattern was found. The DNA aneuploid cancers had a relatively poorer prognosis in patients with unresectable hepatic metastasis. In resected hepatic metastases from colorectal cancer, rate of hepatic recurrence with DNA diploid pattern was lower than that with DNA aneuploid pattern. Survival of patients with DNA diploid metastases (71% alive at 5 years) was significantly better than that of patients with DNA aneuploid metastases (21% alive at 5 years) (p less than 0.05). These results demonstrated that flow cytometric DNA ploidy measurements may have prognostic value for patients with hepatic metastases from colorectal cancer.

Aneuploidy↗

PubMed2006

The role of histone modifications in epigenetic transitions during normal and perturbed development.

Epigenetic mechanisms control eukaryotic development beyond DNA-stored information. DNA methylation, histone modifications and variants, nucleosome remodeling and noncoding RNAs all contribute to the dynamic make-up of chromatin under distinct developmental options. In particular, the great diversity of covalent histone tail modifications has been proposed to be ideally suited for imparting epigenetic information. While most of the histone tail modifications represent transient marks at transcriptionally permissive chromatin, some modifications appear more robust at silent chromatin regions, where they index repressive epigenetic states with functions also outside transcriptional regulation. Under-representation of repressive histone marks could be indicative of epigenetic plasticity in stem, young and tumor cells, while committed and senescent (old) cells often display increased levels of these more stable modifications. Here, we discuss profiles of normal and aberrant histone lysine methylation patterns, as they occur during the transition of an embryonic to a differentiated cell or in controlled self-renewal vs pro-neoplastic or metastatic conditions. Elucidating these histone modification patterns promises to have important implications for novel advances in stem cell research, nuclear reprogramming and cancer, and may offer novel targets for the combat of tumor cells, potentially leading to new diagnostic and therapeutic avenues in human biology and disease.

Animals↗

PubMed1994

An immunohistochemical study of the extracellular matrix in oral squamous cell carcinoma and its association with invasive and metastatic potential.

The expression of extracellular matrices (ECMs) laminin (LN), type IV collagen (IV C), heparan-sulphate proteoglycan (HS-PG), fibronectin (FN), tenascin (TN), decorin and vitronectin (VN) was examined immunohistochemically in 112 primary tumours and 29 metastatic cervical lymph nodes in oral squamous cell carcinoma (OSCC). In highly invasive primary tumours, the expression of LN, IV C and HS-PG in the basement membrane along the tumour-stroma borderline and the expression of decorin and VN in the tumour stroma at the invasive site were all significantly decreased. The expression of FN and TN in the tumour stroma at the same site was markedly increased. In peritumour stroma in metastatic lymph nodes, LN, IV C, HS-PG, decorin and VN were weakly expressed, while FN and TN were strongly expressed. Thus, the staining pattern of the ECMs in the metastatic lymph nodes was similar to that in highly invasive primary tumours. Furthermore, in primary tumours of metastatic cases, the expression of LN, IV C, HS-PG, decorin and VN obviously decreased, while the expression of FN and TN increased when compared with those of the non-metastatic cases. The investigation of ECMs in OSCC was valuable in predicting tumour behaviour.

Carcinoma, Squamous Cell↗

PubMed1988

Suppression of synthesis of tropomyosin isoform 2 in metastatic v-Ha-ras-transformed NIH3T3 cells.

We have reported that the synthesis of tropomyosin isoform 2 (TM2) is significantly suppressed in high-metastatic Lewis lung carcinoma cells compared with that in low-metastatic cells. In order to examine whether the change is also observed in other high-metastatic tumor cells, we compared the pattern of expressions of TM isoforms between NIH3T3 cells and v-Ha-ras-transformed NIH3T3 (pH1-3) cells, the latter of which was highly metastatic when injected into BALB/c nude mice. The results showed that the expression of TM2 was less in pH1-3 cells than in NIH3T3 cells, suggesting that the suppression of TM2 synthesis is involved in the expression of metastatic phenotype.

Animals↗

PubMed1998

Carcinosarcoma of the esophagus with metastases showing osteosarcoma: a case report and review of the literature.

Carcinosarcoma of the esophagus includes both carcinomatous and sarcomatous elements. The classification and histogenesis of carcinosarcoma is controversial. In a polypoid carcinosarcoma diagnosed in a resected esophagus the sarcomatous component was composed of dense interlacing bundles of spindle-shaped cells in the submucosa. Areas with transitional features between the two components were observed. Immuno-histochemical examination showed vimentin-positive cells in the sarcomatous areas. Subsequently, obtained autopsy specimens from the lung, kidney and iliac bone showed metastatic osteosarcoma composed of an interlacing pattern of bone or osteoid components. We suspected that the sarcomatous elements in the esophagus resulted from sarcomatous transformation of carcinoma cells, and that the metastatic lesions showed differentiation of neoplastic cells to the osteosarcoma.

Carcinosarcoma↗

PubMed1984

Local blood flow in Walker 256 metastatic brain tumors.

Local blood flow (F) in metastatic Walker 256 (WL-256) brain tumors produced by the intracarotid artery injection of WL-256 tumor cells in rats was measured using 14C-iodoantipyrine and quantitative autoradiography. Blood flow was variable in the tumors; the overall range was 2 to 222 ml hg-1 min-1 and the maximum range in an individual tumor extended over 150 ml hg-1 min-1. Small tumors had mean blood flows similar to surrounding brain. Medium to large tumors had significantly lower flows; the lowest values were usually measured in necrotic or cystic regions, although low values (less than 20 ml hg-1) were also measured in some viable-appearing tumor regions. Blood flow was significantly reduced in brain adjacent to medium and large but not small tumors. A global depression of brain and tumor blood flow was measured in two animals with hydrocephalus and the largest tumor burden. The blood flow patterns of the WL-256 metastatic tumor model are not uniquely different from other brain tumor models although some individual differences exist.

Animals↗

PubMed1991

Clonality and clonal evolution of hepatocellular carcinoma with multiple nodules.

To determine the clonal evolution of hepatocellular carcinoma, the integrated hepatitis B virus DNA patterns of the main tumor, satellites and/or metastatic lesions were analyzed by Southern-blot hybridization in 28 hepatocellular carcinomas, including three HBsAg-seronegative cases. Unicentric or multicentric hepatocellular carcinoma was confirmed by histopathological criteria in 89% of the cases. Among 17 unicentric hepatocellular carcinomas, minor changes of the integration pattern--including partial loss or addition of the integration sites or both--were detected in the metastatic lesions in 29% of the cases. Furthermore, none of five cases with free-form hepatitis B virus DNA in the primary tumor had detectable free hepatitis B virus DNA in the metastatic lesions. These results suggest that the alteration of integrated hepatitis B virus DNA pattern during the course of tumor growth and metastasis may occur more often than previously perceived and that the switch-off of virus replication may be related to tumor metastatic potential. In eight cases with unilateral, multicentric hepatocellular carcinoma, two clones were detected in six cases, three were seen in another and four were seen in one. One case of note was a 9-yr-old boy with two histological types and two different integration patterns, one associated with vascular invasion and lung metastasis. Three patients with bilateral hepatocellular carcinoma were confirmed to have bicentric or tricentric hepatocellular carcinoma rather than intrahepatic dissemination and had survival rates similar to those in unicentric hepatocellular carcinoma. Three invasive HBsAg-seronegative hepatocellular carcinomas were found to have hepatitis B virus DNA integration and were of unicentric origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Southern↗

PubMed1992

[Endoscopic ultrasonography for preoperative diagnosis of the hilar and mediastinal lymph node metastases in lung cancer].

Fifty patients with lung cancer underwent transesophageal endoscopic ultrasonography (EUS) for preoperative detection of metastases to the hilar and mediastinal lymph nodes. An electronic ultrasonic fiberscope with a linear array (EPB-503-FS, Machida-Toshiba) was used. Later, in surgery, a total of 513 nodes that could have been detected by EUS were removed. Of these, 54 nodes were found to be metastatic histologically, and 459 were non-metastatic. The rate of detection by EUS was 65% (35/54) for the metastatic nodes; the rate was 41% (186/459) for the non-metastatic nodes (p less than 0.01). Metastatic nodes were detected at high rates in every lymph node site. Non-metastatic nodes were detected at low rates in sites 1, 2, and 4, and at the highest rate in site 7. Metastatic nodes had characteristic internal echoes, affected by the extent of tumor and necrosis present in a node, and were detected more easily than non-metastatic nodes. For larger or rounder nodes, metastasis was more common (p less than 0.01). Lymph nodes that could be detected were classified into six types by their internal echo patterns; three of these types were rarely metastatic, and were called 'negative'; the other three were often metastatic, and were called 'positive'. In histological examinations, of the 'negative' nodes found in fact to be metastatic histologically, invasion by the tumor tended to be diffuse and necrosis was minute. The 'positive' nodes that were in fact metastatic tended to have one of two internal echo patterns (depending on the amount of necrosis) when invasion was diffuse, and a third pattern when invasion was localized.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Models of metastatic prostate cancer: a transgenic perspective.

PURPOSE: Transgenic mouse models are proving to be invaluable in our effort to understand the molecular basis of metastatic prostate cancer (CaP). We review and discuss how current animal models have contributed to our understanding of the metastatic cascade and how transgenic technology is being used to develop the next generation of mouse models. Our goal is to provide a review of the recent advances and provide a framework for further studies. MATERIALS AND METHODS: We performed a MEDLINE search of the literature on CaP metastasis transgenic and animal models. RESULTS: We present a summary of the characteristics of nine different animal models of CaP. Each model is unique and provides valuable insight into the molecular mechanisms governing the progression of CaP. Our experience with transgenic models and all the new data from the literature predicts that we will be able to develop genetically engineered mice that accurately mimic the heterogeneity, androgen-independent growth, and metastatic spread seen in clinical disease. CONCLUSION: In order to elucidate the molecular mechanisms of CaP metastasis, it will be necessary to compare gene and protein expression patterns and biochemical analyses of clinical metastatic disease with data obtained from current models. We will also need to refine our ability to engineer and characterize genetic perturbation models. This type of integrative and iterative approach should facilitate better understanding of the molecular biology of CaP metastases.

Animals↗

PubMed1981

Comparative morphology of primary and secondary deposits of prostatic adenocarcinoma.

In 42 patients with metastatic adenocarcinoma of the prostate, histopathologic specimens of the original prostatic biopsy and lymphatic metastasis were classified using the grading system of tumor differentiation described by Gleason et al. The observed similarity between prostatic biopsy morphologic and the morphology in the corresponding lymphatic metastasis supports the concept that the histologic growth pattern of the primary tumor is reduplicated in the metastatic lesions. The observation that a more anaplastic pattern did not appear in the metastatic deposits implies that factors other than cellular loss of differentiation are responsible for the cells' ability to metastasize.

Adenocarcinoma↗