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At least 91 records · Page 5Linked to original sources
PubMed1985

[Metachronous hematogenous metastasis of gastric cancer--histopathologic characteristics of gastric cancer developing of the liver, lung or bone metastasis].

Fifty-seven gastric cancer patients developing metachronous hematogenous metastasis were histopathologically analyzed. In 37 patients who developed metachronous liver metastasis as the main pattern of recurrence, papillary adenocarcinoma was the most frequent histologic type, followed by poorly differentiated adenocarcinoma of the medullary type. In 20 patients with metachronous lung or bone metastasis, poorly differentiated adenocarcinoma of the scirrhous type was the common histologic pattern. From the present data, we assume that liver metastasis of gastric cancer occurs when cancer cell clusters are transported to the liver, where they attach and proliferate, whereas single cells passed through the portal system tend to establish secondary deposits in the lung or bone.

Bone Neoplasms↗
PubMedDate not supplied

Two cases of gastric involvement of esophageal cancer: intramural metastasis and intramural lymph node metastasis.

Cases of esophageal cancer with intramural metastasis to the stomach and esophageal cancer with metastasis to an intramural lymph node of the stomach are herein reported. The former patient was a 52 year-old male. Squamous cell carcinoma (SCC) of the lower esophagus with an intramural metastasis located at the gastric cardia and a small leiomyoma at the fornix were resected. The latter patient was a 70 year-old female. SCC of the lower esophagus and an intramural lymph node metastasis located at the anterior wall of the gastric cardia were resected. The patient died nevertheless of multiple liver metastases. These gastric involvements were detectable by endoscopy before surgery. The clinicopathological features of these esophageal cancers were characterized; the sites were the lower part of the esophagus, and extreme lymphatic and vascular invasions were shown histologically. The gastric tumors were located in the upper third of the stomach, and the findings revealed submucosal tumors. It is therefore important to discriminate other gastric tumors, and to resect them simultaneously with esophageal cancer when a gastric tube has been used for reconstruction after esophagectomy.

Aged↗
PubMed2004

Caffeine suppresses metastasis in a transgenic mouse model: a prototype molecule for prophylaxis of metastasis.

A significant fraction of cancer patients have occult disseminated tumors at the time of primary diagnosis, which usually progress to become clinically relevant lesions. Since the majority of cancer mortality is associated with metastatic disease, the ability to inhibit the growth of the secondary tumors would significantly reduce cancer-related morbidity and mortality. We have investigated whether caffeine, which has been shown to suppress tumor cell invasiveness and experimental metastasis, can suppress metastasis in a spontaneous transgene-induced mammary tumor model. Chronic exposure to caffeine prior to the appearance of palpable mammary tumors significantly reduced both tumor burden and metastatic colonization. However, when caffeine exposure began after the appearance of frank tumors, caffeine suppressed metastasis without changing primary tumor burden. The means by which caffeine suppressed metastatic activity may be associated with inhibition of malignant transformation of mammary epithelial cells, inhibition of conversion of dormant tumor cells to micrometastases, micrometastases to macrometastases, or inhibition of tumor cell adhesion and motility. Gene and protein expression patterns resulting from caffeine treatment showed that metastasis suppression may be associated with up-regulation the mRNA expression of multiple extracellular matrix genes, including Fbln1, Bgn, Sparc, Fbn1, Loxl1, Colla1, Col3a1, Col5a1, ColS5a2, ColSa3, Col6a1, Col6a2, and Col6a3. These data suggested that caffeine or other methyl xanthine derivatives may improve the clinical outcome in patients prior to and following the diagnosis of metastatic disease, and could potentially reduce the morbidity and mortality associated with disseminated tumors.

Animals↗
PubMed2003

Development of brain metastasis 5 years before the appearance of the primary lung cancer: "messenger metachronous metastasis".

We report a patient with a brain metastasis that presented 5 years before the primary adenocarcinoma of the lung from which it originated. The metastasis and the primary tumor were removed. To confirm their common origin, we used comparative genomic hybridization. We have named this type of metastasis "messenger metachronous metastasis." The patient remains well 79 months after the brain metastasectomy and 18 months after the lung surgery.

Adenocarcinoma↗
PubMed2006

Neuromedin U is regulated by the metastasis suppressor RhoGDI2 and is a novel promoter of tumor formation, lung metastasis and cancer cachexia.

Most deaths from urinary bladder cancer are owing to metastatic disease. A reduction in Rho GDP Dissociation Inhibitor 2 (RhoGDI2) protein has been associated with increased risk of metastasis in patients with locally advanced bladder cancer, whereas in animal models, RhoGDI2 reconstitution in cells without expression results in lung metastasis suppression. Recently, we noted an inverse correlation between tumor RhoGDI2 and Neuromedin U (NMU) expression, suggesting that NMU might be a target of the lung metastasis suppressor effect of RhoGDI2. Here we evaluated whether NMU is regulated by RhoGDI2 and is functionally important in tumor progression. We used small interfering RNA knockdown of endogenous RhoGDI2 in poorly tumorigenic and non-metastatic human bladder cancer T24 cells and observed increased NMU RNA expression. Although NMU overexpression did not increase the monolayer growth of T24 or related T24T poorly metastatic human bladder cancer cells, it did augment anchorage-independent growth for the latter. Overexpression of NMU in T24 and T24T cells significantly promoted tumor formation of both cell lines in nude mice, but did not alter the growth rate of established tumors. Furthermore, NMU-overexpressing xenografts were associated with lower animal body weight than control tumors, indicating a possible role of NMU in cancer cachexia. NMU overexpression in T24T cells significantly enhanced their lung metastatic ability. Bioluminescent in vivo imaging revealed that lung metastases in T24T grew faster than the same tumors in the subcutaneous microenvironment. In conclusion, NMU is a RhoGDI2-regulated gene that appears important for tumorigenicity, lung metastasis and cancer cachexia, and thus a promising therapeutic target in cancer.

Animals↗
PubMed2000

Levels of E2F-1 expression are higher in lung metastasis of colon cancer as compared with hepatic metastasis and correlate with levels of thymidylate synthase.

We recently reported that forced overexpression of the transcription factor E2F-1 in human HT-1080 fibrosarcoma cells resulted in corresponding high levels of thymidylate synthase (TS) and resistance to 5-fluoropyrimidines (D. Banerjee et al., Cancer Res., 58: 4292-4296, 1998). Because colorectal metastasis to the lung has higher TS levels than liver metastasis and is less responsive to treatment with 5-fluorouracil (R. Gorlick et al., J. Clin. Oncol., 16: 1465-1469, 1998), it was, therefore, of interest to measure E2F-1 expression in these tumors. In contrast to marginally increased levels of dihydrofolate reductase and topoisomerase I in lung metastasis as compared with liver metastasis, lung tumors had a 5-fold increase in E2F-1 expression as compared with liver tumors, corresponding to the relative levels of TS in these metastases. These data indicate that there exists a close correlation between E2F-1 and TS levels and provide a rationale for targeting this transcription factor, ie., E2F-1, for the treatment of certain cancers.

Adenocarcinoma↗
PubMed1986

[A case of alveolar soft-part sarcoma with recurrent cerebral metastasis--operative management of the cerebral metastasis].

A female patient noticed a painless swelling at the right thigh at the age of 12. Two years later, she had total removal for the tumor and irradiation. The diagnosis of the tumor was alveolar soft-part sarcoma. At the age of 16 she had left pneumonectomy for its metastasis. The next year the metastatic tumor is detected in the right lung. At 21 she was admitted to our service with a diagnosis of cerebral metastasis. Her chief complaints were headache, nausea and visual disturbance. Neurological examination revealed advanced choked disc and left homonimous hemianopsia. CT scan revealed a large vascular tumor in the right occipital lobe and chest film showed multiple metastatic shadows in right lung. A large bloody tumor was removed totally through right occipital craniotomy. She was discharged with a marked improvement of neurological symptom. Since then she had had 8 times of surgical removal for 10 cerebral metastatic tumors. Several chemotherapy was attempted for three times. At first adriamycin was administered after the first removal of cerebral metastasis. Methyl-CCNU and Picibanil was administered after the second removal. Soon after the chemotherapy, metastatic tumor recurred. Cisplatin was administered for the ninth metastasis. None of these chemotherapy had seemed to be benefit in the management. At 27 she had removal of metastatic tumor on chest wall. She died of respiratory embarrassment in thorax at 30. At autopsy she had metastatic tumors in right frontal lobe, right lung, mediastinum, heart, chest wall, and intestine. During her illness, she graduated from high school and college, and got a good job as a secretary.

Adult↗
PubMed1996

An experimental model of bone metastasis by human lung cancer cells: the role of parathyroid hormone-related protein in bone metastasis.

In the formation of bone metastasis, osteoclastic bone resorption is necessary before the expansion of tumor cells from bone marrow to bone, and several cytokines, which possess osteoclast-stimulating activity, could be involved in this step. In this paper, we describe a bone metastasis model in nude mice using human lung squamous cell carcinoma-derived cells (HARA), in which the parathyroid hormone-related protein (PTHrP) gene, one of the most potent osteoclast-activating factors, is strongly expressed. The injection of HARA cells (1 x 10(5)) into the left cardiac ventricle resulted in tumor colonies exclusively in the skeletal system at 4 and/or 8 weeks after inoculation. An anti-PTHrP antibody injected via a tail vein reduced the incidence of bone metastases, number of tumor colonies, and tumor volume after the inoculation of HARA cells. The injection of another line of human lung squamous cell carcinoma-derived cells (QG-56), in which the PTHrP gene is not expressed, resulted in no bone metastasis. These findings suggest that PTHrP plays an important role in the formation of bone metastasis.

Animals↗
PubMed1997

[Metastasis in metastasis].

Double metachron neoplasm was found in a 75 year-old man by the authors, myxoid chondrosarcoma as primer neoplasm of the right leg, and cecum adenocarcinoma. In the centre of myxoid chondrosarcoma's metastasis of the lung adenocarcinoma metastasis occurred. Metastasis in metastasis is a histological rarity.

Adenocarcinoma↗
PubMedDate not supplied

The role of neutrophils as cytotoxic cells in lung metastasis: suppression of tumor cell metastasis by a biological response modifier (PSK).

We aimed to determine the role of neutrophils and the usefulness of a protein-bound polysaccharide (PSK) in the suppression of tumor cell metastasis in the lung in vivo. Circulating neutrophils collected frm tumor-bearing animals (Line-10 hepatocarcinoma) induced a marked decrease in the size and number of metastatic foci in the lung. Although pulmonary macrophages (PAMs), lymphocyte and eosinophil in bronchoalveolar lavage (BAL) fluid increased following tumor cell inoculation, in addition to these findings we found that PSK caused an increase in BAL neutrophil levels causing increased of target cell toxicity and a marked decrease in the size and the number of lung metastatic foci. Superoxide anion generation of blood neutrophils collected from PSK-treated animals with metastasis showed forward acceleration. The presence of neutrophil chemotactic factors was confirmed in the BAL fluid of PSK-treated animals with metastasis, but not leukotriene B4. The results suggest that modulation of the tumor cell microenvironment by activation of neutrophils may prove to be an additional modality in treatment strategy by combining PSK as a biological response modifier with conventional therapies for lung metastasis.

Animals↗
PubMed1998

[Arachnoid metastasis of renal cell carcinoma: review of forms of tumor dissemination and review of its metastasis in the nervous system].

Contribution of one case of renal cells carcinoma, in an adult man, that during evolution developed arachnoid metastasis. The patient was first seen for a brain haemorrhage due to a bleeding metastasis. In later studies, a renal cells carcinoma was found to be the primary site of the brain condition. The evolution showed neurological manifestations in the limbs, and the arachnoid metastasis was detected. The paper includes imaging studies of the referred disease both al brain, renal and spinal level with CT and NMR studies. A revision is made of the different dissemination forms of renal cells tumours, as well as a review of the existing literature with regard to the nervous system metastasis. No case has been found in this review relative to spinal arachnoid dissemination.

Arachnoid↗
PubMed1992

[Clinical characteristics and prognosis of renal cell carcinoma. Statistical evaluation of possible determinants for distant metastasis, venous tumor thrombi, and lymph node metastasis].

To clarify the recent clinical characteristics of renal cell carcinomas and to evaluate possible determinants for metastasis and venous tumor thrombi, the authors reviewed data from 99 renal cell carcinoma patients treated at Nagoya University Hospital between 1980 and 1989. According to Robson's classification, stage I tumors were found in 48 patients, stage II in 9, stage III in 16, and stage IV in 26. Incidentally detected tumors appeared to be on the increase in recent years. Grade 1 tumors were significantly associated with low-stage tumors and expansive growth. Univariate and multivariate analyses using a logistic regression model demonstrated that venous tumor thrombi and histological grade were significantly related to distant metastasis. Univariate analysis revealed relative risks of 4.7 for venous tumor thrombus presence (pV1b-pV2 vs. pV0-pV1a, p = 0.005) and 8.5 for histological grade (grades 2 and 3 vs. grade 1, p = 0.04). Local invasion (pT3 vs. pT2a-pTb: a relative risk of 7.5, p = 0.0009) and infiltration pattern (INF beta and INF gamma vs. INF alpha: a relative risk of 11.5, p = 0.002). were associated with venous tumor thrombi. Local invasion (pT3 vs. pT2a-pT2b: a relative risk of 6.6, p = 0.03) was the only significant determinant for lymph node metastasis. The 5-year actuarial survival rate was 60.0% for all 99 patients. The 5-year survival rates for stage I and II tumors were, respectively, 91.8% and 64.8%.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Renal Cell↗
PubMed2005

Suppression of murine mammary carcinoma metastasis by the murine ortholog of breast cancer metastasis suppressor 1 (Brms1).

The murine ortholog (Brms1) of human breast cancer metastasis suppressor 1 shares 95% identity to the human metastasis suppressor, BRMS1, in amino acid structure. We tested Brms1 for suppression of metastasis of mouse mammary carcinoma cell line 4T1 in syngenic BALB/c mice, using orthotopic (mammary fat pad) injection as well as intravenous injection. As observed for BRMS1, transfection with Brms1 did not inhibit 4T1 primary tumor formation, but significantly suppressed lung colonization. We also show that Brms1 protein interacts with histone deacetylases, indicating involvement of Brms1 in murine Sin3-HDAC complex, like its human counterpart. Thus, because of similarities with its human ortholog, the results suggest that Brms1 will be useful as a model for studying mechanism of action of BRMS1.

Animals↗
PubMed2006

Gene expression profile analysis of an isogenic tumour metastasis model reveals a functional role for oncogene AF1Q in breast cancer metastasis.

To study the molecular mechanisms underlying breast cancer metastasis, gene expression profile analysis was performed on two well-established breast cancer cell lines with high and low metastatic potentials: MDA-MB-435HM and MDA-MB-435LM. The analysis was conducted using cDNA microarrays containing 8000 genes. Of 60 differentially expressed genes, ALL1-fused gene from chromosome 1q (AF1Q), a putative oncogene not described previously in breast cancer, was identified and found to be over-expressed in MDA-MB-435HM cells compared with MDA-MB-435LM cells. The results indicate that AF1Q may play an important role in breast cancer metastasis. To test this hypothesis, we generated an AF1Q high-expression cell line by stable transfection of AF1Q cDNA into MDA-MB-435LM cells. Results showed that over-expression of AF1Q led to a marked increase in the invasive and metastatic potential of MDA-MB-435LM cells in vitro and in vivo, accompanied by the up-regulation of matrix metalloproteinase-2 (MMP-2), MMP-9, transcription factor Ets-1, and RhoC expression in both mRNA and protein levels. Consistent with this observation, reduced AF1Q expression in MDA-MB-435HM cells by small interfering RNA (siRNA) resulted in a significant decrease in the invasive potential of MDA-MB-435HM cells in vitro and in the protein expression of MMP-2, MMP-9, Ets-1, and RhoC, compared with either parental or non-silencing control cells. These data provide functional evidence that oncogene AF1Q may be a novel mediator of metastasis promotion in human breast cancer through regulation of the MMP pathway and RhoC expression.

Blood Proteins↗
PubMed2002

Synergistic effects of L- and P-selectin in facilitating tumor metastasis can involve non-mucin ligands and implicate leukocytes as enhancers of metastasis.

P-selectin facilitates human carcinoma metastasis in immunodeficient mice by mediating early interactions of platelets with bloodborne tumor cells via their cell surface mucins, and this process can be blocked by heparin [Borsig, L., Wong, R., Feramisco, J., Nadeau, D. R., Varki, N. M. & Varki, A. (2001) Proc. Natl. Acad. Sci. USA 98, 3352-3357]. Here we show similar findings with a murine adenocarcinoma in syngeneic immunocompetent mice but involving a different P-selectin ligand, possibly a sulfated glycolipid. Thus, metastatic spread can be facilitated by tumor cell selectin ligands other than mucins. Surprisingly, L-selectin expressed on endogenous leukocytes also facilitates metastasis in both the syngeneic and xenogeneic (T and B lymphocyte deficient) systems. PL-selectin double deficient mice show that the two selectins work synergistically. Although heparin can block both P- and L-selectin in vitro, the in vivo effect of a single heparin dose given before tumor cells seems to be completely accounted for by blockade of P-selectin function. Thus, L-selectin on neutrophils, monocytes, and/or NK cells has a role in facilitating metastasis, acting beyond the early time points wherein P-selectin mediates interactions of platelet with tumor cells.

Animals↗
PubMed2005

Tumour size and vascular invasion predict distant metastasis in stage I breast cancer. Grade distinguishes early and late metastasis.

BACKGROUND: Recent Dutch guidelines recommend adjuvant systemic treatment (AST) for women with high grade stage I breast carcinoma > or =1 cm. High grade is defined as Bloom and Richardson grade 3 (B&R3), Nottingham modification, or mitotic activity (MAI) > or =10/1.59 mm2. AIMS: To investigate the validity of these histological prognostic factors as the exclusive defining criteria. MATERIALS/METHODS: Fifty patients with stage I breast carcinoma who developed distant metastases and 50 matched controls without metastasis were studied; none had received AST. RESULTS: Cases more often had tumours > or =1 cm (p = 0,019), B&R3 tumours (p = 0.059), grade 3 nuclei (p = 0.005), and vascular invasion (p = 0.007). No differences were found for MAI > or =10 (p = 0.46). In multivariate analysis, the only significant variables were vascular invasion and tumour size (odds ratios: 8.21 and 5.35, respectively). In a separate analysis, the 50 cases were divided into 25 patients with early and 25 with late metastasis. Those with early metastasis more often had B&R3 tumours (p = 0.009) and grade 3 nuclei (p = 0.006). No differences were found for tumours > or =1 cm, vessel invasion, or MAI > or =10. Using the present Dutch guidelines for AST, based on B&R3, 20 cases and 11 controls would have received AST. Based on MAI > or =10, 14 cases and 11 controls would have received AST. CONCLUSIONS: Tumour size and vessel invasion are the best prognostic factors for disease free survival in patients with stage I breast cancer. Dutch selection criteria for AST for these patients need to be improved. Some prognostic factors are time dependent, making their use as selection criteria for AST more complicated.

Adjuvants, Pharmaceutic↗
PubMed1993

[A case report of pulmonary metastasis of malignant fibrous histiocytoma (MFH) accompanied by mediastinal lymph node metastasis].

Mediastinal lymph node metastasis associated with pulmonary metastasis is rarely seen in soft tissue sarcoma. A case is presented in which investigation of primary lung cancer (cT2N2M0) in a 78-year-old woman with a history of MFH of the left thigh revealed pulmonary metastasis of MFH accompanied by paratracheal (#2) and anterior mediastinal (#3a) lymph node metastases.

Aged↗
PubMed2006

Identification of breast cancer metastasis-associated proteins in an isogenic tumor metastasis model using two-dimensional gel electrophoresis and liquid chromatography-ion trap-mass spectrometry.

To better understand the molecular mechanisms underlying breast cancer metastasis and search for potential markers for metastatic progression, we have developed a highly metastatic variant of human MDA-MB-435 breast cancer cell line through in vivo stepwise selection of pulmonary metastatic cells caused by parental MDA-MB-435 cells in the athymic mice. Comparative proteomic analysis using 2-DE and LC-IT-MS revealed that 102 protein spots were reproducibly altered more than three-fold between the selected variant and its parental counterpart. Eleven differentially expressed protein spots were identified with high confidence using SEQUEST with uninterpreted tandem mass raw data. Cathepsin D precursor, peroxiredoxin 6 (PDX6), heat shock protein 27 (HSP27), HSP60, tropomyosin 1 (TPM1), TPM2, TPM3, TPM4, 14-3-3 protein epsilon, and tumor protein D54 were up-regulated in the highly metastatic variant, whereas alpha B-crystalline (CRAB) was only detected in its parental counterpart. Differential expression was confirmed for four proteins including PDX6, CRAB, TPM4, and HSP60 by real-time quantitative PCR and Western blotting analysis in our model. Immunohistochemical analysis in 80 breast cancer donors demonstrated a significant association of TPM4 (p = 0.002), HSP60 (p = 0.001), PDX6 (p = 0.002) but not CRAB (p = 0.113) staining with the presence of lymph node metastasis. In addition, TPM4 staining was also associated with clinical stage (p = 0.000), but no significant association was found between TPM4, PDX6, CRAB, and HSP60 expression and tumor size, hormone receptor, and HER-2 status (p > 0.05). The functional implication of these identified proteins was also discussed. These proteomic data are valuable and informative for understanding breast cancer metastasis and searching for potential markers for metastatic progression.

Animals↗