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)

Surgery is the standard treatment of tympano-jugular chemodectomas. Radiation therapy is used only for inoperable forms. Since the tumor most often does not regress completely after irradiation, radiation therapy is generally considered as palliative. From 1979 to 1988, 18 patients with this rare tumor were referred to the Necker Hospital Tumor Center for radiation therapy. These patients have now been followed for 2 to 11 years. Tumors were extensive (Fish Stage C and D) in 75% of the patients and half of these patients showed cranial nerve involvement in addition to the usual otovestibular anomalies. Three patients were referred for recurrent tumors and 7 patients had undergone surgery just prior to radiation therapy. Among the 11 patients treated with the tumor in place, 7 had more or less complete regression of symptoms and radiologic signs, 3 had no further progression of symptoms and radiologic signs and 1 had tumor progression and expired as the result of the disease. No patient receiving post-operative radiation therapy developed clinical or radiological evidence of recurrent tumor. Among the 18 patients treated, 2 died of intercurrent disease. Our experience shows that a dose of 45 Gy is suffisant, leaves no trace, and does not prevent subsequent surgery. In an extensive review of the literature, tumor growth stopped or regressed after radiation therapy in 90% of the patients reported. Therefore, if incomplete surgery or neurological operative sequelae seem unavoidable, we prefer radiation therapy to surgical management of this tumor.
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PMID:[The value of radiotherapy in the treatment of tympano-jugulare chemodectoma. Apropos of 18 cases]. 217 10

Tumor progression has been reported to be often accompanied by a loss of sensitivity to various elements of the immune system. In the present study, three variants of malignancy of AKR lymphoma were compared as to the host reaction they elicit. Splenectomy caused an acceleration of growth of the low-metastasizing tumor, slightly inhibited the growth of the tumor of intermediate malignancy and significantly inhibited the development of the high-metastasizing lymphoma. These results suggest that splenic elements exert an inhibitory effect on the low-metastasizing tumor and a growth-stimulatory effect on the more malignant ones. While decreased sensitivity to various host defense mechanisms following tumor progression has been amply documented, the present study shows a more severe phenomenon: increased malignancy can be accompanied by a deviation of the host immune reaction from tumor growth inhibition to growth stimulation.
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PMID:Change in the role of the spleen from protective to harmful following tumor progression in AKR lymphoma. 222 17

Recent studies have shown that orthotopic (transurethral) transplantation of human bladder cancer cell lines into nude mice permits tumor growth that accurately reflects their clinical malignant status in the original host. Thus, such a system allows a unique opportunity to analyze the genetic events involved in the conversion of low-grade bladder cancer, the vast majority of which are curable, to the high-grade life-threatening form of the disease. Since 5-10% of transitional cell carcinomas (TCCs) have been shown to contain a mutated HRAS gene, and protein expression levels of all forms of HRAS have been correlated with TCC progression, we chose to study the contribution of the HRAS oncogene in bladder tumor progression. We evaluated the effects of transfection of normal or mutated HRAS genes into a human TCC, called RT-4, that behaves as a superficial noninvasive papillary tumor after transurethral orthotopic inoculation into athymic nude mice. We found that overexpression of either transfected normal or mutated HRAS genes converted RT-4 cells to express an invasive phenotype remarkably similar in nature to the clinical behavior of high-grade bladder carcinomas. These results suggest a role for overexpressed normal or mutated RAS genes in human bladder carcinoma progression, and highlight the importance of using orthotopic inoculation systems for evaluation of the contribution of oncogenes to malignant tumor progression.
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PMID:Overexpression of normal and mutated forms of HRAS induces orthotopic bladder invasion in a human transitional cell carcinoma. 224 80

This investigation examined the effect of retinoic acid on tumor progression and immunological status of mice bearing the B16-F10 melanoma (previously selected for high lung-colonizing capacity). Tumor cells were implanted s.c. in syngeneic C57BL/6 mice, half of which were treated with beta-all trans retinoic acid (RA). Although RA failed to exhibit direct toxicity on this variant at the concentration used, the immunologic aberrations induced by the tumors were diminished by i.p. RA administration (at 45 micrograms twice/week for 3 weeks). In mice bearing B16-F10 tumors, tumor burdens were decreased from 2.9% of body weight to 1.6%. The mitogenic responses of splenic lymphocytes to concanavalin A (ConA) were increased in tumor-bearing mice following this RA treatment. The presence of these tumor cells decreased the absolute number of CD4- and CD8-positive splenic lymphocytes. Following RA treatment, the CD8-positive population was increased in tumor-bearing mice, while the CD4+ population was not significantly altered. Since previous studies indicated that plasma membrane fragments (or vesicles) could alter lymphocyte distributions and proliferative capacities, the in vitro shedding of membrane fragments from B16-F10 tumor cells was assayed and observed to be decreased after continuous treatment of cultures with 10(-6) M RA for 21 days. Membrane shedding from B16-F10 cells was inhibited by 48.5% following RA treatment. Based on these in vivo and in vitro results, we suggest that RA treatment may diminish tumor growth by decreasing tumor-induced immunosuppressive events.
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PMID:Effect of retinoic acid on tumor-mediated immunologic alterations in mice bearing a variant of the B16 melanoma. 224 92

The epidermal growth factor and the homologous alpha-tumor growth factor are mitogenic polypeptides that act by binding to the epidermal growth factor receptor. The present study investigated whether increased production of epidermal growth factor/alpha-tumor growth factor or increased density of epidermal growth factor receptors may occur in gastric carcinomas as compared with normal mucosa from the same individuals. Epidermal growth factor receptors were measurable by (125I)EGF-binding assays in 13 of 15 normal mucosas and in 15 of 15 carcinomas. The epidermal growth factor-binding capacity was significantly higher in carcinomas than in mucosa. A comparison of pairs of mucosa and carcinomas showed an increase of epidermal growth factor receptors in 9 of 15 carcinomas, no change in 3, and a decrease in 2 carcinomas. One mucinous adenocarcinoma contained extreme numbers of epidermal growth factor receptors (2445 fmol/mg protein) corresponding to a 320-fold increase over normal mucosa. Epidermal growth factor-like activity was increased in 2 of 22 carcinomas compared with mucosa. We conclude that relative overexpression of epidermal growth factor receptors occurs in a fraction of gastric carcinomas. Whether increased expression of epidermal growth factor receptors is associated with particular patterns of tumor progression needs to be investigated.
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PMID:Increased epidermal growth factor receptors in gastric carcinomas. 200 30

In vivo estimation of intracranial tumor progression is important in tumor treatment response studies in animal models. High resolution MR images at 4.7 T of 9L-gliomas stereotactically implanted in Fisher-344 rat brains were obtained. Due to elongation of T1 at higher fields, tissue contrast is diminished in T1-weighted images. However, normal anatomy and vasogenic edema are clearly discerned in T2-weighted images (echo times of greater than 50 ms and recycle times of greater than 2 sec). Tumor tissue is not always clearly delineated. Images obtained after administration of contrast agents (Gadolinium DTPA), with short TR (0.6 sec) selectively enhanced the tumorous tissue, with little effect upon normal tissue and edema. Good correlation of enhanced tumor lesions has been observed with histological examination of formalin fixed brains. Relaxation times (T1 and T2) of tumor and normal tissues were measured using stimulated-echo and multi-echo sequences, respectively. Serial images corresponding to tumor growth were recorded, from which tumor volume progression was monitored.
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PMID:MRI characterization of 9L-glioma in rat brain at 4.7 Tesla. 233 99

Retinoids are effective in the prevention of N-methyl-N-nitrosourea-induced mammary carcinoma; retinoids and hormonal therapy exert synergy in cancer prevention. In this study, we examined the effects of the dietary supplementation with all-trans retinoic acid (RA) alone or in combination with ovariectomy on the growth of established N-methyl-N- nitrosourea-induced mammary carcinomas in rats. In the first experiment, animals (n = 13) were entered in each of the following treatment groups when their tumors reached 2 cm in diameter: 1, control diet; 2, RA 300 mg/kg diet; 3, ovariectomy (OVX); 4, RA 300 mg/kg diet plus OVX. Animals were sacrificed after 28 days of therapy. In the RA-supplemented animals, tumor progression was less than in the control group without signs of toxicity as assessed by total and individual tumor surface area and weight, and animal weight. OVX produced tumor regression that was not enhanced by the addition of RA. In a second experiment, RA 65- and 130-mg/kg diets were dissolved in corn oil with antioxidants prior to mixing to the diet to improve biodisponibility. This resulted in overall stabilization of tumor growth by RA addition to the diet at either of the 2 doses utilized; the addition of RA 65 mg/kg diet did not modify tumor regression induced by OVX. In conclusion, the dietary supplementation with RA decreased the progression or stabilized the growth of the majority of tumors and only rarely (6%) induced tumor regression; no additive or synergistic effects were found with the combination of RA and ovariectomy.
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PMID:Inhibition of growth of established N-methyl-N-nitrosourea-induced mammary cancer in rats by retinoic acid and ovariectomy. 239 47

Phenomenon of spontaneous regression of cancer indicates that recovery from malignant disease can happen without the application of any so far known therapeutic treatment. The most of the self-cured patients have undergone surgical operation which did not eliminate entire tumor or did not affect malignant tissue at all. Furthermore, regression or reversion of tumors (transformation of tumor cells into normal, nonmalignant cells) can be achieved in plants or amphibia after exposure of tumor cells to the influence of normal, regenerating tissue. Thus, it seems that during tissue regeneration certain local changes in tissue happen (synthesis of some regulatory growth factors) which induce dying of tumor cells or modify main features of malignant cells. Previously we have studied growth of murine malignant tumors in regenerating tissue of liver and skin. Obtained results indicated that under the influence of regenerating tissue anaplasia of fibrosarcoma decreases, as well as do pigmentation and the incidence of live cells in melanoma B16 tissue. Thus, it is obvious that mechanism of regenerating tissue growth control, which can also change characteristics of tumor cells, exists in mammalia, too. In order to analyse whether the same homeostatic mechanism is responsible for the phenomenon of spontaneous regression of human cancer, we have analysed the growth of melanoma B16 in back limb of nonoperated and sham or partially hepatectomized mice. Regeneration of skin and abdominal wall tissue in sham hepatectomized animals slowed down tumor growth, while liver regeneration completely inhibited tumor progression. Tumor growth inhibition was result of tumor tissue necrosis which developed around blood vessels. However, the structure and integrity of blood vessels themselves was normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inhibition of growth of B16 melanoma caused by liver regeneration]. 239 79

Chromosomes from nine morphologically transformed (MT) cell lines (designated MT14 to MT22) of Golden hamster embryo cells induced by X-rays and from tumor-derived cell lines (MT14T to MT22T), obtained after injection of MT cells, were analyzed by the Giemsa banding method. MT cell lines showed a variety of numerical abnormalities. All of the MT cell lines involved trisomy of chromosomes 11 (80 to 100% of cells in each cell line) and 3 (8% of MT22 cells and 100% in other cell lines). Although the latent period for tumor growth differed greatly, eight of nine MT cell lines (MT14 to MT21) produced tumors at the site of injection. All tumor-derived cell lines involved trisomy of chromosome 3 at a 100% rate of incidence. Seven of nine tumor-derived cell lines (MT15T to MT18T, MT20T to MT22T) lost one chromosome 11 from the trisomic condition, resulting in disomy of chromosome 11. These results suggest that trisomies of chromosomes 11 and 3 may play a role in X-ray-induced neoplastic progression.
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PMID:Karyotypic changes with neoplastic conversion in morphologically transformed golden hamster embryo cells induced by X-rays. 240 77

The strong antitumor resistance was induced after the complete cure of a KMT-17 fibrosarcoma in WKA rats treated with bleomycin (BLM, 5 mg/kg/day, ip, for 5 days from Day 8). This suggests that immune responses of the hosts may participate in the therapeutic effects of BLM. The immune responses against the tumor associated antigens (TAA) of KMT-17 tumor cells were examined by assaying the cytotoxic T lymphocyte (CTL) activity of spleen cells after a mixed lymphocyte tumor culture (MLTC). The non-treated tumor-bearing rats showed slight responses on Day 5 and the responses reached the peak on Day 8. On Day 11, however, the responses could not be detected further. On the other hand, the responses were restored and augmented in the BLM-treated rats. The responses could be detected on the next day after the end of BLM treatment (Day 13) and were able to maintain for at least one month. Furthermore, the augmentation of T cell-mediated responses against TAA in BLM-treated rats was found to be due to the elimination of suppressor T cell activity appearing in the course of tumor progression. The T cell-fraction of spleen cells obtained from non-treated tumor-bearing rats inhibited the responses of hyperimmune rats, while the fraction obtained from BLM-treated tumor-bearing and normal rats did not. The antigen presenting cell (APC) activity of macrophages involved in T cell responses was not altered significantly by the tumor growth or BLM treatment. Moreover, macrophages of non-treated tumor-bearing rats did not show any suppressor activity on the T cell responses. The antitumor activity of CTL generating after the MLTC was detected not only by the in vitro 51Cr release assay but also by the in vivo tumor neutralizing assay (Winn's assay).
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PMID:[Enhancement of T cell-mediated immune responses in KMT-17-bearing rats by treatment with bleomycin]. 244 Jul 89


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