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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The given data indicate the presence of a negative correlation between metabolic indices (a decrease of the tolerance to glucose, increase of the blood level of free fatty acids, insulin, cholesterol triglycerides, cortisol, stc) and the indices of cellular immunity, which is determined by the number of rosette-forming cells and blasttransformation reaction to PHA and skin tests. Accordingly, the administration of an antidiabetic drug-phenformin (phenetylbiguanide)--apart from the improvement of metabolic pattern, results in the restoration of the cell-mediated immunity indices. These findings provide a basis for stating the phenomenon of metabolic immunodepression. The metabolic immunodepression may be supposed to prevent immunological surveillance activation, which normally is realized through the signals, provided by cells subjected to somatic mutation. It is noteworthy that the given metabolic conditions (hypercholesterinemia, hyperinsulinemia, the enhanced utilization of free fatty acids) promote the division of somatic cells. Thus, the same metabolic shifts which increase the pull of proliferating cells and, accordingly, increase the possibility of mutation development, also cause the metabolic immunodepression at the same time. These opposite metabolic influences on somatic cells and T-dependent lymphocytes cause the development of the syndrome of cancrophilia. The syndrome of cancrophilia normally arises at pregnancy, in intensive growth of the organism in childhood, accelerated development, stress and during normal ageing. Many carcinogens cause the decrease of tolerance to glucose, the increase in blood-insulin level and elevation of the threshold of sensitivity of the hypothalamus to feedback suppression. This phenomenon is based on the decrease of catecholamine level in thehypothalamus in ageing, stress and the action of some carcinogens. Thus, the syndrome of cacrophilia provides the conditions for cancer development and tumor progression, besides, the tumor itself produces the metabolic shifts typical of cancrophilia. In the light of mutation-metabolic model of cancer development, it is possible to consider the fundamental factors which increase of hinder carcinogenesis.
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PMID:[Mutational-metabolic model of carcinogenesis and the progression of the neoplastic process]. 99 16

26 patients with unresectable locally recurrent adenocarcinoma of the rectum were treated with a mixed beam schedule. 40 Gy photons were delivered to the whole pelvis followed by a neutron boost of 6.6 or 10 Gy. Neutron therapy was carried out with a 14 MeV d-t generator (KARIN) using an isocentric are technique. Fluctuation in neutron dose rate during irradiation was monitored by a computer which controlled the gantry speed. All patients were followed clinically by CEA monitoring and CT-scans. In 18 patients positron-emission-tomography (PET) was used to verify the therapeutic efficacy. All patients were symptomatic with severe pain prior to therapy. After a mean follow-up interval of 12.8 months (range six to 26 months), the palliative effect in terms of pain relief was excellent in 22 patients in spite of the poor general condition of most patients and the large tumor extension. In four patients, further pain symptoms developed again after six to nine months due to renewed tumor progression. We observed proctitis at late side effects in one, enteritis in two and a fistula in one patient six to ten months after therapy. Changes in tumor glucose metabolism were monitored by serial PET examinations in all patients. The typical pattern observed by PET was a decrease in the F-18-Deoxyglucose (FDG) accumulation, approximately six weeks after onset of therapy.
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PMID:Photon-neutron therapy for recurrent colorectal cancer--follow up and preliminary results. 230 Aug 91

The effect of long-term, high-dose therapy with bromocriptine (BR) on the clinical and hormonal response, tumor size and neuro-ophthalmological status was studied in seven acromegalic patients. The mean BR dose was 64 mg/day (range 35 to 80) for a mean period of 11 months (range 10 to 12). In six patients there was a clinical improvement already manifest at low BR doses (10 to 20 mg). Serum growth hormone levels fell substantially (greater than 50%) in five patients, and the growth hormone response to thyrotropin-releasing hormone (TRH) and glucose were similar to those previously reported at lower doses of the drug, as were the prolactin and thyroid-stimulating hormone responses to TRH. In three patients, repeat CT scan disclosed a reduction in tumor size. In none of the patients was there evidence of tumor progression, with the possible exception of one patient who developed an impairment of the visual evoked potential response. These results suggest that when compared to previous studies in which lower doses of BR were used, a high BR dose is not superior in terms of clinical response and hormone secretion, but does appear to increase the percentage of patients who respond with a reduction in tumor size.
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PMID:Bromocriptine treatment of acromegaly: possible dose dependency of the tumor size-reducing effect. 249 29

In a small-cell lung carcinoma (SCLC) tumor specimen as well as in 3 cell lines derived from SCLC biopsies obtained from the same patient at successive times during the clinical course, either the N-myc gene or the c-myc gene appeared to be amplified and expressed. The initial tumor specimen, a lymph-node metastasis, was amplified for N-myc, as was the cell line GLC-14 derived from this metastasis. The cell lines GLC-16 and GLC-19, derived from the recurrent primary tumor biopsies after a complete remission, were amplified for c-myc. This finding implies independent amplification events and supports the idea that the amplification of myc genes is probably a secondary event correlated with tumor progression. Although all 3 cell lines could be classified as classic SCLC cell lines according to their histological characteristics, GLC-16 and GLC-19 clearly possess, in their c-myc amplification and derivation from therapy-resistant tumor cells, features of variant SCLC lines. This may question the significance of the classic/variant classification.
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PMID:Amplification and expression of different myc-family genes in a tumor specimen and 3 cell lines derived from one small-cell lung cancer patient during longitudinal follow-up. 254 36

Positron emission tomographic scanning with fludeoxyglucose F 18 (18F-fluorodeoxyglucose) was used to study acute changes in gliomas after chemotherapy. In six experimental subjects, scans were obtained before and at days 1, 7, and 30 after treatment. Five control patients with gliomas who did not undergo chemotherapy had two scans, 1 month apart. Ratios were calculated between peak tumor regional cerebral metabolic rate for glucose and contralateral white matter. The percent change in ratios relative to each patient's baseline scan was calculated. Ratios in three stable controls remained unchanged over the study interval; in two controls it increased 155% and 36% and both died of tumor progression. In experimental subjects, ratios increased 20% to 100% 24 hours after chemotherapy and then decreased until at 28 days they varied between 22% above and 35% below baseline. The increased fludeoxyglucose F 18 uptake at 24 hours could be from uncoupling oxidative phosphorylation or shunting glucose to ribose phosphates for salvage nucleoside synthesis.
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PMID:Glucose uptake by gliomas after treatment. A positron emission tomographic study. 203 74

We tested clinical significance of hemocirculatory and metabolic values and ratios as determined by positron emission tomography (PET) in twenty-three patients with cerebral gliomas. Regional cerebral blood flow (rCBF), blood volume (rCBV), oxygen extraction fraction (rOEF), and metabolic rates of oxygen (rCMRO2) and glucose (rCMRGl) were measured prior to treatment using PET with 15O2, C15O, 15O2, and 18F-fluorodeoxyglucose tracers. For the quantitative analysis, regions of interest were delineated on tumor regions including peak activity, the contralateral gray and white matter. The regional values and the ratios of tumor/gray matter and tumor/white matter were compared to performance status (PS) according to the five functional grades system which are defined by the Japan Society for Cancer Therapy, tumor progression-free time (PFT), survival time (ST) from the time of the PET study, regardless of type of therapy. As with rCMRGl, the tumor values and the ratios of tumor/gray matter and tumor/white matter correlated significantly with PS (tumor/gray: p less than 0.05, tumor/white: p less than 0.01). Both the gray rCBF and the tumor/gray rCBF ratio had close relation with PS and/or PFT (p less than 0.05). The gray matter rCMRO2 and the tumor/gray matter rCMRO2 ratio related significantly (gray matter: p less than 0.01, tumor/gray: p less than 0.05) to each clinical parameter of PS, PFT, and ST. These indicate that values and ratios as determined by PET can be useful in predicting the prognosis of glioma patients.
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PMID:[Prognostic significance of regional blood flow, blood volume, oxygen extraction fraction, and metabolic rates of oxygen and glucose as measured by positron emission tomography in patients with gliomas]. 261 91

Subcutaneous adipose tissue was examined in 77 patients with breast cancer, 61 patients with lung cancer and in a control group of 23 male and 27 female with non-tumor pathology; the weight and age of controls matched those of cancer patients. The obesity in breast cancer patients was of the hypertrophic type, and of combined type (hypertrophic-hyperplastic) in patients who were more than 50% overweight. The increased level of adipose tissue in lung cancer patients was mostly due to the larger size of adipocytes. The concentration of unsaturated fatty acids in adipose tissue in breast cancer patients was in direct correlation with the level of this tissue and adipocyte size, while, in lung cancer group, this correlation was reversed. There was no inverse correlation between the size and c-AMP level of adipocytes in both cancer groups. Resistance to the inhibitory effect of glucose on lipolysis occurring in adipose tissue was more frequent in cancer patients than in controls. Antilipolytic effect of insulin in subcutaneous adipose tissue of breast cancer patients was less pronounced than in lung cancer group. Liposynthetic activity in adipose tissue was identical in all study groups. Lipolytic activity in adipose tissue was enhanced in both cancer groups, but in the breast cancer group it was in direct correlation with overweight, while in lung cancer patients--with the degree of tumor progression.
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PMID:[Morphometric and biochemical peculiarities of fatty tissue in patients with cancer of the breast and lung]. 630 31

Using a culture cell system, derived from a low-tumorigenic strain of L929 mouse fibroblasts, including cell variants with different malignant behavior in vivo, we have tried to dissociate a group of biological and biochemical transformation-associated properties with respect to the process of neoplastic progression. It is shown that morphologic changes, nonalignment in vitro, and growth in soft-agar are not sufficient alterations for in vivo malignant behavior and, also, not useful indicators for further neoplastic progression. The rate of hexose uptake should also be considered as unrelated to this process. The increase in tumorigenicity, but without the concomitant development of metastasis ability of the cells, was associated with the decrease of a 160k cell surface protein and the diminution of the tumor dose 50%. Finally, further alteration in morphology and the appearance of a 177k cell surface protein were associated with the development of metastasis ability, in an early stage; loss of fibronectin and the ability to grow as macrocolonies in increasing concentrations of deoxyglucose appeared as associated to more advanced stages of neoplastic progression. On the whole, the approach of taking the in vivo behavior, and not the in vitro properties, as end-point for the study of transformation is recommended on the basis of this and a previous paper.
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PMID:Neoplastic progression evidenced in the L929 cell system. II. In vitro growth properties and biochemical characteristics of cell variants with different malignant behavior. 713 25

To date, the structure of the autocrine motility factor (AMF), a tumor-secreted cytokine which stimulates cell migration in vitro and metastasis in vivo, is unknown. Here, AMF secreted by Gc-4 PF murine fibrosarcoma into a protein-free conditioned media was isolated, purified, and microsequenced. The results demonstrate that AMF is the previously cloned cytokine and enzyme designated as neuroleukin, and phosphohexose isomerase (PHI), which has been independently implicated in cell motility, and to be a cancer progression marker. PHI catalyzes isomerization of glucose 6-phosphate to fructose 6-phosphate and is specific for both sugars. Murine AMF exhibits the enzymatic properties of PHI and rabbit heart PHI-stimulated mouse fibrosarcoma cells' motility similar to those of the endogenous AMF. Specific PHI inhibitors (carbohydrate phosphates) inhibited enzymatic activity and AMF-induced cell motility.
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PMID:Tumor cell autocrine motility factor is the neuroleukin/phosphohexose isomerase polypeptide. 867 49

Cells in tumors may be exposed to adverse conditions such as nutrient deprivation, acidic pH and hypoxia. It has been shown previously that exposure to hypoxia, acidosis and glucose starvation in vitro increases the experimental metastatic ability of murine KHT-LP1 sarcoma, SCC-VII squamous carcinoma and B16 melanoma cells. This effect was most marked when cells were allowed to recover under normal in vitro growth conditions before injection. In the present study we examined whether the invasive capacity of the cells could be influenced by these modifications of the cell microenvironment. We used Matrigel, a basement membrane-like preparation in a two-chamber invasion assay to address this issue. Both KHT-LP1 and SCC-VII murine cell lines showed an increased ability to invade through Matrigel after hypoxia, and glucose starvation, but there was no consistent change in invasive capacity following acidosis exposure. The results for hypoxia and glucose starvation are in agreement with our previous studies of metastatic ability for these cell lines and we confirmed this for KHT-LP1 cells exposed to hypoxia in the current study. In parallel with the invasion assays, we compared cathepsin (L + B) content of the cells in treated and control suspensions. The effect observed varied according to the cell line and the treatment received (hypoxia, glucose starvation). There was an increase of cathepsin content for KHT-LP1 cells exposed to hypoxia and this increase correlated well with the increase of the invasion ability through Matrigel. We did not observe any increase of cathepsin for hypoxia-treated SCC-VII or for KHT-LP1 and SCC-VII cells treated with glucose starvation. These results suggest that transient hypoxia and glucose starvation can increase the invasive ability of tumor cell lines and thus may cause tumor progression by facilitating the invasive step of the metastatic process. The increased levels of cathepsin (L + B) in the KHT-LP1 cells treated with hypoxia, compared to control non-treated cells, may play a part in this increased invasive capacity.
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PMID:Exposure to hypoxia, glucose starvation and acidosis: effect on invasive capacity of murine tumor cells and correlation with cathepsin (L + B) secretion. 900 2


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