Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

119 patients with stage-IV renal cell carcinoma were treated using immunotherapy with autologous tumor vaccine. The immunization was carried out at monthly intervals, the patients were restaged every 3 months using X-ray, ultrasound scanning or computed tomography as well as bone scintigraphy in the follow-up. The patients' follow-up periods run from 6 to 66 months averaging in 38.5 months. 6 complete remissions, 4 partial responses and 29 stable diseases were seen, whereas 54 patients had progressive disease. Patients with a T1 primary tumor all survived the follow-up period irrespective of whether lymph node metastases (n = 2), venous invasion (n = 12) or distant metastases (n = 6) were present at the time of operation. Follow-up periods run from 12 to 48 months (averaging 23 months). Patients with T2 tumors showed survival up to 50 months postoperatively, of these only 3 died. Follow-up averages 30 months. The 3 patients died within the first year after operation. Patients with very large primary tumors showed the poor prognosis normally expected. 23 of these 40 patients died after a mean follow-up of 15 months. These results may indicate that immunotherapy can slow down tumor progression and induce objective responses. Those patients with small primary lesions apparently benefit from the treatment even though metastases are present at the time of diagnosis.
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PMID:Immunotherapy of metastasizing renal cell carcinoma. Results of a multicentered trial. 266 60

Four genetic marker systems were investigated in 102 patients with renal cell carcinoma. The previously observed excess of the transferrin (TF) variant C3 among male patients was confirmed. Interestingly, an excess of TFC3 and a deficit of the haptoglobin heterozygote, HP2-1, were associated with diploid tumor DNA content and Stage I, particularly in male patients. The results are discussed in terms of a possible genetic influence on tumor progression.
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PMID:Genetic variation of haptoglobin and transferrin in relation to DNA content and stage in renal cell carcinoma. 291 16

We treated 19 patients with progressive metastatic renal cell carcinoma with continuous infusion of 5-fluoro-2-deoxyuridine, 52 per cent of whom had previously received and failed chemotherapy. Implantable pumps were used for automatic drug delivery. 5-Fluoro-2-deoxyuridine was infused continuously for 14 days at monthly intervals. The starting dose was 0.15 mg. per kg. per day (intravenous) or 0.25 mg. per kg. per day (intra-arterial). Intravenous doses were increased or decreased in increments of 0.025 mg. per kg. per day as permitted by toxicity. Abdominal pain, diarrhea and mucositis limited the intravenous infusion, while malaise, anorexia and hepatic function abnormalities limited intra-arterial infusion. Of 18 evaluable patients we observed 1 complete, 4 partial (objective response rate 28 per cent) and 2 minor responses. The duration of response ranged from 2 to greater than 18 months. During a median follow up of 7.5 months (range 2 to 21 months) only 4 of the 18 patients had objective tumor progression. Over-all survival for the 19 patients was 94 per cent. Continuous infusion of 5-fluoro-2-deoxyuridine may be effective for the treatment of progressive renal cell carcinoma.
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PMID:Progressive metastatic renal cell carcinoma controlled by continuous 5-fluoro-2-deoxyuridine infusion. 296 42

The most challenging aspect of cancer treatment remains the management of invasive and metastatic tumor growth. Recent progress in the development and use of biologic response modifiers for immunomodulation has raised the possibility that the immune system can be used as an additional antitumor treatment modality in conjunction with surgery, chemotherapy, and/or radiotherapy for the treatment of established tumors and their metastases. As a model for adoptive chemoimmunotherapy (ACIT) of renal cancer we have used a murine renal cancer (Renca) of spontaneous origin that mimics the tumor progression characteristically observed for human renal cell carcinoma. In the present study, we demonstrate that broadly cytotoxic lymphocytes, generated by in vitro culture with human recombinant interleukin 2, and used in conjunction with the chemotherapeutic drug doxorubicin hydrochloride, are effective in treating invasive and metastatic renal cell cancer. Administration of ACIT i.v. or i.p., alone, or after nephrectomy of the tumor-bearing kidney, did not cure mice with stage II (locoregional invasive tumor) or stage III (lymph node metastases) disease. In contrast, nephrectomy followed by simultaneous bicompartmental i.v. and i.p. ACIT administration cured 80% of mice with either stage II or stage III Renca. These data demonstrate that simultaneous bicompartmental ACIT affords dramatically improved cure rates for advanced and metastatic Renca. This effect most likely results from efficient control of both locoregional and metastatic tumor growth.
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PMID:Successful treatment of advanced murine renal cell cancer by bicompartmental adoptive chemoimmunotherapy. 349 54

In 153 patients with verified neoplasias of the genitourinary tract, urinary neopterin excretion was monitored under different conditions. As control, urinary neopterin values were taken from 208 male and 209 female volunteers. Neopterin excretion was measured by high performance liquid chromatography. Patients with early tumor stages, both with bladder tumor and carcinoma of the prostate, presented almost normal urinary neopterin levels. The difference of urinary neopterin excretion between low and high stages in bladder tumor (T0-1 versus T2-4) as well in carcinoma of the prostate (stage A-B versus stage C-D) is highly significant (p less than 0.001). In the group of patients with renal cell carcinoma we could not find any correlation between tumor stage and neopterin excretion. The basal urinary neopterin values in patients with testicle tumors were as follows: 1 of 6 patients stage-I seminomatous tumors and 2 of 4 patients with stage-I non-seminomatous tumors demonstrated elevated neopterin levels. In the higher stages all patients, in both groups, exhibited pathologically increased neopterin excretion. During therapy and follow-up: all 24 stage-I (seminomatous and non-seminomatous tumors) patients showed normal neopterin levels: 1 of 3 stage-II (non-seminomatous tumors) patients and all 5 stage-IV (seminomatous and non-seminomatous tumors) patients had elevated urinary neopterin excretion. Our experience suggests that neopterin measurements may supplement laboratory examinations in patients with malignant tumor diseases of the genitourinary tract, providing meaningful information in regard to early detection of tumor progression, tumor recurrence and follow-up.
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PMID:The value of urinary neopterin as an immunological parameter in patients with malignant tumors of the genitourinary tract. 387 60

Acquired dysfibrinogenemia has not been previously reported as a paraneoplastic marker for malignancy. This report describes the clinical course of a patient who at the time of diagnosis of nonmetastatic renal cell carcinoma had dysfibrinogenemia characterized by prolongation of the thrombin and Reptilase times and increased sialic acid content of the purified fibrinogen. The thrombin and Reptilase times returned toward normal values after nephrectomy but became abnormal with the development of nonhepatic metastases. It is concluded that acquired dysfibrinogenemia can be part of a paraneoplastic syndrome and is a sensitive plasma marker for tumor progression.
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PMID:Acquired dysfibrinogenemia. Paraneoplastic syndrome in renal cell carcinoma. 398 42

A variety of cytogenetic aberrations have been reported in sporadic and familial renal cell carcinoma. Rearrangements of the short arm of chromosome 3 (3p), trisomy 17, and nuclear hyperdiploidy have been reported to be common clonal chromosome changes. We analyzed a total of ten tumor-derived cell lines from patients who underwent nephrectomy for renal cell carcinoma employing conventional cytogenetics. All patients received an immunomodulatory therapy based on recombinant interleukin-2 (rIL-2). Tumor stage and grade, histo- and cytopathology, and patients' response to immunotherapy were assessed and correlated statistically to rearrangement of 3p, trisomy 17, and nuclear hyperdiploidy. Trisomy 17 as clonal aberration could be revealed only in papillary renal cell carcinoma, whereas tumors with compact or tubulopapillary growth pattern lacked this abnormality (p < 0.002). One of 3 patients with diploid or near-diploid karyotype (< or = 49 chromosomes) achieved a partial remission while two presented with stable disease after immunotherapy. In contrast, all 6 patients with tumor progression upon rIL-2-based immunotherapy revealed hyperdiploid (> 49 chromosomes) karyotypes. The correlation between hyperdiploidy and tumor progression was found to be statistically significant (p < 0.029). Interestingly, the only patient achieving an objective tumor remission after immunotherapy presented with a normal diploid karyotype. Our findings suggest tumor hyperdiploidy as an adverse prognostic factor in renal cell carcinoma patients receiving rIL-2-based immunotherapy.
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PMID:Cytogenetic studies in renal cell carcinoma patients receiving low-dose recombinant interleukin-2-based immunotherapy. 750 70

We have recently identified on rat chromosome 10q a germline mutation in the tuberous sclerosis gene (Tsc2), the gene predisposing to renal carcinoma (RC) in the Eker rat. The homozygous mutant condition is lethal at around the 13th day of fetal life. In heterozygotes, RCs invariably develop in the first year of life. Histologically, RCs develop through multiple stages from early preneoplastic lesions (i.e., phenotypically altered tubules) to adenomas. The wild-type allele mutation has been found even in the earliest preneoplastic lesions, fitting Knudson's two-hit hypothesis and supporting the hypothesis that Tsc2 is a tumor suppressor gene. In this study, homozygous deletion of the Ink4 homologue on rat chromosome 5q was observed in 14 of 24 (58%) RC-derived cell lines. This may represent involvement of a second tumor suppressor gene, contributing to tumor progression. Considering previous results of studies of homozygous deletion of the Ifn alpha gene in five of 24 cases (21%) and the Ifn beta gene in one of 24 cases (4%), the order of the genes may be Ink4-Ifn alpha-Ifn beta. Microsatellite instability was not observed in 26 Eker rat tumors.
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PMID:Molecular genetic basis of renal carcinogenesis in the Eker rat model of tuberous sclerosis (Tsc2). 754 21

The differentiation of tissues and organs during ontogeny increases the necessity of integration of the different structures. These developmental processes of integrations by body fluids, immunologic, endocrine and nervous systems culminate in mammals, since they possess the most diversified system of body fluids. Typical of the most developed mammals are the bone marrow, the lymphatic system with regional lymph nodes and consequently the pathologic development of the diversity of leukemias, malignancies without stroma. In the German literature the leukemias are considered systemic diseases because the floating cells they discharge are more or less uniformly pathologically underdeveloped. The leukemias are named according to the major abnormal cell type (e.g. monocytic acute leukemia). Acute and chronic is the distinction of the time limitation regarding the development and duration of the disease. More complicated is the discharge of motile cells from primary tumors or daughter tumors deriving from solid tumors. These motile cells enter into the circulation via the lymphatic spaces or by penetration of the endothelium of the blood vessels. They move freely in the circulatory system until settling in a more or less distant region. The process of detecting these cells is known as carcinocythemia. Other movable cells during neoplastic progression are those populating effusions in the coelomic cavities. Non-movable, that is only growing in succession like a tissue chain are those tumors which distribute by direct tumor spread within the veins, keeping the connection with the primary tumor. This condition is especially well-known in renal cell carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of circulating neoplastic cells. 772 18

A phase I-II clinical trial was conducted to determine the maximum-tolerated dose (MTD) of oral cyclosporine (CsA) and vinblastine in patients with metastatic renal cell cancer (RCC) as well as to estimate the response rate. Sixteen patients received a 5 mg/kg oral loading dose of CsA followed by 3 days of CsA in 4 divided daily doses escalating from 10 mg/kg per day up to 17 mg/kg per day. Vinblastine (Vbl) was administered as an intravenous bolus on the morning of the 3rd day with dose escalation from 6 to 10 mg/m2. Cycles were repeated every 4 weeks until tumor progression. Forty-nine cycles of CsA with vinblastine were administered. The maximum tolerated dose of Vbl was 10 mg/m2, with neutropenia as the dose-limiting toxicity resulting in one death. CsA could not be escalated above 17 mg/kg per day because of nausea and vomiting. Other toxicities included constipation (100%), malaise (100%), temporary increase in pain (36%), and one seizure that may have been drug-related. There were no clinically significant changes in renal function or serum bilirubin. Mean peak whole-blood CsA level at the highest CsA dose level was 919 ng/ml (range: 414-1,827) with a trough prior to Vbl injection of 451 ng/ml (range: 128-1,229). There were no tumor responses. The combination of oral CsA and Vbl is not nephrotoxic but is poorly tolerated. In most patients optimal blood levels of CsA for reversal of MDR cannot be reliably achieved, and vinblastine dose intensity must be compromised because of the significant toxicity of this regimen.
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PMID:Phase I-II study of vinblastine and oral cyclosporin A in metastatic renal cell carcinoma. 774 14


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