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PubMed1990

Generation of metastatic variants by transfection of a nonmetastatic rat mammary epithelial cell line with DNA from a metastatic rat mammary cell line.

Transfection of rat mammary (Rama) 37 epithelial cells, which yield nonmetastasizing adenomas in syngeneic Wistar-Furth rats, with HindIII-fragmented cellular DNA and the drug-resistance plasmids pSV2gpt or pSV2neo yields drug-resistant transformants with a frequency of 10(-4)-10(-5). Transformant cell lines transfected with the following, pSV2gpt alone, pSV2gpt and Rama 37 DNA, pSV2gpt and DNA from a metastasizing cell line Rama 800 (CT set), pSV2neo and salmon sperm DNA, pSV2neo and Rama 800 DNA (C set), all yield tumors when injected subcutaneously into syngeneic rats. A few transformants obtained by cotransfection with DNA from Rama 800 cells produce metastases in lungs and/or lymph nodes. The incidence of such metastases for two transfectants, termed CT4-41 and C18P, is significant at 20 and 24%, respectively, but only half (48%) that achieved with Rama 800 cells. Reintroduction into rats of cells cultured from a metastatic tumor of CT4-41 and of C18P, and from their lung or lymph node metastases, produces either a similar incidence (20-24%) or a significantly higher (48-52%) incidence of metastasis than that of the original transfectants. Cells cultured from nonmetastatic tumors fail to produce any metastatic lesions. When [32P]-labeled gpt or neo DNAs are hybridized to EcoRI-digested cellular DNA of the CT4-41 or C18P series of cell lines, tumors or metastases, gpt binds to one major fragment of 3,800 basepairs, and neo to two major fragments of 5,700 and 4,200 basepairs. The same cell lines produce hybridizing mRNAs of 1,500 and 1,900 bases for the CT4-41 series and 2,000-2,400 bases for the C18P series. It is suggested that transfection of DNA from the metastatic cells causes the nonmetastatic cells to become metastatic, in a genetically dominant manner, but additional steps are required for this process to become established and expressed at a level equivalent to that of the original, metastasizing donor cells.

Animals↗

PubMed1983

Doxorubicin, mitomycin-C, and 5-fluorouracil (DMF) in the treatment of metastatic hormonal refractory adenocarcinoma of the prostate, with a note on the staging of metastatic prostate cancer.

Sixty-two patients with metastatic hormonal refractory adenocarcinoma of the prostate received a combination of doxorubicin, mitomycin-C, and 5-fluorouracil (DMF). Thirty (48%) of the patients achieved an objective response. Response criteria excluded disease "stabilization" as a manifestation of response. Four clinical prognostic categories were identified: osseous I (OI) had metastatic axial skeletal involvement (23 patients); osseous II (OII) had axial and extremity skeletaL involvement (18 patients); visceral I (VI) had pulmonary metastasis (9 patients); and visceral II (VII) had pulmonary metastasis and involvement of other viscera (12 patients). The 20 responding patients survived a median of 47.5 weeks, whereas the 32 nonresponding patients survived a median of 23.8 weeks (n = 0.002). Response rates were highest among patients with OI (52%) and VI (88%) disease; response rates were lower amont patients with OII (33%) and VII (33%) disease. Responding patients in each clinical category survived longer than nonresponding patients except for those patients with VII disease. The median duration of response for patients with OI disease was 11 months, for OII 9.5 months, for VI patients it was 6.5 months, and VII patients it was 5 months. DMF is an effective treatment of metastatic hormonal refractory prostate cancer, resulting in consistent objective responses. The staging system employed identifies four clinical categories of metastatic prostate cancer and allows for accurate comparison of diet and stratification of study populations.

Adenocarcinoma↗

PubMed1992

The difference in immunological properties between lymph node metastatic and non-metastatic cell lines of MCA-induced fibrosarcoma of C4W mice.

To pursue the process of lymph node metastasis, i.e, the preferential tumor growth in lymph node, we have established the non-metastatic M2B cell line which was derived from 3-methylcholanthrene-induced fibrosarcoma of C4W mouse and a metastatic cell line, M2BLN-M+ which was obtained from metastatic lymph nodes of irradiated C4W mouse which was subcutaneously implanted with cultured tumor cells, because implanted tumor cells were derived from the spontaneous metastatic lymph node of the parental M2B tumor, but regressed in naive C4W mouse. We examined the characteristics of both tumor cell lines in terms of the immunological cellular interactions. M2BLN-M+ showed unexpectedly to be more susceptible to cytotoxicity of immune effectors (NK cell, macrophage and cytotoxic T lymphocyte) than M2B did. When cultured both tumor cells with these effector cells, the growth inhibition of M2BLN-M+ was greater than that of M2B. The regional lymph node of tumor-bearer, however, showed no effective cytotoxic activity as reported by others. On the contrary, when cultured both tumor cells with non-immune lymph node cells, to be surprised, the proliferation of M2B was markedly suppressed, while that of M2BLN-M+ was slightly inhibited. The lymph node cells of M2B-bearing mice showed stronger cytostatic activity to M2B. The results suggest that the cytostatic activity of lymph node cells will be a pivotal factor, concerning the establishment of lymph node metastasis.

Animals↗

PubMedDate not supplied

An unusual initial manifestation of metastatic papillary thyroid carcinoma: radioiodine uptake in lymph node metastatic lesions in a patient with Graves' disease.

OBJECTIVE: To report an unusual manifestation of metastatic papillary thyroid carcinoma with functional metastatic lesions demonstrated by radioiodine scanning and to discuss the relationship of Graves' disease and thyroid carcinoma. METHODS: A case report is presented, and the current literature is reviewed. RESULTS: An 82-year-old man had symptoms and laboratory results suggestive of thyrotoxicosis. 123I thyroid uptake scanning demonstrated lateral uptake, which directed attention to the lateral aspect of the neck and resulted in subsequent identification of previously overlooked lymphadenopathy. Total thyroidectomy, including excision of the central compartment and right jugular chain lymph nodes, was performed. CONCLUSION: In two previous reports of similar cases of metastatic thyroid carcinoma, imaging was done with use of a different scanning agent. To our knowledge, this is the first published case report of functional metastatic lesions imaged with 123I before thyroidectomy. This preoperative finding facilitated clinical management of the patient's thyroid cancer and thyrotoxicosis.

Aged↗

PubMedDate not supplied

Identification of metastasis-associated genes by transcriptional profiling of metastatic versus non-metastatic colon cancer cell lines.

In order to define genes which mediate liver tropism of colon cancer metastasis we have compared the transcriptional profile of 5600 full-length genes using the Affymetrix HuGene FL array technology of the non-metastatic colon cancer cell lines KM12C and the two metastatic cell lines, KM12SM and KM12L4A, which are derived from KM12C. We present data on genes which are up- and downregulated in the metastatic cell line and those which are selectively upregulated in one of the metastatic cell lines. We have sub-grouped the deregulated genes into different categories, such as immune response, modulation of transcription, enzymes, cell cycle/apoptosis, interferon- and tumor necrosis factor-regulated genes, tumor antigens and transmembrane receptors, intracellular signaling, cytoskeleton and extracellular matrix associated proteins, 'others' and genes of unknown function.

Animals↗

PubMedDate not supplied

Identification of genes associated with metastasis of mammary carcinoma in metastatic versus non-metastatic cell lines.

Cell lines 4A4 and 2C5 are the respective metastatic and non-metastatic variants (nude mouse system) derived from the human mammary carcinoma cell line MDA-MB-435. In order to identify genes associated with or functionally involved in metastasis, we have extended our previous transcriptional profile from 5000 to 12,000 genes using the Affymetrix Gene Chip array technology. Based on a threshold level of a change factor of > or = 2.5, we found that the steady-state level of 40 genes (0.3%) was up-regulated and conversely 89 genes (0.7%) were down-regulated in the metastatic cell line 4A4. The de-regulated genes were classified into categories such as tumor antigens/transmembrane receptors, enzymes, mediators of signaling, cell migration and angiogenesis, cell-cycle-, apoptosis-, differentiation- and growth-factor related genes, tumor suppression, transcription factors and genes encoding components of the extracellular matrix and the cytoskeleton. As possible mediators of invasion we identified DGCR6, osteopontin, autotaxin and the 65 kD phosphoprotein p65. In addition, three sugar-modifying enzymes were up-regulated in cell line 4A4. Profound differences in G-protein-mediated signaling and down-regulation of the tumor-suppressor genes DPC4, BARDI and DLC-1 were noted in the metastatic cell line 4A4.

Animals↗

PubMedDate not supplied

Expression of the KAI1 metastasis suppressor gene in non-metastatic versus metastatic human colorectal cancer.

BACKGROUND: The importance of KAI1 to colorectal cancer (CRC) progression is unclear, with conflicting data regarding changes in KAI1 expression during tumour progression. MATERIALS AND METHODS: In situ hybridisation and immunohistochemistry, with a semiquantitative scoring system, were used to assess KAI1 mRNA and protein levels, respectively, in normal colon samples (43), and non-metastatic (24) or metastatic (33) primary cancers, and liver metastases (48). RESULTS: There was significant loss of KAI1 mRNA and protein staining in non-metastatic primary tumours versus normal tissues (Bonferroni, p < 0.05) but levels recovered to near normal in metastatic primary tumours and liver metastases. Increased KAI1 expression significantly correlated with distant metastases (Mann-Whitney, p = 0.0001, mRNA; p = 0.033, protein), cancer-specific survival (Cox regression analysis p = 0.0002, mRNA; 0.0493, protein) and overall patient survival (p = 0.0001, mRNA). Multivariate analysis (Cox proportional hazards model) confirmed high KAI1 mRNA expression was an independent prognostic indicator of distant metastasis (p < 0.0001), cancer-specific survival (p < 0.0001) and overall patient survival (p < 0.0001). CONCLUSION: These data indicate a complex relationship between KAI1 and progression of human CRC, in which expression is reduced in localised primary tumours, but regained in disease associated with metastasis.

Analysis of Variance↗

PubMed1998

[Different integrin-induced adhesion of highly liver metastatic and little metastatic colon carcinoma cells in an extracellular matrix].

Poorly and highly liver metastatic colon carcinoma cell lines have different integrin-mediated adhesion to extracellular matrix. Specific integrin-mediated interactions between tumor cells and extracellular matrix (ECM) in the host organs are important for organ-specific metastasis. In colon carcinoma integrin expression differs depending on the metastatic potential of the tumor. Integrin-mediated adhesion of poorly (HT-29P) and highly liver-metastatic (HT-29LMM) colon carcinoma to extracellular matrix (ECM; Collagen I-C I, Collagen IV-C IV, Laminin LN, Fibronectin FN, Vitronectin VN) was investigated. HT-29LMM showed significant better adhesion to LN (45% vs. 26%; p < 0.001) and FN 20% vs. 1%; p < 0.001). No adhesion was found to VN. RGD-oligopeptides completely inhibited adhesion to FN. Using inhibition with anti-integrin-mAB it was shown, that adhesion to C I and C IV is mediated by alpha 2 beta 1-integrin, adhesion to LN by alpha 6 beta 1 and adhesion to FN by alpha v beta 1. These results have shown that adhesion of HT-29 cells is mediated by different integrins depending on ECM components. Poorly and highly metastatic cells possessed different patterns of adhesion to various substrates.

Cell Adhesion↗

PubMed1995

Metastatic variants of the B16 melanoma: metastasis is related to environmental conditions. Phenotypic changes in vitro and metastatic colonization potential in nude mice.

Variants of B16 melanoma exhibit strikingly different metastatic potential in AY/a (YB16 tumours) and a/a C57BL/6J (MB16 tumours) syngeneic mice. This study focused on relative pigmentation and metastatic potential in eight subline cultures initiated from B16 control and YB16 and MB16 tumours. During 6 months of in vitro growth in minimal essential medium, cells displayed a continuous decrease in their ability to form spontaneous lung colonies in 140 syngeneic mice with only persistence of enhanced metastasis-related characteristics depending on genetic change in yellow AY/a mice. Conversely, in a parallel experiment in 101 syngeneic mice in vitro, cells had a greater capacity to generate experimental metastases; this might be related to successive different environmental factors. In order to compare these prior results obtained in syngeneic mice, the above eight secondary cell lines were inoculated subcutaneously into Swiss nude mice. The primary tumours thus obtained were then serially transplanted monthly during 4 months. The new results obtained in a total of 277 mice showed that metastatic properties of cells were enhanced or restored in nude mice. Various tumour cell environments seem to be responsible for selective pressures that determine the melanoma metastatic potential. New, enhanced, heritable, metastasis-related characteristics can occur in melanoma cells as a result of genetic and metabolic changes and immunologic deficiency of the host. Apparent tumour-host relationship should not be neglected, since it has a clear influence on neoplastic diversity and malignant behaviour.

Animals↗

PubMed1994

Serum gangliosides in mice with metastatic and non-metastatic brain tumors.

The content of serum gangliosides was examined in VM and C57BL/6J (B6) mice that contained subcutaneous metastatic (VM) and non-metastatic (CT-2A) brain tumors, respectively. Gas-liquid chromatography (GLC) and high performance thin-layer chromatography (HPTLC) were used to analyze the serum gangliosides. N-glycolylneuraminic acid (NeuGc) accounted for greater than 90% of the total serum sialic acid content in each mouse strain (5.53 nmol and 2.05 nmol per ml serum, respectively). GM2-NeuGc was the major serum ganglioside detectable in both the normal and tumor-bearing mice of each strain. Shedding of tumor gangliosides into the serum occurs in various murine non-neural tumors and in human gliomas and neuroblastomas, but has not been previously studied in murine brain tumors. Our results show that serum ganglioside concentration was reduced in VM mice bearing the metastatic VM tumor, but was increased in B6 mice bearing the non-metastatic CT-2A tumor. These changes in concentration, however, were not associated with marked changes in serum ganglioside distribution. As serum gangliosides are synthesized in the liver, the differences in serum ganglioside concentration in the tumor-bearing mice may arise more from changes in liver function than from differences in tumor shedding.

Animals↗

PubMedDate not supplied

Use of octreotide in the treatment of digestive neuroendocrine tumours. Seven year experience in 20 cases including 9 cases of metastatic midgut carcinoid and 5 cases of metastatic gastrinoma.

The authors report their experience with octreotide in 20 patients (median age 57 years, 10 M, 10 F) from 1984 to 1991; 16 had metastatic APUDoma: 1 PPoma with VIPoma, 1 glucagonoma, 5 gastrinoma including 1 associated to PP-oma, 9 mid-gut carcinoid; 3 patients had multiple-endocrine neoplasia type I (MEN-I) with Zollinger-Ellison syndrome (ZES) and 1 patient a non-metastatic VIPoma. Octreotide (200-750 micrograms/day) was administered bid or tid with regular laboratory controls and morphological assessment. There was a striking improvement of symptoms, particularly in the carcinoid group (reduction of flushing in all patients and of diarrhoea in 3/5), in the patient with gastrinoma + acromegaly (regression of congestive heart failure) and in the patient with non-metastatic VIPoma. The hormonal markers were markedly reduced, particularly gastrin, PP (except in the patient with PPoma + VIPoma), VIP, GH and Somatomedin-C and urinary 5HIAA in 4/9 patients with carcinoid. There was only one partial regression of metastases (gastrinoma) and 4 apparent stabilizations of tumour growth, in the 16 metastatic cases. Among them, 4 patients died: 1 glucagonoma, 1 PPoma + VIPoma, 2 mid-gut carcinoids after a treatment of 5, 16, 30, 36 months, respectively. The patient with acromegaly + ZES died after 6 years of treatment at age 81. A patient with prolactinoma, resected insulinoma, hyperparathyroidism and ZES was not improved by a short course of octreotide (hypoglycemia); he died later of recurrent insulinoma. In conclusion, octreotide is a useful drug to control most of the symptoms related to gut endocrine tumours; it may inhibit tumour growth.

Adolescent↗

PubMed1995

[Growth pattern and metastatic behaviour of orthotopically metastatic model of human hepatocellular carcinoma in nude mice].

Growth pattern, metastatic behaviour and serial alph-a-fetoprotein (AFP) level of highly metastatic model of human hepatocellular carcinoma in nude mice (LCI-D20), which constructed by using orthotopic implantation of histologically intact patient specimens, were studied by implanting into the liver, subcutis and peritoneum of nude mice. Pathologic (by light and electronmicroscopic examination) and biologic (chromosome karyotype and DNA contents by flow cytometry) characteristics of LCI-D20 were also observed. The results showed that transplantability of LCI-D20 was 100% in 12 generations (passage time: 20 days) and all of these mice implanted tumors died within 40 days after transplantation due to serious metastasis. After LCI-D20 implanted into the liver of nude mice, growing implant-tumors in progress were negatively related to their double time during animal survival. LCI-D20 maintained 100% (70/70) metastatic rate in nude mice that showed early intrahepatic metastasis and late lymphatic and pulmonary metastasis. The high metastatic potentials of LCI-D20 tumor cells were kept in subcutis and peritoneum (70%, 100% respectively). The increase of the serial AFP secreting from the tumor cells was correlated with the implantation tumor growth rate (797.5 micrograms/L/5th week). The data from histological and electronmicroscopic findings, chromosome karyotype and DNA content analysis of the tumor cells revealed characteristics of human hepatocellular carcinoma. The results indicated that LCI-D20 exhibited the variety of clinical behaviours seen in hepatoma patients and it could be a useful model for investigating the metastasis mechanism of human hepatoma and anti-metastasis therapy.

Adult↗

PubMed1996

Suppression of metastatic potential of high-metastatic Lewis lung carcinoma cells by vanadate, an inhibitor of tyrosine phosphatase, through inhibiting cell-substrate adhesion.

Treatment of high-metastatic Lewis lung carcinoma A11 cells with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor, resulted in a dose- and time-dependent suppression of cell spreading on various extracellular matrix components such as Matrigel, fibronectin, laminin and type IV collagen, while the treatment did not significantly inhibit attachment of the cells to these substrates. Orthovanadate slightly and reversibly inhibited the in vitro cell growth of A11 cells, but the suppression of cell spreading was not directly due to the inhibition of cell growth. Orthovanadate-treated A11 cells showed reduced invasive ability in a reconstituted basement membrane invasion assay and experimental metastatic ability. Protein tyrosine phosphorylation level in A11 cells was elevated after treatment with orthovanadate. The increase in tyrosine phosphorylation level was partially diminished by the tyrosine kinase inhibitor ST638, concomitantly with restoration of the suppressed cell spreading as well as invasive and metastatic abilities. These results suggest that protein tyrosine phosphorylation influences invasive and metastatic potential of tumor cells possibly through regulating cell-substrate adhesion.

3T3 Cells↗

PubMed1999

Suppression by ganglioside GD1A of migration capability, adhesion to vitronectin and metastatic potential of highly metastatic FBJ-LL cells.

Ganglioside GD1a, which is highly expressed in poorly metastatic FBJ-S1 cells, has been shown to inhibit the serum-induced migration capability of highly metastatic FBJ-LL cells. In the present study, the capacity of FBJ-S1 cells to adhere to vitronectin was found to be about half that of FBJ-LL cells. Pre-treatment of FBJ-LL cells with GD1a decreased this capacity by 30% that of the control, whereas GM1-pre-treatment caused only a 10% decrease, indicating that GD1a specifically inhibits FBJ-LL cell adhesion to vitronectin. Since FBJ-LL cells contain almost no GD1a, transfectants capable of expressing GD1a to varying degrees were produced in this study by transfection of FBJ-LL cells with GM2/GD2-synthase cDNA. Decrease in the serum-induced migration capacity of these transfectants was accompanied by an increment in GD1a expression. Adhesion of the transfectants to vitronectin decreased by 30% as compared with mock-transfected cells. Within 4 to 5 weeks after GD1a-expressing transfectant and mock-transfected cells were transplanted into mice, metastatic nodules were observed in liver, lung, kidney and adrenal glands of mock-transplanted mice, but not in those with GD1a-expressing transfectants, indicating that GD1a suppresses the metastasis of FBJ-osteosarcoma cells, possibly by inhibiting cell migration and cell adhesion. The involvement of the ganglioside in the suppression of metastasis is clearly demonstrated in the present study.

Animals↗

PubMed1976

Carcinoma metastatic to the eye and orbit III. A clinicopathologic study of 28 cases metastatic to the orbit.

Two hundred and twenty-seven cases of carcinoma metastatic to the eye and orbit have been reviewed previously. The orbit alone was involved in 28 cases: theses lesions constitute the basis of this clinicopathologic study. The most common signs and symptoms produced by orbital metastasis included exophthalmos (75%1, pain (29%), decreased vision (29%), periorbital swelling (25%), a visible mass (21%), ophthalmoplegia, and diplopia (18%). The ophthalmologists' preoperative (or premortem) clinical diagnoses were: orbital mass, 36%; metastatic carcinoma, 29%; leukemia, 7%; melanosarcoma, 4%; mixed tumor of lacrimal gland, 4%; and meningioma, 4%. The sites of the primary tumors in the 28 patients with orbital metastasis were as follows: breast, eight; lung, four; genitourinary tract, four; pancreas, one; and ileum, one. In 10 patients the site of the primary carcinoma was not determined. In 17 of the 28 patients, symptoms of orbital metastasis preceded detection of a primary tumor elsewhere in the body. In 10 of the remaining 11 patients, detection of the primary tumor had preceded the onset of orbital symptoms. In one patient, symptoms of the primary tumor and of orbital metastasis appeared at about the same time. The median survival of patients with carcinoma metastatic to the orbit was 15.6 months from the time of orbital surgery. This was much better than the median survival of the 227 patients in the overall study (7.4 months) and far better than the median survival of the patients with metastasis to the anterior segment of the eye (only 5.4 months).

Adenocarcinoma↗

PubMed1981

Immunoselection in vitro of a non-metastatic variant from a highly metastatic tumor.

Immunoselection of a non-metastatic variant of the highly metastatic MDAY-D2 tumor of DBA/2 mice was achieved by means of an antiserum directed to the LY6.2 surface marker of MDAY-D2. While the new tumor (MDAY-D2.L61) expresses no detectable LY6.2, other measurable surface markers including H2d, FcR and TAA remain unchanged. The phenotypic behavior of MDAY-D2.L61 is that of a non-metastatic tumor and has remained stable after 1 year of maintenance in vivo and in vitro. Immunoselection can now be used to derive variants with stable phenotypic behavior from heterogeneous parent tumor cell populations.

Animals↗

PubMed1987

Karyotypic analyses of metastatic and non-metastatic mouse tumor cells by G- and C-banding.

Cytogenetic studies using G- and C-banding were performed in order to compare non-metastasizing BWO mouse thymoma cells with their metastatic BW-IS-Li and BW-O-Li1 variants. BW-IS-Li and BW-O-Li1 cells were obtained from liver metastases generated respectively after intra-splenic or intravenous inoculation of mice with BWO cells. BW-O-Li1 cells contained normal chromosomes 4 and 18 which were never found in BWO or BW-IS-Li cells. As they also contained several markers common to the BWO parental cell line, our data provide definite evidence that the BW-O-Li1 cell line results from spontaneous in vivo cell fusion between a BWO cell and a normal host cell. Chromosome 3 was also shown to be "rearrangement-prone" and was less represented among metastatic cell variants. These variants also lack a C-band-deficient marker chromosome which was found in most of the BWO cells. However, as many complex chromosome rearrangements were found in all 3 cell lines, at least some chromosomal material may be present in a hidden form. We were not able in this particular cell system to link the presence or absence of a single chromosome, chromosome fragment or rearrangement to the acquisition or expression of metastatic properties.

Animals↗

PubMed1988

Effects of metastatic cascades on metastatic patterns: studies on colon-26 carcinomas in mice.

The present studies are based on autopsy data showing that in upper esophageal and lower rectal carcinomas, hematogenous metastasis occurs mainly first to the lungs, and cancer cells from pulmonary metastases generate arterial metastases. In lower esophageal and upper rectal carcinomas, hematogenous metastases occur first in the liver, then in the lungs, and are further disseminated by the arterial route. The arterial metastatic patterns are different in the 2 groups. One possible explanation for these differences in pattern is that liver "residence" is associated with different metastatic behavior; this has been tested in a model system. Experiments with the transplantable colon-26 carcinoma in mice reveal that, when cancer cells from common s.c. transplant sites are grown in the liver, lungs or liver-and-lungs, and then injected into the bloodstream of fresh recipients via the left ventricle, the portal vein or the tail vein, different patterns and degrees of colonization of 11 different target sites are observed. These results are consistent with the hypothesis that growth of cancers in different anatomic sites may modify the subsequent arterial metastatic patterns, due to site-induced changes occurring in cancer cell populations, which influence metastasis from metastases or so-called "cascade" processes.

Animals↗