UMLS:C0001418 - FACTA Search

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Query: UMLS:C0001418 (adenocarcinoma)
68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cytotoxic activities, of the peripheral blood lymphocytes (PBL) and regional lymph node lymphocytes (LNL) generated by incubation with recombinant IL-2 (rIL-2) in vitro, have been studied to assess their effects on autologous pulmonary adenocarcinoma cells from 21 patients with lung cancer. The lymphokine-activated killer (LAK) activities of PBL were 22.9 +/- 14.8% for autologous pulmonary adenocarcinoma cells and 44.9 +/- 20% for PC-9 cells. A previous coculture of autologous tumor cells with PBL (ATS-LAK) showed no increase in induction of cytotoxicity to autologous tumor cells. The LAK activities of LNL were significantly lower than those of PBL. The cytotoxicities of rIL-2 activated lymphocytes seemed lower in well differentiated pulmonary adenocarcinoma than in moderately and poorly differentiated adenocarcinoma, and higher in patients with lymph node metastasis than in those without; they appeared, however, not to be related to clinical stage or degree of infiltration of T-zone histiocytes into the cancer stroma. The cytotoxicity to autologous tumor cells was not significantly different in the presence of the Ia antigen expressed on tumor cells, but the cytotoxicity to Ia positive PC-9 cells was significantly higher for rIL-2 activated lymphocytes from patients with lung cancer cells which were Ia positive than from those where they were Ia negative. The presence of Ia antigen on tumor cells seemed important for antitumor activity.
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PMID:Induction of lymphokine-activated killer activities in peripheral blood lymphocytes and regional lymph node lymphocytes against PC-9 cultured adenocarcinoma and autologous pulmonary adenocarcinoma cells. 349 85

A good therapeutic response following local transfer of lymphokine-activated killer (LAK) cells was obtained in a patient with cardiac tamponade due to breast carcinoma. A 41-year-old female was admitted with complaints of dyspnea and tachycardia. She had undergone left mastectomy at the age of 37 years and had received continuous oral administration of tamoxifen. Chest roentgenogram revealed cardiomegaly (CTR = 65%) and cardiac echogram showed marked retention of pericardial effusion. The cytology of the effusion was class V (adenocarcinoma). Cardiac tamponade proved refractory to combination chemotherapy using adriamycin, cyclophosphamide and 5-fluorouracil, and the effect of paracentesis was only temporary. Autologous peripheral blood lymphocytes were obtained through the cubital vein and cultured in vitro with 2 units/ml of human recombinant IL-2, (TGP-3, Takeda Pharm. Co.). After 4 days of cultivation, LAK cells were transferred intrapericardially 3 times. The cumulative infusion dose was 1.2 X 10(8) cells and the amount of combined IL-2 administration was 100 units/each transfer. Twenty-four days after initial infusion of LAK cells, the effusion disappeared. After then, recurrence has not been observed for 287 days. This case is the first trial of LAK therapy against pericarditis carcinomatosa and seems to be a useful way of treating this uncontrollable state without any serious side effects.
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PMID:[A case of pericarditis carcinomatosa showing good response following local transfer of lymphokine-activated killer (LAK) cells]. 349 13

Cytotoxic activity of lymphocytes cultured in IL-2 against autologous primary lung cancer cells was studied in relation to curativity, prognosis and relapse rate. A total of 51 patients, 44 males and 7 females, consisting of those with adenocarcinoma (n = 27), squamous cell carcinoma (n = 19), large cell carcinoma (n = 2), small cell carcinoma (n = 1), lung sarcoma (n = 1), and carcinoid (n = 1), were evaluated. Pathological stages of the patients were stage I (n = 16), stage II (n = 1), stage III (n = 28), and stage IV (n = 6). Thirteen patients (25.5%) underwent curative surgery, 23 patients (45.1%) received relative curative surgery and 15 patients (29.4%) received non-curative surgery. The mean value of cytotoxic activity in the patients who received curative surgery was 34.7 +/- 15.3%, relative curative surgery 26.5 +/- 18.9%, and non-curative surgery 42.8 +/- 22.3%. Among the patients who underwent curative and relative curative surgery, 23 patients survived more than 2 years and 13 patients died of cancer recurrence. Mean value of cytotoxic activity in the former (36.7 +/- 15.9%) was significantly (p less than 0.01) higher than that in the latter (17.1 +/- 14.7%). Positive rate (percentage of patients whose CA exceeded 15%) of the former (86.9%) was also higher than that of the latter (46.1%). Comparison between the survival curves of the positive cases (CA 15.0%) and negative cases (CA less than 15.0%) revealed a significantly better prognosis for the former (generalized Wilcoxon test: W/square root VarW = 2.198). The mean cytotoxic activity in the cases of local recurrence (25.7 +/- 16.6%, n = 7) was higher (p less than 0.10) than that in the cases with distant metastases (9.3 +/- 6.3%).
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PMID:[Cytotoxic activity of autologous lymphocytes against lung cancer cells; correlation of prognosis and recurrence pattern]. 349 20

Natural killer activity against K562 targets and recombinant interleukin-2 induced cytotoxicity to NK resistant targets (MEL-4 and T24) was investigated in 15 melanoma patients. Before elective surgery no differences in cytotoxic activities were demonstrated when compared with patients with colorectal adenocarcinoma and controls. No correlation with the depth of the melanoma lesion was observed. Numbers of precursors of IL-2 induced killers in melanoma patients were in normal range. In conclusion, no defects in non-specific NK and IL-2 induced behavior in peripheral blood of melanoma patients were found. Other factors, specific, non-specific, related or unrelated to the tumor side should be thus considered.
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PMID:Effect of human recombinant interleukin-2 on cytotoxic response of peripheral blood mononuclear cells in melanoma patients before surgery. 350 Jun 90

NK activity of human peripheral blood lymphocytes (PBL) for cells of the human myeloid line K562, and antibody-dependent cellular cytotoxicity (ADCC) of PBL for cells of human lung adenocarcinoma line PC-9 were determined by the human tumor clonogenic assay (HTCA). Incubation of K562 cells or anti-PC-9 serum treated PC-9 cells with PBL before plating inhibited the formation of colonies of these tumor cells. The percent inhibition of tumor cell colony formation was dependent on the effector/target ratio, the incubation time before plating and, in the case of PC-9 cells, on the dilution of anti-PC-9 serum. PBL activated with human T-cell growth factor (TCGF), lymphokine-activated killer (LAK) cells, significantly augmented the inhibition of colony formation of K562 cells, compared to the control lymphocytes. The increase in colony inhibition was dependent on the concentration of TCGF and the time of incubation of PBL with TCGF. The HTCA determining the colony inhibition of K562 cells incubated with LAK or PBL correlated with the 51Cr-release assay (p less than 0.001). The HTCA determining the colony inhibition of anti-PC-9 serum-treated PC-9 cells incubated with PBL also correlated with the 51Cr-release assay (p less than 0.001). We found that the NK activity and ADCC of lymphocytes on K562 and PC9 tumor lines could be detected with HTCA.
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PMID:Detection of NK activity and antibody-dependent cellular cytotoxicity of lymphocytes by human tumor clonogenic assay--its correlation with the 51Cr-release assay. 387 46

Human peripheral blood or lymph node lymphocytes, obtained from patients with a variety of lung cancer, were incubated in vitro with mitomycin C-treated tumor monolayers in the presence of T-cell growth factor. The cytotoxicity of these lymphocytes for autologous tumor cells (autologous killer activity) was assessed by a 4-hr 51Cr-release assay. Cytotoxic activity was observed in 14 out of a total of 20 cases. Lymphocytes from patients with squamous cell carcinoma, large cell carcinoma and carcinoid exhibited positive activity levels of 11.1 +/- 1.8, 16.3 and 23.9% respectively. Nine out of 13 patients with adenocarcinoma exhibited positive activity with a mean value of 8.8 +/- 6.8%. No lymphocyte activity against small cell carcinoma was observed. Natural killer (NK) activity did not always correlate with autologous killer (AK) activity. Treatment of lymphocytes with monoclonal anti-human lymphocyte antibody revealed differences in effector cell populations concerning these two activities; AK activity was abrogated only by treatment with anti-human Lyt 3 antibody and complement, whereas NK activity was abrogated by anti-human Lyt 1, 2 and 3 and partially by anti-human Ia antibody. These results indicate that AK activity is mediated exclusively by T cells, but that NK activity is mediated by several subpopulations of lymphocytes such as T cells, null cells and others.
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PMID:Cytotoxicity tests against cultured human lung cancer cells with autologous lymphocytes activated in vitro by mitomycin C-treated tumor monolayers in the presence of T-cell growth factor. 630 Apr 83

This study delineates the temporal relationship between immune complex formation and tumor growth, and provides one possible explanation for host immunosuppression during tumor growth. The authors have studied serial circulating immune complex (CIC) levels and interleukin (IL) elaboration by peripheral blood cells (IL-1 production by adherent mononuclear cells [AMC]; and IL-2 generation by peripheral blood mononuclear cells [PBMC]) during the growth of syngeneic tumor isografts in an inbred rat model. Male Wistar/Furth (W/Fu) rats were injected, subcutaneously (SC) with 2 X 10(6) W163 ( a dimethylhydrazine [DMH]-induced colon adenocarcinoma) cells into their hind limbs. Serial CIC levels, (measured by the antigen nonspecific polyethylene glycol turbidity assay) and IL-1 and IL-2 production were measured before isografting and weekly thereafter. Progressive local tumor growth occurred for 3 weeks followed by regional lymph node metastases during the fourth week. During local tumor growth, there was a progressive rise in CIC levels (123% rise compared with baseline value; P less than 0.05) which correlated with a fall in both IL-1 and IL-2 generation (r = -0.768). At the time of regional metastasis, the mean CIC levels declined, and there was a further significant decrease in IL production (IL-1 = 0.9% and IL-2 = 10% of controls in tumor bearers). These results show that progressive tumor growth results in decreased IL production by host PBC, and suggest that CIC may be involved in regulating IL generation.
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PMID:Effects of tumor growth on interleukins and circulating immune complexes. Mechanisms of immune unresponsiveness. 660

Localization of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and of their ligands, lymphocyte function-associated antigen-1 and very late activation antigen-4, was determined in non-small cell lung carcinomas and tumor-free lung. Messenger RNA expression for interleukins (IL) IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, tumor necrosis factor-alpha, transforming growth factor-beta, interferon-gamma, granulocyte-macrophages colony stimulating factor, and human perforin-1 was assessed by in situ hybridization on the same tissues. Intercellular adhesion molecule-1 was expressed in all blood vessels, whereas only a low number of vessels displayed vascular cell adhesion molecule-1 immunoreactivity. Tumor infiltrating lymphomononuclear cells consisted of lymphocyte function-associated antigen-1-positive cells and of a lower number of very late activation antigen-4-positive cells. All squamous cell carcinomas consisted of intercellular adhesion molecule-1-positive neoplastic cells infiltrated by lymphocyte function-associated antigen-1-positive tumor infiltrating lymphomononuclear and CD-la-positive Langerhans cells, whereas only a minor number of adenocarcinomas displayed a consistent number of intercellular adhesion molecule-1-positive neoplastic cells. Tumor infiltrating lymphomononuclear cells showed a wider production of cytokines when compared to bronchus-associated lymphoid tissue of tumor-free lung. Moreover, cells producing interferon-gamma, IL-4, and IL-5 were more numerous in squamous cell carcinomas than in adenocarcinomas. These findings indicate that the lung squamous cell carcinoma might represent a neoplastic microenvironment able to induce activation of tumor infiltrating lymphomononuclear cells more efficiently than the adenocarcinoma.
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PMID:Cytokine production and expression of adhesion molecules and integrins in tumor infiltrating lymphomononuclear cells of non-small cell carcinomas of the lung. 751 25

The immune effectors and the cellular mechanisms responsible for tumour rejection of two different tumours transduced with different cytokines have been characterized by immunocytochemistry and in situ hybridization. A colon (C-26) and a mammary (TS/A) adenocarcinoma engineered to release, respectively, 90 pg/ml of G-CSF (C-26/G-CSF) and 30 U or 6000 U of IL-2 (low B1.30 and high B4.6000 level of IL-2, respectively) were compared for the type of infiltrating leucocytes and for the repertoire of secondary cytokines produced by the leucocytes recruited at the tumour site. The results indicate that in both systems tumour rejection is associated with prominent infiltration of CD45+/RB6-8C5+ polymorphonuclear (PMN) leucocytes expressing mRNA for IL-1 alpha, IL-1 beta and TNF alpha. TS/A B1.30 and B4.6000 also showed a small proportion of infiltrating T lymphocytes, expressing IFN gamma and IL-4 mRNA, which were virtually absent in the C-26/G-CSF tumour. In mice injected with C-26/G-CSF cells after 600 rad irradiation, the tumours grew to about 1.5 cm and then regressed completely. During the regression phase, T lymphocytes were recruited within C-26/G-CSF, and the infiltrating leucocytes were similar, in terms of PMN/macrophages/T lymphocytes ratio, to those found during the memory response elicited by injection of a challenging dose of parental TS/A into mice pre-immunized with B1.30 IL-2-producing cells. The memory response was characterized by a CD4/CD8 ratio of 0.4 and by IFN-gamma and IL-4 mRNA expression, whereas the T lymphocytes present within regressing C-26/G-CSF were mostly CD4 (CD4/CD8 ratio of 2.1) and expressed IFN gamma mRNA only. The gene transfers of cytokines as different as G-CSF and IL-2 are able to inhibit tumour take through a similar anti-tumour immune response mostly due to non-specific effectors (PMN), thus resembling acute inflammation phenomena. Regression of C-26/G-CSF initially established in irradiated mice as well as rejection of TS/A tumour injected into B1.30 immunized mice are similar to a chronic infection but the immune reaction elicited by C-26/G-CSF has an impaired T-lymphocyte function.
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PMID:Different tumours, transduced with different cytokine genes as G-CSF and IL-2, show inhibition of tumour take through neutrophil activation but differ in T cell functions. 752 63

Little is known about the activation level of tumor-infiltrating lymphocytes (TIL) in human lung adenocarcinoma. We investigated the activation of fresh TIL at cellular and molecular levels and compared it with autologous and healthy normal peripheral blood lymphocytes (PBL) for baseline level. TIL were extracted from 12 primary lung adenocarcinomas by mechanical disruption without enzyme use and isolated by double-density Ficoll gradients. Flow-cytometry analysis of TIL subset distribution revealed that the majority was composed of T lymphocytes, and double labeling with alpha-CD3 and adhesion/activation markers revealed T cell subsets expressing CD49a, CD49b, CD54, and CD15, each of which was almost absent in autologous T peripheral blood lymphocytes (T-PBL). Moreover, the proportions of T-TIL expressing CD58, CD65, or CD25 were increased severalfold compared to T-PBL. Lymphokine gene activation in TIL was assessed by mRNA reverse transcriptase/polymerase chain reaction (RT-PCR) and primers for interleukin(IL)-2, IL-4, interferon (IFN) gamma, granulocyte/macrophage-colony-stimulating factor (GM-CSF), and tumor necrosis factor (TNF) beta. Semiquantitative comparisons between patients' TIL and PBL and healthy normal and activated PBL were performed by computerized image analysis. RT-PCR gel band products were quantified in relative units as a function of their size and intensity. TIL expressed detectable lymphokine mRNA but seemed poorly activated with respect to the total number of lymphokine genes and the amount of mRNA compared with alpha-CD3-activated healthy PBL. IL-2, IFN gamma, and TNF beta did not appear to be expressed at higher levels in TIL than in autologous or healthy normal PBL. However, two-thirds of the patients had TIL distinguishable from autologous PBL by specific expression of GM-CSF and from healthy normal PBL by expression of IL-4. These results show that lung adenocarcinoma TIL populations had little lymphokine gene activation despite the presence of several T cell subsets expressing different adhesion/activation markers. The lack or deficient combination of lymphokine production may be a factor that prevented efficient activation of TIL in these tumors.
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PMID:High expression of adhesion molecules/activation markers with little interleukin-2, interferon gamma, and tumor necrosis factor beta gene activation in fresh tumor-infiltrating lymphocytes from lung adenocarcinoma. 764 Dec 14

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