摘要:

The biological and analytical components of variability of tumor markers should be distinguished from the variations due to tumor progression. The aim of the present study was to evaluate tumor marker variability in the follow-up of patients resected for breast cancer. So far, we have carried out 2,085 CEA and 2,550 CA 15-3 determinations in 435 patients. The total variability of both CEA and CA 15-3 was widely scattered among different subjects (CEA coefficient of variation 0-105%; CA 15-3 coefficient of variation 0-89.2%). The biological variability of CA 15-3, which was calculated in a limited number of cases, was scattered between 0 and 23% and was higher than the intra-assay variability. From these findings we conclude that when evaluating serial marker assays the intra-individual variability should be assayed initially to obtain a reference value of individual variability in relapse-free conditions.

ISSN:1010-4283    

DOI:10.1159/000217847

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

The carbohydrate moieties of glycoproteins in plasma membrane are known to correlate with the induction of cell differentiation in some kinds of cells. We investigated the asparagine-linked sugar chains of neuroblastoma and ganglioneuroma cell membranes. The acidic oligosaccharides were bi-, tri-, and tetraantennary complex-type sugar chains with Manα→(Manα)Manβ→GlcNAcβ→( ± Fucα- > )GlcNAc as their cores. A comparative study of the oligosaccharides of these cells showed that the biantennary complex-type sugar chain with bisecting N-acetylglucosamine residues increased and high-molecular-weight oligosaccharides decreased in ganglioneuroma cells. It is suspected that asparagine-linked sugar chains correlate with the differentiation stage of ne

ISSN:1010-4283    

DOI:10.1159/000217848

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

The cell is a complex system functioning outside a thermodynamic equilibrium. The prediction of cellular functions based exclusively on molecular evidence is still impossible because of the large number of interacting molecules and the nonlinear interactions between cellular subsystems. The system cell displays a surprisingly small spectrum of macroscopically observable degrees of freedom. Their number and characteristics, however, are different in normal and neoplastic growth. As illustrated by image analytical, microanalytical and other cell biological data we demonstrate that certain cellular observables – termed order parameters – may serve as indicators for normal and neoplastic growth. The data indicate that the transition between normal and neoplastic growth can be understood as a phase transition of the mitogenic signalling network. In this interpretation, the order parameters of normal and neoplastic cells are the result of cellular self-organizat

ISSN:1010-4283    

DOI:10.1159/000217849

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

Natural killer (NK) cells are believed to contribute to the clinical efficacy of cancer immunotherapy using recombinant interleukin-2 (rIL·2) in humans. In previous trials of high-dose i.v. rIL-2, however, no correlation has been established between circulating NK cells and treatment response. Between January 1989 and October 1990, we treated a total of 47 outpatients with advanced tumors using low-dose s.c. rIL·2 and interferon-α-2 (rIFN-α). Therapy consisted of a 2-day rIL·2 pulse at 18 million IU/m2/ day, followed by 6 weeks of rIL-2 (3.6 × 106-4.8 × 106 IU/m2/day × 5 days/week) and rIFN-α (5 × 106-6 × 106U/m2 × 3/week). Before and after therapy, we phenotypically evaluated circulating lymphocytes and correlated them with clinical response. During 6-week therapy, peripheral blood lymphocytes bearing the CD 5 6 (NK-cell-associated) surface antigen were increased significantly (p 0.1). After one 6-week treatment cycle, CR/PR patients had significantly more peripheral NK cells, when compared with patients in SD (1.6-fold) and PD (1.9-fold) (p 0.4). These data demonstrate that s.c. rIL·2 and s.c. rIFN-α produce a significant increase in peripheral blood NK cells; this expansion correlates significantly with treatment response in advanced tumor patients receiving long-term combination immunotherapy at o

ISSN:1010-4283    

DOI:10.1159/000217850

出版商:S. Karger AG    

年代:1993

数据来源: Karger

摘要:

The objectives of this study were (1) to quantify galaptin, an endogenous lectin, and galaptin-binding glycoconjugates present in normal serum, (2) to determine if these components were altered in the serum and effusions of carcinoma patients with advanced disease, and (3) to determine if ovarian carcinoma cells synthesize and release soluble galaptin inhibitors. Serum from healthy females (n = 10) had a mean galaptin content of 96 ± 40 ng/ml. Galaptin levels in carcinoma patient serum (n = 29) were depressed (mean 21 ± 23 ng/ml; p < 0.0001). Galaptin was not detected in 6 of 8 ovarian carcinoma patient sera. Effusions (n = 17) had a mean galaptin content of 358 ± 326 ng/ml. Assays involving inhibition of binding of galaptin-peroxidase conjugates to asialofetuin were carried out to evaluate the levels of galaptin-binding glycoconjugates in serum and effusions. The mean inhibition titer of normal serum (n = 12) was 75 ± 38. Patient serum (n = 28) had an elevated inhibitor content (mean titer = 304 ± 155; p < 0.0001). Effusions (n = 17) also had a higher inhibitor content relative to normal serum (mean titer = 247 ± 202; p = 0.0037). Ovarian carcinoma cells isolated from effusions and cultured in vitro were shown to synthesize and release into the medium galaptin-binding glycoconjugates of molecular mass 100-200 kD. An ovarian carcinoma cell line, A121, released galaptin-binding glycoconjugates of molecular mass ≥ 200 kD into the medium. The data presented show that the levels of soluble galaptin and galaptin-binding glycoconjugates in the serum of advanced cancer patients are perturbed relative to normal femal

ISSN:1010-4283    

DOI:10.1159/000217851

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:1010-4283    

DOI:10.1159/000217852

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:1010-4283    

DOI:10.1159/000217853

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:1010-4283    

DOI:10.1159/000217854

出版商:S. Karger AG    

年代:1993

数据来源: Karger

ISSN:1010-4283    

DOI:10.1159/000217846

出版商:S. Karger AG    

年代:1993

数据来源: Karger