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PubMed2001

Modulatory effects of neonatal exposure to TCDD, or a mixture of PCBs, p,p'-DDT, and p-p'-DDE, on methylnitrosourea-induced mammary tumor development in the rat.

The role of organochlorine (OC) exposure in the etiology of breast cancer remains controversial. Thus, our objective was to determine whether the most abundant and toxic OCs found in human milk could, when ingested during the neonatal period, modulate the development of mammary tumors in the rat. We prepared a mixture composed of p,p'-dichlorodiphenyltrichloroethane (DDT), its major metabolite, p,p'-dichlorodiphenyldichloroethene (DDE), and 19 polychlorinated biphenyls (PCB) based on their concentrations found in the milk of Canadian women. Neonate rats at 1, 5, 10, 15, and 20 days of age were gavaged with this mixture, at 10, 100, and 1,000 times the amount that a human baby would consume. An additional group received 2.5 microg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg body weight (bw) by gavage at 18 days of age, instead of the mixture. On day 21, all treatment groups, except for a control group and a 1,000-mix group, received a single intraperitoneal injection of methylnitrosourea (MNU, 30 mg/kg bw), the initiator of the carcinogenic process. The average number of rats per treatment group was 33. Rats were sacrificed when their tumors reached 1 cm in size, or at 308 days of age. We prepared mammary tumors and mammary gland whole mounts for histologic analysis. There were no significant effects when only the malignant or only the benign tumors were considered. After all benign and malignant lesions were pooled, the number of mammary tumors differed among all MNU-treated groups (p = 0.02) with more lesions developing in the MNU-1,000[times] (median = 4.5; p = 0.05) and MNU-TCDD (median = 5.5; p = 0.07) compared to the MNU-0 rats (median = 2). Compared to the MNU-0 group, the percentage of rats that developed palpable tumors (benign plus malignant) was slightly higher (p = 0.06) in the MNU-TCDD group, but not in the MNU-1,000[times] group. The percentage of palpable tumors that were malignant was higher (p = 0.02) in the MNU-100[times] group (15/16, 94%) than in the MNU-0 group (10/18, 56%). The highest dose of the mixture delayed (p = 0.03) the development of tumors, but this was not observed with the MNU-TCDD treatment. These results suggest that neonatal exposure to high doses of organochlorines could favor the development of MNU-induced mammary lesions, but also delays the development of palpable tumors in the rat.

Alkylating Agents↗
PubMed1994

Interaction between CD44 and hyaluronate is directly implicated in the regulation of tumor development.

CD44 is implicated in the regulation of tumor growth and metastasis but the mechanism by which expression of different CD44 isoforms determines the rate of primary and secondary tumor growth remains unclear. In the present study we use a human melanoma transfected with wild-type and mutant forms of CD44 to determine which functional property of the CD44 molecule is critical in influencing tumor behavior. We show that expression of a wild-type CD44 isoform that binds hyaluronic acid augments the rapidity of tumor formation by melanoma cells in vivo, whereas expression of a CD44 mutant, which does not mediate cell attachment to hyaluronate, fails to do so. The importance of CD44-hyaluronate interaction in tumor development is underscored by the differential inhibitory effect of soluble wild-type and mutant CD44-Ig fusion proteins on melanoma growth in vivo. Whereas local administration of a mutant, nonhyaluronate binding, CD44-Ig fusion protein has no effect on subcutaneous melanoma growth in mice, infusion of wild-type CD44-Ig is shown to block tumor development. Taken together, these observations suggest that the tumor growth promoting property of CD44 is largely dependent on its ability to mediate cell attachment to hyaluronate.

Animals↗
PubMed2003

Hepatocyte transformation and tumor development induced by hepatitis C virus NS3 c-terminal deleted protein.

AIM: To study the effect of hepatitis C virus nonstructural protein 3 c-terminal deleted protein (HCV NS3-5') on hepatocyte transformation and tumor development. METHODS: QSG7701 cells were transfected with plasmid pRcHCNS3-5' (expressing HCV NS3 c-terminal deleted protein) by lipofectamine and selected in G418. The expression of HCV NS3 gene and protein was determined by PCR and immunohistochemistry respectively. Biological behavior of transfected cells was observed through cell proliferation assay, anchorage-independent growth and tumor development in nude mice. The expression of HCV NS3 and c-myc proteins in the induced tumor was evaluated by immunohistochemistry. RESULTS: HCV NS3 was strongly expressed in QSG7701 cells transfected with plasmid pRcHCNS3-5' and the positive signal was located in cytoplasm. Cell proliferation assay showed that the population doubling time in pRcHCNS3-5' transfected cells was much shorter than that in pRcCMV and non-transfected cells (24 h, 26 h, 28 h respectively). The cloning ratio of cells transfected with pRcHCNS3-5', pRcCMV and non-transfected cells was 33 %, 1.46 %, 1.11 %, respectively, the former one was higher than that in the rest two groups (P<0.01). Tumor development was seen in nude mice inoculated with pRcHCNS3-5' transfected cells after 15 days. HE staining showed its feature of hepatocarcinoma, and immunohistochemistry confirmed the expressions of HCV NS3 and c-myc proteins in tumor tissue. The positive control group inoculated with HepG2 also showed tumor development, while no tumor developed in the nude mice injected with pRcCMV and non-transfected cells after 40 days. CONCLUSION: 1.HCV NS3 c-terminal deleted protein has transforming and oncogenic potential. 2. Human liver cell line QSG7701 may be used as a good model to study HCV NS3 pathogenesis.

Animals↗
PubMed2006

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

The tumor suppressor PTEN is frequently inactivated in human cancers. A major downstream effector of PTEN is Akt, which is hyperactivated via PTEN inactivation. It is not known, however, whether diminished Akt activity is sufficient to inhibit tumorigenesis initiated by Pten deficiency. Here we showed that the deficiency of Akt1 is sufficient to dramatically inhibit tumor development in Pten+/- mice. Akt1 deficiency had a profound effect on endometrium and prostate neoplasia, two types of human cancer, in which PTEN is frequently mutated, and also affected thyroid and adrenal medulla tumors and intestinal polyps. Even haplodeficiency of Akt1 was sufficient to markedly attenuate the development of high-grade prostate intraepithelial neoplasia (PIN) and endometrial carcinoma. These results have significant implications for cancer therapy.

Adrenal Gland Neoplasms↗
PubMed1987

Regulation of tumor development: the biphasic effects of silica and of lipopolysaccharide on natural resistance.

The impact on tumor development of the BRM silica and LPS was assessed through analysis of changes in NR parameters in vivo and in vitro. Although injection of the fumed silica Cab-o-sil 3 days before a threshold s.c. inoculum of L5178Y-F9 cells increased the tumor frequency in syngeneic DBA/2 mice, tumors recovered from silica-treated animals exhibited an augmented resistance to NAb and to in vivo NR. Cab-o-sil increased in vivo NR and induced a biphasic modulation of anti-tumor NAb and NK activities. The appearance of more autonomous tumors in Cab-o-sil-treated mice corresponding with a stimulation of NR parameters, suggests that the adjuvant activity of silica also contributes to its co-carcinogenic effect by accelerating tumor development. While injection of LPS 2-3 days before a threshold tumor inoculum lowered the tumor incidence, the survival of tumor cells injected within 1 day of LPS was increased. A corresponding early decrease in NAb activity occurred, in contrast with increases in NK cell and NAb levels previously observed after 5 days. This biphasic effect of LPS on NR effectors assayed in vitro was also seen on in vivo NR. Although their frequency was higher, tumors initiated during the period of LPS-induced NR abrogation exhibited greater reductions in NAb binding and sensitivity to NR than tumors from control mice. These data extend the support for NAb acting against tumor cells in vivo and reveal the dual nature of NR in tumor development, defending against small tumor foci and driving the progression of the surviving neoplasm.

Animals↗
PubMed1994

Timely immunization subverts the development of peripheral nonresponsiveness and suppresses tumor development in simian virus 40 tumor antigen-transgenic mice.

Tolerance to tumor cell-expressed molecules and selection of cells that evade immune surveillance during tumor progression create effective barriers to immunotherapy. We investigated the cytotoxic T-lymphocyte response to simian virus 40 (SV40) tumor (T/t) antigen in two lineages of transgenic mice bearing the same rat insulin promoter-SV40 T/t antigen (RIP Tag) hybrid gene. RIP1-Tag2 mice, which express Tag as embryos, are tolerant to Tag, whereas RIP1-Tag4 mice, which express the transgene in pancreatic islet beta cells several weeks after birth and develop insulinomas, can be immunized to generate active Tag-specific cytotoxic T lymphocytes as determined by in vitro assays. Indeed, RIP1-Tag4 mice immunized with Tag by SV40 infection prior to the time of endogenous transgene expression also mount an effective in vivo cellular immune response to the Tag-expressing pancreatic beta cells, and Tag-induced tumor growth is significantly delayed (up to 1 year). However, after the transgene is expressed, RIP1-Tag4 mice are unable to mount a tumor-inhibiting response upon immunization, although Tag-specific cytotoxic T cells can still be demonstrated in vitro. Our data suggest that Tag-specific T cells are rendered unresponsive in vivo in RIP1-Tag4 mice and that the establishment of this unresponsiveness to Tag can be prevented by SV40 immunization only before the onset of the transgene expression. In the older, successfully immunized mouse, decreased immune surveillance and selection of cells with down-regulation of major histocompatibility complex class I expression most likely set the stage for insulinoma development.

Animals↗
PubMed1997

Massive mammary gland infection and pregnancy-dependent mammary tumor development in mice infected neonatally with mouse mammary tumor virus (SW) but not in mice infected as adults, despite a dramatic local response.

Mouse mammary tumor virus (MMTV) (SW) caused a high incidence (65%) of pregnancy-dependent adenocarcinomas in BALB/c(SW) mice infected as newborns by suckling their mothers' milk. These tumors were type B adenocarcinomas which developed early, at about 1 year of age. Uninfected breeding females and those infected at an age of 8 weeks by injection of virus had the same low incidence of malignant tumors (13%), and the tumors developed later (at approx. 23-24 months). The low incidence of tumors in adult-infected mice was correlated with partial infection of the mammary glands, and delayed transmission of MMTV(SW) to the offspring. Although the virus was rapidly disseminated in both types of infection, the responses of neonatally infected and adult-infected mice to MMTV(SW) infection and viral superantigen (vSAG) presentation were different. Activation by and presentation of the vSAG was impaired in mice infected neonatally, and tolerance induction by clonal deletion was delayed. Local activation was dramatic in mice infected as adults and clonal deletion followed rapidly. Although interaction between B and T cells is needed for completion of the virus life cycle and viral amplification, the strong local immune response to MMTV(SW) in adult-infected mice limits mammary gland infection, and protects them against mammary tumor development.

Adenocarcinoma↗
PubMed1975

Tumor development after polyoma infection in athymic nude mice.

Nude (nu/nu) mice in a CBA/H background show an age-dependent ssuceptibility to tumor development after polyoma virus infection (strain LID-1) when compared with nu/ + or CBA/H mice, which is apparent when 15- or 30-day-old mice are used: tumor incidence was 83 to 90% in nudes and 0 to 10% in controls. Latent perids for tumor development were also shortened in nudes. However, with increasing age nude mice become partially resistant and only 25% develop tumors when infected at 120 days of age. This partial resistance could be transferred with spleen cells to newborn mice. The cells in spleen responsible for this transfer can be eliminated by lysis with anti-Ig and complement or by pre-treatment of the donor with 100 mg/kg of cyclophosphamide and were not affected by treatment in vitro with anti-Thy.1.2 or procedures that remove adherent cells and/or macrophages. When the cells in 15-day-old nu/ + spleen were studied, both anti-Ig or anti-Thy.1.2 treatment eliminated tranfer of resistance to newborn. Virus replication in tissues of nude mice was increased 5 days after infection when compared with nu/ + but became comparable by day 15 after infection. Hemagglutination-inhibition antibodies in serum of nude and nu/ + had comparable titers when measured early after infection but higher titers were observed in nu/ + later after infection.

Age Factors↗
PubMed1993

Accelerated tumor development in interferon-treated B6.C-Hyal-1 a mice.

The Hyal-1 locus, which we have previously described and mapped to mouse chromosome 9, influences the serum levels and molecular weight forms of hyaluronidase. We have also shown that the growth of two transplantable tumors, the 3LL carcinoma and the B16F10 melanoma, is influenced by the alleles at Hyal-1, in that the tumors develop more slowly in congenic B6.C-Hyal-1a (also called HW23) mice than in the parental Hyal-1b C57BL/6 mice. Here we present evidence that tumor development is stimulated and mortality is accelerated in B6.C-Hyal-1a mice grafted with 3LL carcinoma cells when treated with alpha/beta interferon (IFN-alpha/beta) or with IFN-beta, whereas in IFN-treated C57BL/6 mice 3LL tumor growth is inhibited. Likewise, in B6.C-Hyal-1a mice grafted with B16F10 melanoma cells, IFN-alpha/beta treatment results in stimulation of tumor growth, whereas in IFN-treated C57BL/6 mice tumor growth, whereas in IFN-treated C57BL/6 mice tumor growth is inhibited and mortality delayed. Thus, IFN-alpha/beta treatment of B6.C-Hyal-1a mice results in stimulation of tumor development and sometimes in accelerated mortality. This is the opposite of the usually described effect of IFN treatment in mice, which is inhibition of tumor development and delayed mortality, as was indeed observed in the C57BL/6 mice in the present experiments. These results provide the first indication that host genes can up- or down-regulate the antitumor activity of IFN and that, on some genetic backgrounds, IFN treatment enhances rather than inhibits tumor development. This may help to explain the apparent discordance between mouse model studies, which hitherto have consistently reported inhibition of tumor formation by IFN, and the clinical trials, in which only a limited percentage of individuals show tumor regression while others have no beneficial effect or even have progression of disease in spite of the IFN treatment.

Alleles↗
PubMed1979

Prevalent types of tumors developing in neonatally thymectomized mice.

Tumor development was observed for 24 months in neonatally thymectomized (nTx) and normal (C3H/HeMs x 129/J)F1 mice. Thymectomy was performed at 3 days of age. Ovarian (29%, with significant difference from the control at P less than 0.001), pituitary (6%, P less than 0.08), and lymphoreticular tumors (16%, P less than 0.05) were observed in higher incidence in nTx females compared with normal controls, resulting in a significant increase in overall tumor incidence (99 tumors in 114 nTx females vs. 37 tumors in 71 normal females, P less than 0.01). No apparent difference in overall tumor incidence was observed between nTx and non-Tx males. Also, there was no higher risk for lung, liver, and mammary tumors in males and females after neonatal thymectomy. The finding that increased tumor incidence was limited to endocrine and lymphoreticular tissues does not support the concept of immune surveillance of carcinogenesis, but rather suggests the importance of tumor-prone conditioning of endocrine or immune systems as a result of neonatal thymectomy.

Animals↗
PubMed2002

Deficiency of c-Jun-NH(2)-terminal kinase-1 in mice enhances skin tumor development by 12-O-tetradecanoylphorbol-13-acetate.

The c-Jun NH(2)-terminal kinase (JNK) has been implicated in regulating cell survival, apoptosis, and transformation. However, the distinct role of JNK isoforms in regulating tumor development is not yet clear. We have found previously that skin tumor formation induced by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), is suppressed in JNK2-deficient (Jnk2(-/-)) mice. Here, we show that JNK1-deficient (Jnk1(-/-)) mice are more susceptible to TPA-induced skin tumor development than wild-type mice. The rate of tumor development in Jnk1(-/-) mice was significantly more rapid than that observed in wild-type mice (P < 0.0001). At the end of 33 weeks of TPA promotion, the number of skin tumors and tumors >1.5 mm in diameter per mouse in Jnk1(-/-) mice was significantly increased by 71% (P < 0.03) and 82% (P < 0.03), respectively, relative to the wild-type mice. Furthermore, the carcinoma incidence and the number of carcinomas per mouse were also higher in Jnk1(-/-) mice. Strikingly, Jnk1(-/-) mouse skin was more sensitive to TPA-induced AP-1 DNA binding activity and phosphorylation of extracellular signal-regulated kinases and Akt, which are two important survival signaling components. These results suggest that JNK1 is a crucial suppressor of skin tumor development.

Animals↗
PubMed1991

Alterations in tumor development in vivo mediated by expression of wild type or mutant p53 proteins.

To study the mechanism of p53 involvement in malignant transformation, we compared the tumor development patterns induced by a parental p53 nonproducer pre-B cell line with those by cell lines generated from this parental cell line following transfection of either wild type or mutant p53. It was found that whereas mutant p53 facilitated tumor development, expression of wild type p53 restrained tumor development. Cell lines expressing the wild type p53 induced the development of faster regressing tumors than the parental cell line. The parental p53 nonproducer and the wild type p53 producer regressor tumors underwent in vivo cell differentiation, manifested as IgG production. Mutant p53, producer cell lines, on the other hand, failed to show any immunoglobulin synthesis and gave rise to highly proliferative lethal tumors. Our results support the conclusion that these pre-B cells develop regressor tumors because they have undergone differentiation. Whereas the wild type p53 facilitates this differentiation, mutant p53 cells block it. We suggest that, in addition to inactivating the growth-suppressive activity of wild type p53, the expression of mutant p53 facilitates malignant transformation.

Animals↗
PubMed2005

[Human normal biliary epithelial cells transformation and tumor development induced by hepatitis C virus core protein].

OBJECTIVE: To study the effect of hepatitis C virus core protein (HCV-C) on human normal biliary epithelial cells (BEC) transformation and tumor development. METHODS: BEC cells were transfected with plasmid pcDNA HCV-C (expressing HCV-C) by lipofectamine and selected in G418. The expression of HCV-C gene and protein was determined by PCR and immunohistochemical staining, respectively. Biological effect of transfected cells was observed through cell proliferation assay, anchor independent growth, and tumor development in nude mice. The expression of HCV-C protein in the induced tumor was evaluated by immunohistochemistry. RESULTS: HCV-C was strongly expressed in BEC cells transfected with plasmid pcDNA HCV-C and the positive signal was located in cytoplasm. The HCV-C expression protein in the induced cytoplasm. Cell proliferation assay showed that the population doubling time in the pcDNA HCV-C transfected cells was much shorter than that in the pcDNA3 and non-transfected cells (14 h, 28 h, 30 h respectively). The cloning efficiencies of transfected cells with pcDNA HCV-C, pcDNA3 and non-transfected cells were 36%, 2.5% and 1.5%, respectively (P < 0.01). Tumor developed in nude mice inoculated with pcDNA HCV-C transfected cells after the inoculation. HE staining showed bile duct carcinoma character and immunohistochemistry confirmed HCV-C expression in the tumor tissue. The positive control group also showed tumor development, while no tumor mass obtained in the nude mice inoculated with pcDNA3 and non-transfected cells even 36 days after the injection. CONCLUSION: HCV-C protein showed human normal biliary epithelial cells transformation and tumorigenic features.

Animals↗
PubMed2003

[Hepatocyte transformation and tumor development induced by hepatitis C virus NS3 N-terminal protein].

OBJECTIVE: To study the effect of hepatitis C virus nonstructural protein 3 N-terminal protein (HCV NS3-5') on hepatocyte transformation and tumor development. METHODS: QSG7701 cells were transfected with plasmid pRcHCNS3-5' (expressing HCV NS3 N-terminal protein) by lipofectamine and selected in G418. The expression of HCV NS3 gene and protein was determined by PCR and immunohistochemistry respectively. Biological effect of transfected cells was observed through cell proliferation assay, anchor independent growth, and tumor development in nude mice. The expression of HCV NS3 and c-myc protein in the induced tumor was evaluated by immunohistochemistry. RESULTS: HCV NS3 was strongly expressed in QSG7701 cells transfected with plasmid pRcHCNS3-5' and the positive signal was located in cytoplasm. The HCV NS3 expression and c-myc protein in the induced cytoplasm. Cell proliferation assay showed that the population doubling time in the pRcHCNS3-5' transfected cells was much shorter than that in the pRcCMV and non-transfected cells (24 h, 26 h, 28 h respectively). The cloning efficiencies of transfected cells with pRcHCNS3-5', pRcCMV and non-transfected cells were 33.0%, 1.5%, 1.1% respectively (P < 0.01). Tumor developed in nude mice inoculated with pRcHCNS3-5'transfected cells 15 days after the inoculation. HE staining showed hepatocarcinoma character and immunohistochemistry confirmed HCV NS3 and c-myc expression in the tumor tissue. The positive control group also showed tumor development, while no tumor mass obtained in the nude mice inoculated with pRcCMV and non-transfected cells even 40 days after the injection. CONCLUSION: HCV NS3 N-terminal protein showed cell transformation and tumorigenic features.

Animals↗
PubMed1997

Effect of tissue factor deficiency on mouse and tumor development.

Previous reports suggest that tissue factor (TF) may play an essential role in embryonic vascular development and tumor angiogenesis. To further examine this relationship, the morphology of fully developed TF-deficient embryos and the growth of TF-deficient teratomas and teratocarcinomas were analyzed. In a 129/Sv genetic background, TF null embryos do not survive beyond mid-gestation. In contrast, 14% of 129/Sv x C57BL/6 TF-deficient embryos escape this early mortality and survive to birth. On gross and microscopic inspection, these late gestation, TF-deficient embryos appear normal. The growth and vascularity of TF(+/+), TF(+/-), and TF(-/-) teratomas and teratocarcinomas are indistinguishable. Thus, tumor-derived TF is not required for tumor growth and angiogenesis and the combined data do not support an essential role for TF in embryonic vascular development.

Animals↗
PubMed1996

Polyoma tumor development in neonatally polyoma-virus-infected CD4-/- and CD8-/- single knockout and CD4-/-8-/- double knockout mice.

CD4-/- or CD8-/- single knockout as well as CD4-/-8-/- double knockout mice were infected with polyoma virus as newborns or 1 week after birth. The animals were followed for tumor development and virus persistence. Double knockout mice developed tumors at a higher incidence (29%) than either the CD8-/- or CD4-/- single knockout mice (11% and 2%, respectively). Persistence of polyoma virus was examined by PCR in one third of all animals included in the study. Seven of the 17 CD4-/-8-/- double knockout mice gave positive evidence of virus persistence up to 6 months p.i. where virus DNA was present in most organs. Corresponding tests in single knockout mice gave positive results of persistent viral DNA in 2 of the 19 CD8-/-and 2 of the 7 CD4-/-mice. In the single knockout mice polyoma DNA could only be detected in a more limited variety of organs compared to the double knockouts.

Animals↗
PubMed2005

Suppression of tumor development and metastasis formation in mice lacking the S100A4(mts1) gene.

The S100A4(mts1) protein stimulates metastatic spread of tumor cells. An elevated expression of S100A4 is associated with poor prognosis in many human cancers. Dynamics of tumor development were studied in S100A4-deficient mice using grafts of CSML100, highly metastatic mouse mammary carcinoma cells. A significant delay in tumor uptake and decreased tumor incidences were observed in S100A4(-/-) mice compared with the wild-type controls. Moreover, tumors developed in S100A4(-/-) mice never metastasize. Immunohistochemical analyses of these tumors revealed reduced vascularity and abnormal distribution of host-derived stroma cells. Coinjection of CSML100 cells with immortalized S100A4(+/+) fibroblasts partially restored the dynamics of tumor development and the ability to form metastasis. These fibroblasts were characterized by an enhanced motility and invasiveness in comparison with S100A4(-/-) fibroblasts, as well as by the ability to release S100A4 into the tumor environment. Taken together, our results point to a determinative role of host-derived stroma cells expressing S100A4 in tumor progression and metastasis.

Animals↗
PubMedDate not supplied

Sonographic estimation of liver tumor development induced by oral administration of thioacetamide in rat.

Animal models for various types of cancer are of great help in the study of tumors and antitumor effects. Subcutaneous models have been widely utilized because they can be produced easily by subcutaneously implanting tumor cells into animals. Although subcutaneous models are very convenient for examining tumor development, they are definitely different from clinical manifestations of original tumors. In orthotopic animal models for internal tumors, however, it is difficult to examine tumor development without sacrificing animals. We demonstrate here that the occurrence and growth of liver tumors induced by oral administration of thioacetamide into rats were clearly observable by ultrasonography, and that the sonographic estimation was accurate. It was observed sonographically that the number and volume of liver tumors increased proportionately with TAA treatment periods. These results indicate that sonography is a useful and non-invasive method to investigate liver tumor development in rats.

Administration, Oral↗