Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of cellular and humoral immunity in the localization of blood-borne, bone marrow-derived ADCC effector cells into the T1699 mammary adenocarcinoma was investigated. Administration of ALG before tumor inoculation caused total immunosuppression and resulted in minimal in situ inflammation. ALG treatment started at the time of tumor inoculation suppressed the delayed hypersensitivity response below a detectable level but permitted a significant antibody response. Under these circumstances, the localization of ADCC effector cells into the tumors appeared normal. Similarly, administration of ALG at later stages of tumor growth, where ALG acts as an anti-inflammatory agent, did not interfere with the normal infiltration of ADCC effector cells in situ, although the delayed hypersensitivity response was totally suppressed. When melphalan treatment was used to produce tumor-bearing mice with an intact delayed hypersensitivity response but devoid of a significant antibody response, the drug-treated animals were found to have high levels of ADCC effector cells in situ. These results demonstrate that although the in situ inflammatory reaction appears to be immunologically inflammatory reaction appears to be immunologically dependent, neither the delayed hypersensitivity nor the antibody response is solely responsible for the localization of ADCC effector cells in the T1699 mammary tumor.
 ...
PMID:Immunologic factors influencing the intra-tumor localization of ADCC effector cells. 65 77

In our previous studies we found that the slower growth of syngeneic, immunogenic MC-induced sarcoma (MC-Sa) in aging rats was followed by the higher activity of spleen lymphocytes in ADCC assay. The purpose of the present paper was to study infiltrating cells of immunogenic and non-immunogenic MC-Sa and to estimate in situ ADCC activity in relation to the growth of MC-Sa transplants in adult and aging rats. It was found that MC-Sa's were infiltrated mainly by lymphocytes. Among cells infiltrating tumor the high percentage of cells with Fc receptor was present. During progressive tumor growth the percentage of infiltrating cells and also FcR+ cells significantly decreased within immunogenic MC-Sa, but did not change in the case of the non-immunogenic MC-Sa. In cell infiltrates of both tumors no differences between adult and aging rats were observed. At early stages of the tumor growth the cells active in ADCC assay were present within both MC-Sa. The slower growth of immunogenic MC-Sa in aging rats compared with adults was connected with longer maintenance of ADCC activity in situ. In the case of non-immunogenic MC-Sa, which grew at similar rate in both groups of rats, no differences in ADCC activity between adult and aging animals were observed. It is suggested that in situ ADCC activity may be one of the mechanisms responsible for the slower growth of immunogenic MC-Sa in aging rats.
 ...
PMID:Methylcholanthrene-induced tumors in adult and in aging rats: infiltrating cells and their ADCC activity. 210 60

The effect of murine anti-canine lymphoma monoclonal antibodies (MAbs) on tumor cell lysis by thioglycolate activated murine macrophages in vitro and tumor growth inhibition in athymic mice was studied. All IgG1 and IgG2a MAbs tested were able to promote specific destruction of canine lymphoma 17-71 cell line by activated macrophages. A correlation between higher ADCC activity and MAb isotype was not clearly evident. In vivo IgG2a and IgG1 MAbs inhibited the growth of canine lymphoma. These results suggest that MAbs of IgG type have potential in immunotherapy of dogs with lymphoma since they have high tumoricidal activity in vivo.
 ...
PMID:In vivo destruction of canine lymphoma mediated by murine monoclonal antibodies. 210 65

It has recently been shown that human T-cell subpopulation can be identified functionally via surface receptors for Fc fragment of immunoglobulins. We detected peripheral blood T-cells bearing the Fc receptor for IgG molecules (T gamma cell) in patients with brain tumors who manifested a variety of immunological abnormalities. We also analyzed immunological values of T gamma cells which were thought to be suppressor and/or a part of killer T cells, comparing with other immunological parameters. The percentage of T gamma cells was significantly higher in patients with malignant brain tumors than in normal controls (6.54 +/- 1.6%). The values of T gamma cells in patients with glioma, metastatic brain tumor, benign brain tumor were 15.4 +/- 4.8%, 14.9 +/- 3.2%, and 8.1 +/- 3.7%, respectively. In the patients with glioma, the values increased in the uncontrolled group compared with the well-controlled group. Furthermore, the values were decreased by surgical removal of the tumor. On immunological study of T gamma cells in the patients with glioma, there was a definite correlation between the values of T gamma cells and ADCC activity. Furthermore, the T gamma cells in the patients showed higher ADCC activity than in normal controls. The values of T gamma cells also correlated with blastogenesis of the peripheral blood lymphocytes by PHA (r = -0.742, p less than 0.001) and Con A (r = -0.662, p less than 0.001). These results suggest that T gamma cells are playing two important roles in patients with glioma such as suppressor function and ADCC activity, and that these cells may change according to the tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Clinicoimmunological values of measurement of IgG-Fc receptor positive T cells in the patients with malignant brain tumors]. 293 80

Four mouse monoclonal antibodies (mAb) (8C, IgG2a; M2A, IgG2a; M2D, IgG2b; 10B, IgG1) directed against the human ovarian adenocarcinoma cell line HEY were compared for their ability in the free form and as immunotoxins made with recombinant ricin A chain (rRA) to inhibit the growth of HEY cells. For in vitro studies cultured HEY cells were assayed for protein synthesis and plated in agarose to form colonies, and for in vivo studies they were injected intraperitoneally (i.p.) into BALB/c nu/nu (nude) mice at a challenge dose (3 X 10(5) cells) which produced carcinomatosis with ascites, leading to death 30 days following injection. In the free form, mAB 8C was the most potent in inhibiting colony formation in the complement (C)-mediated and ADCC (antibody-dependent cell-mediated cytoxicity) assays in vitro. This mAb was also the only one capable of prolonging survival of mice, both in tumor cell neutralization, and tumor growth inhibition experiments. The four mAb-rRA immunotoxins were effective in inhibiting protein synthesis in vitro in the presence of 10(-7) M monensin. However, in vivo, only 8C-rRA and M2A-rRA were capable of prolonging survival of mice in tumor growth inhibition experiments. Our results suggest that mAb 8C might be useful in the free form and as an 8C-rRA immunotoxin for i.p. immunotherapy of ovarian cancer.
 ...
PMID:Comparison of growth inhibition of a human ovarian adenocarcinoma cell line by free monoclonal antibodies and their corresponding antibody-recombinant ricin A chain immunotoxins. 326 79

Investigations on the relationship between the aging of the immune system and the tumor growth are the trigger of our studies. The purpose of the present paper was to determine a relation between cytotoxic activity of the spleen lymphocytes in ADCC assay and the MC-induced sarcoma growth in adult and aging rats. In ADCC assay the mouse leukemia L1210 labeled with Cr and sensitized with rabbit anti-L1210 serum was used as target cells. In aging rats with MC-Sa tumors the lymphocyte activity in ADCC was increased or remained unchanged in the comparison with normal animals. On the contrary, in adult rats with MC-Sa tumors ADCC activity was decreased. In comparative studies between the groups of adult and aging rats a reverse relationship between the tumor growth and the lymphocyte activity in ADCC was found. In aging rats the level of ADCC was higher than in adults, but the tumor growth was slower. We suggest that ADCC phenomenon may be involved in an antitumor response, especially effective in aging rats.
 ...
PMID:ADCC in aging rats with methylcholanthrene-induced sarcoma (MC-Sa). 350 42

We had earlier shown that tumor-bearing results in an inactivation of IL-2-dependent effector cells by host macrophage-derived PGE2, and that chronic indomethacin therapy (CIT) aimed at blocking prostaglandin synthesis, combined with multiple rounds of IL-2, can cure experimental metastases of a variety of tumors in mice. We have now tested the efficacy of this therapy on spontaneous as well as experimental metastasis of C3-L5 mammary adenocarcinoma in C3H/HeJ mice. Mice transplanted s.c. with C3-L5 cells (and showing visible spontaneous lung metastases between days 7 and 10) were given CIT starting on day 15, plus 2 5-day rounds of IL-2 or IL-2 alone. Mice injected i.v. with 10(4) C3-L5 cells (and showing lung micrometastases on day 5) were placed on CIT on day 5 and given 3 5-day rounds of IL-2 or treated with IL-2 alone. Control mice received vehicles alone. Results revealed that combined CIT + IL-2 therapy in the spontaneous metastasis model caused a regression of primary tumors, a marked reduction in lung metastases scored on days 25-35 and a marked prolongation of host survival (79% cured). Survivors rechallenged with 10(4) tumor cells i.v. on day 210 resisted tumor growth. In the experimental metastasis model, this therapy also markedly reduced lung metastases and prolonged animal survival (50% cured). In both models, the combination therapy led to the presence of highly active tumoricidal (for C3-L5 and YAC-1 lymphoma targets) lymphocytes with AGM-1+, Lyt-2- and Thy-1 +/- phenotype and macrophages in the spleen and the lungs, and ADCC-promoting activity in the serum. CIT + IL-2 therapy can thus effectively eradicate spontaneous and experimental mammary adenocarcinoma metastasis in mice. It activates natural effector cells in situ, generates ADCC-promoting activity in the serum and results in resistance to tumor take in this moderately immunogenic tumor model.
 ...
PMID:Eradication of spontaneous and experimental adenocarcinoma metastases with chronic indomethacin and intermittent IL-2 therapy. 851 59

Chimeric receptors that redirect effector cell function to tumor cells or virus-infected cells have received much attention. Given the high affinity of Fc(epsilon)RI for immunoglobulin E (IgE) and low serum IgE levels, redirection of effector cells using Fc(epsilon) receptor may provide a novel, versatile, and effective anti-tumor strategy. We have used a mouse perforin 5'-promoter to express a single-chain human Fc(epsilon) receptor in the mouse cytotoxic T lymphocyte cell line, CTLL-R8. Upon ligation of the chimeric Fc(epsilon) receptors by IgE, a signal for effector function is transmitted via the intracellular domain of CD3zeta. Selection in G418-containing medium produced CTLLR8 transfectant clones that: (1) expressed chimeric Fc(epsilon) receptor as determined by flow cytometry; (2) bound human IgE antibodies with high affinity as determined by Scatchard analysis; (3) specifically rosetted IgE-coated SRBC; (4) lysed target cells in IgE-mediated ADCC and reverse ADCC assays; and (5) retarded tumor growth in a Winn assay. Therefore these chimeric Fc(epsilon) receptors can effectively redirect cytotoxicity to tumor cells. Future efforts will assess the versatility and efficacy of these IgE-binding chimeric receptors to redirect killer cell function in animal tumor models.
 ...
PMID:The use of chimeric human Fc(epsilon) receptor I to redirect cytotoxic T lymphocytes to tumors. 897 74

The anti Her-2/neu monoclonal antibody Trastuzumab has strong inhibiting effects on tumor growth in vitro and in vivo and is therefore used for immunotherapy in breast cancer patients. Due to necessity of frequent applications, however, cost intensiveness of Trastuzumab treatment and its limited duration of affectivity, an active immunization inducing a perhaps preventive and long-term immunity to Her-2/neu remains a desirable goal. We attempted to induce anti Her-2/neu antibodies by peptide vaccination and to test their efficacy in inhibiting tumor cell growth in vitro. By computer aided analyses, 7 putative B cell epitopes of Her-2/neu were defined and synthesized. These peptide epitopes were coupled to tetanus toxoid and used for immunization in BALB/c mice. Among these peptides, immunizations with 2 single peptides or a combination of 2 peptides induced anti-peptide antibody levels, primarily of the IgG1 isotype. These antibodies were also directed against the native Her-2/neu antigen, as shown in precipitation assays and ELISA with cell lysates of the Her-2/neu overexpressing breast cancer cell line SK-BR-3. Isolated IgG fractions from immune sera incubated with SK-BR-3 cells led to a moderate inhibition of the tumor cell growth in vitro, as well as to complement dependent cell lyses comparable to that achieved by incubation with Trastuzumab. Moreover, peptide immunization in rabbits generated anti-Her 2-neu IgG that, in contrast to mouse sera, were able to mediate a 31-46% lysis of SK-BR-3 cells in ADCC experiments. We conclude from our data that immunization with Her-2/neu peptides successfully induced humoral immune response with anti-tumor activity in an animal model.
 ...
PMID:Inhibition of tumor cell growth by antibodies induced after vaccination with peptides derived from the extracellular domain of Her-2/neu. 1460 Oct 58

Genome-wide expression profiling revealed overexpression of the gene encoding frizzled homologue 10 (FZD 10), a cell-surface receptor for molecules in the Wnt pathway, as a potential contributor to synovial sarcomas (SS). Northern blotting and immunohistochemical staining confirmed that expression levels of FZD 10 were very high in nearly all SS tumors and cell lines examined but absent in most normal organs or in some cancers arising in other tissues. Treatment of human SS cells with small-interfering RNA (siRNA) to FZD 10 decreased the amount of its product and suppressed growth of SS cells. Moreover, a polyclonal antibody specifically recognizing the extracellular domain (ECD) of FZD 10 was markedly effective in mediating ADCC against FZD 10-overexpressing synovial sarcoma cells in vitro. Injection of the antibody into SS xenografts in nude mice attenuated tumor growth, and TUNEL assays revealed clusters of apoptotic cells in antibody-treated xenografts. Taken together, these findings suggest that a humanized antibody against FZD 10 might be a promising treatment for patients with tumors that overexpress FZD 10; minimal or no adverse reactions would be expected because FZD 10 protein is not abundant in vital organs.
 ...
PMID:Therapeutic potential of antibodies against FZD 10, a cell-surface protein, for synovial sarcomas. 1600 99


1 2 3 Next >>