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

A variety of methods for urinary diversion are employed in patients with gynecologic malignancies depending on whether there is an obstruction or fistula formation due to either tumor growth or radiotherapeutic injury. Percutaneous nephrostomy (PCN) has a low complication rate and is a good method for palliative urinary diversion or may precede some form of permanent diversion to restore the kidney function first. Indication for palliative diversion in tumor obstruction depends on many individual factors. A relative contraindication is tumor progression during therapy. 6-month survival was about 70% in patients with previously untreated tumors or recurrences. This rate is far better than reported in earlier studies, so that a palliative diversion has to be considered for these patients. Also a high rate of recanalization after therapy could be observed in the untreated group, allowing the PCN to be removed. However, this has not been shown to be a prognostic factor. In the individual patient some other aspects, such as quality of life and social status, have to be taken into account before a final decision can be made. Ureteral obstruction after radiotherapy is a rare finding and often mistaken for a more likely recurrence. Different methods to restore the urinary tract, such as reimplantation of the ureter, should be used as a first choice. When the stenosis is due to radiocystitis, enterocytoplasty will often be indicated. Diversion has then to be omitted. The poor quality of life because of permanent incontinence due to fistula formation makes diversion mandatory even if life expectancy is very short. Surgical closure of a large radiogenic fistula is rarely successful. In this situation, ileal conduit has proven its efficacy for long-term urinary diversion.
 ...
PMID:Urinary diversion in gynecologic malignancies. 245 37

To investigate the role of transforming growth factor alpha (TGF alpha) in tumor development, we introduced the human TGF alpha (hTGF alpha) cDNA into cultured primary mouse epidermal cells or papilloma cells using a replication-defective retroviral vector and analyzed skin grafts constructed with such cells. Expression of the exogenous gene was confirmed by detection of hTGF alpha mRNA by northern RNA blot analysis, and the secreted hTGF alpha was measured by ELISA of culture supernatants. Tumor cells expressing hTGF alpha produced benign tumors (papillomas), which were 1.5- to 2-fold larger than tumors of parental cells when tested as skin grafts on nude mice. Grafts of normal cells that expressed hTGF alpha produced normal skin. When mixtures of parental tumor cells and normal mouse keratinocytes were grafted to nude mice, papilloma formation was suppressed and tumors that did form were small. Grafts of hTGF alpha-producing papilloma cells combined with either normal epidermal cells or hTGF alpha-producing epidermal cells yielded large tumors. Mixed grafts containing keratinocytes expressing hTGF alpha and parental papilloma cells also produced large tumors. While the tumor size was substantially increased by hTGF alpha expression, the tumors that developed in all groups were histologically benign and reached a stable size 4-5 wk after grafting. These results indicate that expression of hTGF alpha by either tumor cells (autocrine) or adjoining normal cells (paracrine) can stimulate tumor growth, particularly when tumor growth is suppressed by normal tissue. However, expression of this growth factor did not appear to influence tumor progression directly.
 ...
PMID:TGF alpha stimulates growth of skin papillomas by autocrine and paracrine mechanisms but does not cause neoplastic progression. 247 36

ZME-018 monoclonal antibody (MAb, IgG2a subclass, 0.04 mg), recombinant human tumor necrosis factor-alpha (rHuTNF-alpha, 10(4) units), and recombinant human interferon-gamma (rHuIFN-gamma, 10(6) units) were injected intravenously into athymic nude mice bearing human malignant melanoma (Brown C5513) xenografts. Sixty-four animals were injected subcutaneously with 0.2 ml tumor chunks 4 days prior to administration of one or more of the treatments. The mice were randomized into eight groups so that mean tumor volume/group before initiation of treatment was similar (212-360 mm3); (a) saline, 2X; (b) rHuTNF-alpha, 1X; (c) rHuIFN-gamma, 1X; (d) ZME-018, 1X; (e) rHuIFN-gamma + rHuTNF-alpha, 1X each; (f) rHu-IFN-gamma + ZME-018 + rHuTNF-alpha, 1X each; (g) rHuTNF-alpha + ZME-018, 2X each; (h) rHuTNF-alpha + ZME-018, 3X each. The order of administration of the agents in those groups given more than one modality is as shown above and each injection was separated by a 24 h period. Tumor volume was measured daily for 9 days after the beginning of treatment. Compared to control mice, minimal suppression of tumor growth was noted when ZME-018, rHuTNF-alpha, or rHuIFN-gamma was used singly, but significantly (p less than or equal to 0.05) slower tumor progression occurred in animals given rHuIFN-gamma + rHuTNF-alpha or ZME-018 + rHuTNF-alpha when compared to controls. Histopathologic analyses of tumor biopsies obtained at 1 and 4 days after the last treatment for each group indicated that 15-95% necrosis was present. Necrosis was most striking in the animals given rHuIFN-gamma + rHuTNF-alpha or the ZME-018 MAb alone. However, the group receiving all three agents exhibited a tumor growth rate similar to that seen in the controls and demonstrated minimal necrosis. These results suggest that ZME-018, rHuIFN-gamma, and rHuTNF-alpha may be useful in the treatment of human melanoma. However, the effects of administration of all three of these agents in a single host needs to be evaluated further.
 ...
PMID:Effects of monoclonal antibody, recombinant interferon-gamma, and tumor necrosis factor-alpha in the treatment of human melanoma xenografts. 251 78

The epidermal growth factor (EGF) and alpha-tumor growth factor are mitogenic proteins which bind to the EGF-receptor and may play a role in carcinogenesis or tumor progression. Our study investigated whether colorectal carcinomas and adenomas express altered levels of EGF-receptors or overproduce EGF-like activity by comparing histologically normal mucosa to carcinomas resected from the same patients. EGF-receptors were characterized by radioligand binding studies. Carcinomas contained unchanged or decreased levels of EGF-receptors in 13/16 and moderately increased levels in 3/16 patients as compared to normal mucosa. Adenomas obtained from 2 patients with familial polyposis coli and from a third patient with a coincident carcinoma had similar numbers of EGF-receptors as normal mucosa. EGF-like growth factors, in contrast, were significantly elevated in carcinoma extracts as compared to extracts from normal mucosa of the same patients. Adenomas did not contain elevated levels of EGF-like activity. We conclude that increased expression of EGF-receptors is infrequent in colonic adenocarcinomas. Increased production of EGF-like growth factors may frequently occur but seems to be associated with tumor progression rather than with premalignant lesions as represented by adenomas.
 ...
PMID:Epidermal growth factor receptors and epidermal growth factor-like activity in colorectal mucosa, adenomas and carcinomas. 254 69

The interrelationship among localization of tumor, local extension, lymph node metastasis and various histological grades was investigated in 31 consecutive series of prostate cancer treated by radical prostatectomy. Surgical specimens were examined by step sections cut perpendicular to the urethra. Each tumor was graded histologically in accordance with WHO-Mostofi grading (evaluated by nuclear anaplasia and structural differentiation), Gleason's and M.D. Anderson's grading systems. The areas of the prostate was divided into 4 quadrants delimited vertically along the urethral axis and transversely at the level of utricle, i.e. anterior/superior, anterior/inferior, posterior/superior and posterior/inferior quadrants. Topographical localization and extension of each tumor was examined in accordance with the above area subdivision. Every tumor was growing at least in the posterior/inferior area. All cases with tumor progression to the anterior/superior area also revealed extensive tumor growth in the other two or three quadrants. Therefore, prostate cancer appears to be originated from the posterior/inferior area of the prostate and terminated in the anterior/superior area as local extension. In 31 cases examined, capsular invasion was noted in 22, seminal vesicle invasion in 16, and lymph node metastasis in 12 cases. All cases with seminal vesicle invasion also showed capsular invasion. None of the cases without capsular and/or seminal vesicle invasion had lymph node metastasis. Thus, it is inferred that prostate cancer is initially growing locally, extending to the capsule and seminal vesicle and then metastasizes to the pelvic lymph nodes. As for the histological grading, higher grade tumors tended to show higher incidence of capsular and seminal vesicle invasion and lymph node metastasis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Pathomorphological study of local extension and progression of prostate cancer]. 260 Dec 22

Various human tumor tissues contain different growth factors. In some cases progression of tumors is paralleled by elevated levels of these substances in blood or in tumor tissue. There is evidence that these growth promoting peptides might stimulate tumor growth. The growth of most tumors was associated with insulin-like substances (MW 45,000). We isolated and purified a substance immunologically cross-reactive with insulin (SICRI) from human melanoma. We found the molecular weight of affinity purified SICRI to be approximately 120,000. Our in vitro experiments with human renal carcinoma cells and growth factors suggest an important role of these molecules in tumor progression.
 ...
PMID:Growth factors in human tumors. 265 14

Our recognition that cancer evolves by clonal selection and that the basis for this selection is the growth advantage provided by the inappropriate expression or suppression of genes present in all normal cells allows us to anticipate that the pathways of this evolutionary process may be discovered. If a finite number of such pathways exist with some commonality between various tumors, there is the possibility to anticipate the mechanisms that cell clones might use for both carcinogenesis and tumor progression and to deal with evolving clones before their survival potential becomes overwhelming. As our biochemical understanding increases we may develop the capability to do the following: to identify individuals who have inherited or acquired defective cancer suppressor genes; to identify precursor lesions more exactly; to characterize the degree of progression of a newly diagnosed tumor (has the metastatic phenotype evolved?); to develop antibodies against cell membrane proteins necessary to tumor progression; to produce immune probes that carry cytotoxins or isotopes to specific cell populations; and to take advantage of cell signals to modify tumor growth. The potential for application of the New Biology to cancer medicine seems endless.
 ...
PMID:The new biology of cancer: future clinical applications. 265 85

The incidence of the lethal growth of 10(1) L1210 murine leukemia cells in mice was higher in intraperitoneal (i.p.) (97%) than in intradermal (i.d.) (17%) inoculation, and survival time of mice was shorter in i.p. than i.d. inoculation. It was supposed that resident peritoneal cells (PC) enhanced tumor progression. I.d. inoculation of 10(1) L1210 cells mixed with 10(6) PC induced a lethal tumor growth at higher incidence than that of 10(1) L1210 cells alone or the mixture of 10(1) L1210 cells and 10(4) peripheral blood mononuclear cells (PBM) did. Furthermore, co-inoculation of a tumorigenic number of L1210 cells (10(3] with 10(6) PC resulted in marked shortening of median survival time of mice. Similar growth enhancing effect of PC was observed in Meth 1 fibrosarcoma. Meth A fibrosarcoma and colon carcinoma 26 (C26). Further study showed that PC, intact or X-rayed, helped the in vitro tumor growth under the conditions in which L1210 alone did not grow at all, whereas PBM had no enhancing effect to L1210 growth. We characterized the cells involved in tumor growth enhancement by the in vivo and in vitro tests. Plastic dish adherent cells of PC which were Mac-1 positive, large in size and resistant to X-ray, enhanced L1210 growth, whereas non-adherent cells which were Mac-1 negative and small in size, did not. These data suggest that the cells responsible for enhancing activity of tumor progression in the peritoneal cavity were macrophages (M phi).
 ...
PMID:Environmental conditions favorable for tumor progression in peritoneal cavity induced by peritoneal cells without tumor selectivity. 268 89

The past decade transplants of human tumors in nude mice have been increasingly used as an experimental model for local tumor growth and dissemination. A few human melanoma cell lines have been described that give rise to metastases in nude mice after subcutaneous inoculation. First we give an overview of some relevant literature with respect to the pathogenesis of tumor metastasis, models to study human cancer metastasis, neoplastic progression and the detection of antigens involved in metastasis. Finally we describe our results concerning the morphological and immunohistochemical profile of six different human melanoma cell lines and their xenograft lesions in nude mice using a set of monoclonal antibodies recognizing different categories of human melanoma-associated antigens. From the data we conclude that the nude mouse mouse model appears suitable to study the role of melanoma-associated progression markers in the pathogenesis of metastasis.
 ...
PMID:Progression markers in metastasizing human melanoma cells xenografted to nude mice (review). 268 99

Pooled F(ab')2 fragments of three MAbs against distinct epitopes of carcinoembryonic antigen (CEA) were used for radioimmunotherapy of nude mice bearing a subcutaneous human colon carcinoma xenograft. 9-10 d after transplantation when tumor nodules were in exponential growth, 36 mice were treated by intravenous injection of different amounts of 131I-labeled MAb F(ab')2. All 14 mice injected with a single dose of 2,200 (n = 10) or 2,800 microCi (n = 4) showed complete tumor remission. 8 of the 10 mice treated with 2,200 microCi survived in good health for 1 yr when they were killed and shown to be tumor free. Four of nine other mice treated with four fractionated doses of 400 microCi showed no tumor relapse for more than 9 mo. In contrast, all 15 mice injected with 1,600-3,000 microCi 131I-control IgG F(ab')2 showed tumor growth retardation of only 1-4 wk, and 15 of 16 mice injected with unlabeled anti-CEA MAb F(ab')2 showed unmodified tumor progression as compared with untreated mice. From tissue radioactivity distributions it was calculated that by an injection of 2,200 microCi 131I-MAb F(ab')2 a mean dose of 8,335 rad was selectively delivered to the tumor, while the tissue-absorbed radiation doses for the normal organs were: peripheral blood, 2,093; stomach, 1,668; kidney, 1,289; lung, 1,185; liver, 617; spleen, 501; small intestine, 427; large intestine, 367; bone, 337; and muscle, 198. These treatments were well tolerated since out of 19 mice with complete tumor remission only 4 required bone marrow transplantation and 17 were in good health for 6-12 mo of observation. The results demonstrate the selective destruction of established human colon carcinoma transplants by intravenous injection of either single or fractionated doses of 131I-MAb F(ab')2.
 ...
PMID:Ablation of human colon carcinoma in nude mice by 131I-labeled monoclonal anti-carcinoembryonic antigen antibody F(ab')2 fragments. 270 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>