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At least 73 records · Page 4Linked to original sources
PubMed2002

Comparison of accumulated allele loss between primary tumor and lymph node metastasis in stage II non-small cell lung carcinoma: implications for the timing of lymph node metastasis and prognostic value.

Although the Tumor-Node-Metastasis staging of non-small cell lung carcinoma (NSCLC) is the most effective predictor of survival, the clinical outcome of patients at each stage is variable on an individual case basis. We tested the value of incorporating information about the tumor heterogeneity of NSCLC into microsatellite allelotyping in a cohort of 48 node-positive stage II patients (T1N1M0 and T2N1M0). Microsatellite allelotyping involved microdissection of the invasive component of primary tumor and lymph node metastasis at multiple target sites followed by loss of heterozygosity (LOH) analysis at specific regions on chromosomes 1p, 3p, 5q, 7q, 8q, 9p, 10q, 17p, and 18q using 16 markers. All microsatellites manifested LOH ranging from 44 to 76% in primary tumor and showed various degree of heterogeneity between primary tumor and lymph node metastasis. LOH on 3p and 5q in the lymph node metastases was associated significantly with shortened survival of the patients (P = 0.033 and 0.004, respectively), whereas no single LOH in the primary tumors showed association with prognosis. For the analysis of the accumulated load of allele loss, fractional allele loss (FAL) was calculated for each sample. The maximal FAL of lymph node metastasis was significantly lower than that of primary tumor (P = 0.0015), possibly reflecting the early lymphatic spread. High maximal FAL of lymph node metastasis was significantly correlated with an adverse outcome (P = 0.012), whereas maximal FAL of primary tumor did not show any prognostic significance (P = 0.552). A composite mutational profile for each patient based on the allelotyping of the primary tumor and lymph node deposits may make a significant contribution to a more accurate prognosis of stage II NSCLC.

Aged↗
PubMed2005

Metastasis suppression by breast cancer metastasis suppressor 1 involves reduction of phosphoinositide signaling in MDA-MB-435 breast carcinoma cells.

Several molecules that suppress metastasis without suppressing tumorigenicity have been identified, but their mechanisms of action have not yet been determined. Many block growth at the secondary site, suggesting involvement in how cells respond to signals from the extracellular milieu. Breast cancer metastasis suppressor 1 (BRMS1)-transfected MDA-MB-435 cells were examined for modifications of phosphoinositide signaling as a potential mechanism for metastasis suppression. 435/BRMS1 cells expressed <10% of phosphatidylinositol-4, 5-bisphosphate compared with parental cells, whereas levels of the PtdIns(4)P and phosphatidylinositol-3-phosphate were unchanged. Inositol (1,4,5)-trisphosphate [Ins(1,4,5)P(3)] were decreased in 435/BRMS1 cells by approximately 50%. Phosphatidylinositol-3,4,5-trisphosphate levels were undetectable in 435/BRMS1 cells, even when stimulated by exogenous insulin or platelet-derived growth factor. Immunofluorescence microscopy to examine cellular distribution confirmed that phosphatidylinositol-4,5-bisphosphate distribution with cells was unchanged but was uniformly decreased throughout the cell. Although the gross morphology of 435/BRMS1 cells is similar to the parent, filamentous actin was more readily apparent in 435/BRMS1. Intracellular calcium, measured using Fluo-3 and Fura-2 fluorescent calcium indicator dyes, was somewhat lower, but not statistically different in 435/BRMS1 compared with parental cell. However, when stimulated with platelet-derived growth factor, MDA-MB-435 cells, but not 435/BRMS1 cells mobilized intracellular calcium. Taken together, these results implicate signaling through phosphoinositides in the regulation of breast cancer metastasis, specifically metastasis that can be suppressed by BRMS1.

Breast Neoplasms↗
PubMed1989

Drug treatments for metastasis of the Lewis lung carcinoma: lack of correlation between inhibition of lung metastasis and survival.

The abilities of the Eli Lilly compounds LY150310, LY189332, and LY135305 to inhibit spontaneous metastasis and to increase animal survival were evaluated. These compounds represent widely varied structures and were evaluated because they have been found to inhibit thromboxane synthetase, cyclooxygenase, and thrombin activation, respectively. These biochemical processes have been proposed in the literature as targets for antimetastatic drugs. The purpose of this investigation was twofold: (a) to compare the antimetastatic activities of the Eli Lilly compounds to those of the reference antimetastatic compounds nafazatrom and RA233, and (b) to examine the correlation between inhibition of spontaneous lung metastasis and survival. Spontaneous metastasis of the Lewis lung carcinoma was used to evaluate the antimetastatic activity of the compounds. In this model 5 x 10(5) tumor cells were implanted into the gastrocnemius muscle, the primary tumor was resected on Day 14, and metastatic lung lesions were counted on Day 25. Compounds were administered every 12 h on Days 5 through 19. Nafazatrom, LY150310, LY189332, and LY135305 were found to inhibit spontaneous lung metastasis in a dose-dependent manner. The ED50 values for the respective inhibitions with these compounds were 50, 0.5, 2, and 0.35 mg/kg/day; the respective therapeutic indexes (LD50/ED50) were 7, 180, 255, and 511. To evaluate the effect of nafazatrom, LY150310, LY189332, and LY135305 on animal survival, the compounds were given at maximally antimetastatic doses of 200, 60, 20, and 6 mg/kg/day, respectively. Two dosing schedules were used: (a) on Days 5 through 19 and (b) on Day 5 until death. Neither the median survival times nor the numbers of long-term survivors were significantly changed with any of the compounds at any dosing schedule. RA233, given to a maximally tolerated dose of 200 mg/kg/day on Day 5 until death, did not inhibit lung metastasis and did not increase median survival time. Postmortem examination of animals dosed with nafazatrom, LY150310, LY189332, and LY135305 showed complete inhibition in lung lesions and the appearance of lesions in the liver, kidney, spleen, and brain. The results of this investigation show that the effect a compound has on the number of metastatic lesions in a target organ may not be predictive of its effect on survival. To successfully translate laboratory data into the clinic, survival should be considered as a predictor of a compound's potential clinical utility.

Aniline Compounds↗
PubMed1997

Suppression of metastasis in human breast carcinoma MDA-MB-435 cells after transfection with the metastasis suppressor gene, KiSS-1.

Based on the observation that chromosome 1q deletions are not infrequent in late-stage human breast carcinomas, we tested whether the recently discovered human melanoma metastasis suppressor gene, KiSS-1, which maps to chromosome 1q32-q41, could suppress metastasis of the human breast carcinoma cell line MDA-MB-435. Parental, vector-only transfectants and KiSS-1 transfectant clones were injected into the mammary fat pads of athymic nude mice and assessed for tumor growth and spontaneous metastasis to regional lymph nodes and lungs. Expression of KiSS-1 reduced metastatic potential by 95% compared to control cells but did not suppress tumorigenicity. Metastasis suppression correlated with a decreased clonogenicity in soft (0.3%) and hard (0.9%) agar. Although the overall rate of cell adhesion to extracellular matrix components was unaffected, KiSS-1 transfectants spread on immobilized type-IV collagen more rapidly than did control populations. Invasion and motility were unaffected by KiSS-1. Based on the predicted structure of the KiSS-1 protein, our results imply a mechanism whereby KiSS-1 regulates events downstream of cell-matrix adhesion, perhaps involving cytoskeletal reorganization. In addition to its already described role in melanoma, our results show that KiSS-1 also functions as a metastasis suppressor gene in at least some human breast cancers.

Animals↗
PubMed2003

Antitumor efficacy of reticulol from Streptoverticillium against the lung metastasis model B16F10 melanoma. Lung metastasis inhibition by growth inhibition of melanoma.

Reticulol was isolated from the culture broth of the strain Streptoverticillium sp. NA-4803. Recticulol (M.W. 222.2) exhibited a potent in vitro cytotoxicity against A427, a human lung tumor cell line, and B16F10, a mouse melanoma cell line. In the trypan blue staining assay for B16F10 cells, the cell viability by reticulol treatment was significantly decreased in a dose-dependent manner. The in vivo assay for the lung metastasis-blocking effect showed that reticulol injected intravenously suppressed the increase in colonies on the lung in a dose-dependent manner. In addition, the survival rate of tumor-implanted mice treated with reticulol was closely associated with its antitumoral efficacy. Reticulol administered via the peritoneum of mice showed less metastasis inhibition than that injected intravenously. To demonstrate the mechanism for inhibition of metastasis, the inhibitory effect of reticulol for matrix metalloproteinase-2 or -9 involved in melanoma metastasis was investigated; however, they were not observed on zymogram gel. In addition, the antitumor efficacy of reticulol was not associated with cell cycle arrest or apoptosis. Therefore, it was inferred that reticulol known as a phosphodiesterase inhibitor directly inhibited the growth of B16F10 melanoma, showing necrotic response. These results suggest that reticulol protects its lung metastasis via the bloodstream by inhibiting the growth of B16F10 melanoma at the cellular level.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2004

Histopathologically-diagnosed splenic metastasis in a hepatocellular carcinoma case with adrenal metastasis.

We encountered a patient with hepatocellular carcinoma (HCC), with adrenal gland metastasis, in whom splenic metastasis was diagnosed histopathologically. A 59-year-old man visited our hospital in May 2001 with chief complaints of abdominal distension and pretibial pitting edema. Multiple HCCs associated with HCV-positive liver cirrhosis were detected. Transarterial embolization (TAE) was performed a total of 4 times for HCCs. A left adrenal gland metastatic lesion was detected and it was found to increase in diameter from 3 cm to 6 cm over a four-month period; left adrenalectomy was performed in June 2002. Because of marked splenomegaly and findings of hypersplenism, the spleen was also resected. Although no metastatic lesions were evident on macroscopic examination of the spleen, a small metastatic lesion from moderately differentiated HCC, approximately 0.5 mm in diameter, was detected histopathologically. Splenic metastasis from HCC is rare, usually occurring with metastases involving other organs. Our patient also had adrenal gland metastasis. Therefore, hematogenous metastasis to the congested spleen via the systemic circulation was suspected.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Value of serum carbohydrate antigen 19-9 for predicting extrahepatic metastasis in patients with liver metastasis from colorectal carcinoma.

BACKGROUND/AIMS: Serum levels of carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) are frequently elevated in patients with colorectal carcinoma. However, the predictive utility of these two markers has not been fully investigated in patients with liver metastasis. METHODOLOGY: We retrospectively analyzed data obtained from 90 hepatectomy or non-hepatectomy patients with liver metastases from colorectal carcinoma. We examined correlation between serum levels of CEA and CA19-9 and other clinicopathologic factors and performed univariate and multivariate analyses to determine the impact of these tumor markers on extrahepatic metastasis after admission to our hospital. RESULTS: CEA elevation correlated to advanced age (> or = 60 years), and CA19-9 elevation correlated with the site (colon) of primary tumor. Univariate analysis showed that treatment without hepatectomy, > or = 4 hepatic tumors, and CA19-9 elevation had been an adverse effect on extrahepatic disease-free survival time after admission. Multivariate analysis showed that CA19-9 elevation (risk ratio, 1.84) and treatment without hepatectomy (risk ratio, 1.62) had a significant effect on extrahepatic disease-free time. CONCLUSIONS: In patients with colorectal liver metastasis, elevation of serum CA19-9 is a risk factor for extrahepatic metastasis, and CEA appears to be useless for predicting extrahepatic metastasis in these patients.

Adult↗
PubMed1994

Inhibition of the metastasis of Lewis lung carcinoma by antibody against urokinase-type plasminogen activator in the experimental and spontaneous metastasis model.

A selective inhibitory antibody, raised against human high molecular weight urokinase-type plasminogen activator (HMW-uPA), was examined to determine whether it would inhibit production of experimental and spontaneous lung metastasis by murine Lewis lung carcinoma (3LL) cells. Polyclonal antibody to human uPA cross-reacts with the murine uPA and inhibits murine uPA activity. When examined with an in vitro assay system using a modified Boyden chamber, the anti-catalytic IgG to uPA suppressed the invasion of tumor cells through Matrigel. Anti-uPA IgG inhibited neither the cell proliferation nor the binding of tumor cells to Matrigel, and showed no significant suppression of chemotactic migration of tumor cells to fibronectin. In an in vivo spontaneous metastasis assay, multiple subcutaneous (s.c.) injections of anti-uPA IgG (up to a concentration of 200 micrograms [= 500 inhibitory unit/mouse/day] for 7 days immediately after s. c. tumor cell inoculation significantly inhibited the formation of lung metastasis in C57BL/6 mice in a dose-dependent manner. The inhibition of lung metastasis was not due to direct antitumor effects of anti-uPA IgG. In an in vivo experimental metastasis assay, multiple s. c. injections of anti-uPA IgG for 7 days after intravenous (i. v.) tumor cell inoculation did not reduce the number of lung tumor colonies. These results suggest that uPA more efficiently regulates the mechanism involved in the entry into vascular circulation of tumor cells (intravasation) than in extravasation, during the metastatic process.

Animals↗
PubMed2003

Mechanisms of peritoneal metastasis after operation for non-serosa-invasive gastric carcinoma: an ultrarapid detection system for intraperitoneal free cancer cells and a prophylactic strategy for peritoneal metastasis.

PURPOSE: This aims of this study are to establish an ultra-rapid quantitative reverse transcription-PCR (RT-PCR) protocol that enables the diagnosis of i.p. cancer spread during operation, to reveal the mechanisms of peritoneal metastasis from non-serosa-invasive gastric carcinoma, and to evaluate the effect of the extensive intraoperative peritoneal lavage (EIPL) using the ultra-rapid quantitative RT-PCR as a prophylactic strategy for peritoneal metastasis. EXPERIMENTAL DESIGN: Peritoneal lavage samples from 63 patients with non-serosa-invasive gastric carcinoma were obtained at laparotomy and immediately after lymph node dissection. To identify the free cancer cells in the samples, carcinoembryonic antigen- and cytokeratin 20-specific RT-PCRs were performed using the LightCycler method in combination with an automated mRNA extractor. In addition, EIPL was performed in five cases with serosa-invasive gastric carcinoma, and its efficacy was evaluated by the ultra-rapid quantitative RT-PCR protocol. RESULTS: The method enabled us to complete the detection of cancer cells within approximately 70 min. Both the carcinoembryonic antigen and cytokeratin 20 mRNA in i.p. lavages after lymph node dissection were identified in three (14.3%), four (26.7%), and six (46.2%) patients with submucosal, muscularis propria, and subserosal tumors, respectively. Lymph node metastasis was the independent predictor of the existence of i.p. free cancer cells. The ultra-rapid quantitative RT-PCR demonstrated that EIPL reduced free cancer cells from 3.8 x 10(5) +/- 1.4 x 10(5) cells to 2.8 +/- 1.5 cells/100 ml lavage after six to eight washes, and they disappeared after seventh to ninth wash. CONCLUSIONS: The present study proved that lymph node dissection opened lymphatic channels and spread viable cancer cells into the peritoneal cavity. It is suggested that the combination of the novel detection system with the intraoperative therapy of EIPL can be a useful prophylactic strategy for peritoneal metastasis from gastric carcinoma.

Aged↗
PubMed2002

Interleukin-12 administration is more effective for preventing metastasis than for inhibiting primary established tumors in a murine model of spontaneous hepatic metastasis.

PURPOSE: The effect of interleukin-12 (IL-12) on tumor growth at the primary site and its therapeutic efficacy against metastasis were examined using a model of spontaneous hepatic metastasis. METHODS: IL-12 was peritumorally injected into RL male1 tumor-bearing BALB/c male mice at the different tumor stage. RESULTS: Striking inhibition of hepatic metastasis in both athymic and euthymic mice was induced by the administration of IL-12 irrespective of the stage of tumor progression. In contrast, IL-12 failed to produce any antitumor effect in athymic mice which lack conventional T cells. These results suggest that the antitumor effect of IL-12 is mediated mainly by T cells, and that the antimetastatic effect is mediated mainly by natural killer (NK) and/or NKT cells. Next we examined the direct effect of IL-12 on these cells. IL-12-induced T-cell proliferation was remarkably augmented in the early stage, then decreased dramatically in the advanced stage, while IL-12-induced cytotoxic activity, mediated by NK and NKT cells, was not attenuated even in the advanced stage. This dissociation in IL-12 responsiveness appeared to be the reason for the remarkable antimetastatic effect but insufficient antitumor effect of IL-12 in the advanced stage. CONCLUSION: The findings of this study support the clinical use of IL-12 for immunotherapy against either occult or evident liver metastasis.

Animals↗
PubMed1992

A novel Arg-Gly-Asp containing peptide specific for platelet aggregation and its effect on tumor metastasis: a possible mechanism of RGD peptide-mediated inhibition of tumor metastasis.

A novel cyclic tetrapeptide containing L-arginine-glycine-L-aspartic acid-L-phenylglycine (cyclo-RGDPhg) was synthesized and found to be a potent inhibitor of platelet aggregation induced by highly metastatic murine squamous cell carcinoma (SCCVII) cells (IC50 = 3.3 microM) as well as ADP (1.5 microM). This cyclic peptide, however, showed similar or less inhibitory activities on adhesion of SCCVII cells to fibronectin, vitronectin and type IV collagen as compared with those of parent linear tetrapeptide, RGDS. These results show that cyclo-RGDPhg peptide is a highly specific antagonist for gpIIb/IIIa on platelets. Moreover, this peptide failed to suppress pulmonary metastasis of SCCVII cells in an experimental metastasis model. These results indicate that RGD peptide-mediated inhibition of tumor metastasis is attributed to the suppression of cell adhesion but not platelet aggregation. These also suggest that platelet aggregation is not an essential step during blood circulation of tumor cells for the completion of metastasis.

Animals↗
PubMed2005

Characteristic differences between patients who have undergone surgical treatment for lung metastasis or hepatic metastasis from colorectal cancer.

OBJECTIVE: The characteristic differences between patients with lung or liver metastases from colorectal carcinoma (CRC) have not yet been clarified. A small group of these patients demonstrate a better prognosis, and the selection criteria for resection of liver and/or lung metastasis are not well defined. It is important to compare and analyze the most common metastatic sites, which include liver metastases and lung metastases. The objective of this study was to compare the characteristics of the two groups in order to identify patients who benefitted from surgical resection of CRC. METHODS: We retrospectively reviewed the medical charts of 80 patients who had undergone resection for liver or lung metastasis from CRC in Fukuoka University Hospital between June 1991 and December 2004. These patients were grouped according to surgical therapy received for the metastases, and separated into two groups, as follows: LUM, lung metastases resection; LIM, liver metastases resection. We evaluated these groups for a set of several factors. RESULTS: The characteristic factors between the two groups (LUM vs. LIM) demonstrated significant differences according to histological differentiation, venous invasion, and lymphatic permeation. There was a statistical difference in the disease-free interval (DFI) between the two groups (947.06 +/- 840.39 days in LUM vs. 246.03 +/- 229.26 days in LIM). Although serum CEA levels at resection of metastasis showed significant differences between the groups (LUM, 13.25 +/- 31.55 ng/ml; LIM, 55.21 +/- 99.52 ng/ml), the primary serum CEA levels were not significantly different. Overall survival rates at 5 years were 37.0 % for LUM and 42.8 % for LIM. There was no significant difference in the survival rate of the LUM vs. the LIM group after resection of metastasis. The Cox proportional hazards regression model was used to determine serum CEA status at the time of the metastases and showed a significant difference indicating poor prognosis for patients with LUM, but the results were not significant for LIM cases. CONCLUSIONS: Candidates for surgical treatment for lung or liver metastases from CRC may be an acceptable for the same valuable approach, even if characteristic differences were observed in each group.

Carcinoembryonic Antigen↗
PubMed2006

Imaging steps of lymphatic metastasis reveals that vascular endothelial growth factor-C increases metastasis by increasing delivery of cancer cells to lymph nodes: therapeutic implications.

Preclinical and clinical studies positively correlate the expression of vascular endothelial growth factor (VEGF)-C in tumors and the incidence of lymph node metastases. However, how VEGF-C regulates individual steps in the transport of tumor cells from the primary tumor to the draining lymph nodes is poorly understood. Here, we image and quantify these steps in tumors growing in the tip of the mouse ear using intravital microscopy of the draining lymphatic vessels and lymph node, which receives spontaneously shed tumor cells. We show that VEGF-C overexpression in cancer cells induces hyperplasia in peritumor lymphatic vessels and increases the volumetric flow rate in lymphatics at the base of the ear by 40%. The increases in lymph flow rate and peritumor lymphatic surface area enhance the rate of tumor cell delivery to lymph nodes, leading to a 200-fold increase in cancer cell accumulation in the lymph node and a 4-fold increase in lymph node metastasis. In our model, VEGF-C overexpression does not confer any survival or growth advantage on cancer cells. We also show that an anti-VEGF receptor (VEGFR)-3 antibody reduces both lymphatic hyperplasia and the delivery of tumor cells to the draining lymph node, leading to a reduction in lymph node metastasis. However, this treatment is unable to prevent the growth of tumor cells already seeded in lymph nodes. Collectively, our results indicate that VEGF-C facilitates lymphatic metastasis by increasing the delivery of cancer cells to lymph nodes and therapies directed against VEGF-C/VEGFR-3 signaling target the initial steps of lymphatic metastasis.

Animals↗
PubMed2000

Molecular biology of breast cancer metastasis. Genetic regulation of human breast carcinoma metastasis.

The present is an overview of recent data that describes the genetic underpinnings of the suppression of cancer metastasis. Despite the explosion of new information about the genetics of cancer, only six human genes have thus far been shown to suppress metastasis functionally. Not all have been shown to be functional in breast carcinoma. Several additional genes inhibit various steps of the metastatic cascade, but do not necessarily block metastasis when tested using in vivo assays. The implications of this are discussed. Two recently discovered metastasis suppressor genes block proliferation of tumor cells at a secondary site, offering a new target for therapeutic intervention.

Antigens, CD↗
PubMedDate not supplied

Paratracheal lymph node metastasis is associated with cervical lymph node metastasis in patients with thoracic esophageal squamous cell carcinoma.

BACKGROUND: We determined which lymph node metastases were associated with cervical lymph node metastases of thoracic esophageal squamous cell carcinoma. METHODS: A total of 6464 lymph nodes derived from 155 consecutive patients with thoracic esophageal squamous cell carcinoma were stained by immunohistochemistry (antibody: AE1/AE3). Lymph node metastases were mapped according to the mapping scheme of the American Thoracic Society, as modified by Casson et al. (Ann Thorac Surg 1994;58:1569-70). Patients were divided into two groups: those with and without cervical lymph node metastasis (CLNM). Mapping data were examined by uni- and multivariate analysis. RESULTS: Hematoxylin and eosin-positive and AE1/AE3-positive lymph node metastases were found in 59% and 77% of patients, respectively. Twenty-one (55%) of 38 patients in the CLNM(+) group and 30 (26%) of 117 patients in the CLNM(-) group had AE1/AE3-positive lymph node metastasis in the thoracic paratracheal lymph node. Paratracheal lymph node metastasis is only one independent factor for (CLNM), whereas upper thoracic paraesophageal lymph node and pulmonal hilar lymph node status were also significant in univariate analysis. Three (43%) of seven patients with cervical jumping metastasis from the thoracic esophagus had micrometastasis in the paratracheal lymph node. CONCLUSIONS: The paratracheal lymph node is most associated with (CLNM) of thoracic esophageal squamous cell carcinoma.

Aged↗
PubMed1999

[Expression of tumor metastasis suppressor gene KAI1/CD82 in human cancer cell lines with different metastasis potential].

OBJECTIVE: To investigate the correlation of a newly-defined tumor metastasis suppressor gene KAI1/CD82 and metastatic potential of human cancer cell lines. METHODS: Expressions of KAI1/CD82 in eight human cancer cell lines of prostate, lung and melanoma with different metastasis potential were studied by Northern blot hybridization and the mutation were detected by PCR-SSCP. RESULTS: Expressions of KAI1 mRNA decreased in human prostate cancer cell lines PC3 and PC3M, and lung cancer cell line PG which were metastatic cancer cell lines (integral light density values: 0.0319, 0.0266 and 0.0549, respectively). Expression of KAI1 mRNA showed high level in PAa, a human lung cancer cell line with no metastasis (integral light density value: 0.7313). In human melanoma cell lines with different metastasis potential (WM35, WM1341b, WM983a and WM451), expression of KAI1 showed moderate expression (integral light density values are 0.1798, 0.1582, 0.1501, 0.1800 respectively). PCR-SSCP analysis indicated the existence of band shift in exon 7 of KAI1 gene in PC3, PG and PC3M. CONCLUSION: Decreased KAI1/CD82 expression may be associated with enhanced metastatic potential in prostate cancer cell lines and lung cancer cell line other than melanoma cell lines. The decreased expression may be partially nelaled with mutation of KAI1 gene.

Adenocarcinoma↗
PubMed2003

[A case of advanced cancer with liver metastasis and paraaortic lymph node metastasis responding remarkably to combination chemotherapy of low-dose CDDP, 5-FU and CPT-11].

A 57-year-old male patient with upper epigastric discomfort was introduced to our hospital from another clinic because of gastric cancer. Several examinations showed massive liver metastasis and paraaortic lymph node metastasis from Type-3 gastric cancer beneath the posterior wall of the pyloric antrum. First we tried infusion of CDDP (10 mg/day for days 1-5 and 8-12) and continuous infusion of 5-FU (500 mg/day for 14 days). Concurrently, we added infusion of CPT-11 (80 mg/day on days 1,8). After 3 courses of chemotherapy, the tumor had decreased remarkably in size. Moreover, liver metastasis and paraaortic lymph node metastasis had vanished. This regimen thus appears to be effective for advanced gastric carcinoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Necessity of preoperative screening for brain metastasis in non-small cell lung cancer patients without lymph node metastasis.

BACKGROUND: The exclusion of brain metastasis is important to determine the optimal treatment plan in patients with non-small cell lung cancer (NSCLC). However, a routine examination using magnetic resonance imaging (MRI) for the brain remains controversial in preoperative patients with resectable disease. METHODS: To assess the necessity of routine brain MRI for preoperative patients, a retrospective analysis for a consecutive series of 338 patients with NSCLC was performed. Among the 338 patients, 141 patients who were considered to have potentially resectable diseases through an examination of the chest plus an upper abdominal computed tomography scan and bone radioisotope scan with no neurological symptoms received MRI for examination of brain metastasis. RESULTS: The incidence of brain metastasis detected by MRI was 2.1% (three of 141) in all patients, 0% (zero of 80) in patients with N0 disease, 5.2% (one of 19) in N1, and 4.7% (two of 42) in N2 cases. CONCLUSION: In patients with resectable NSCLC, a brain MRI is not considered to be useful due to the low incidence of asymptomatic brain metastasis.

Adult↗