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

Ten episodes of Torulopsis glabrata fungemia occurring in nine patients with terminal illnesses are described. Eight patients had underlying malignancies and one patient had a plastic anemia. Two episodes of fungemia were considered transient since they were clearly related to the administration of intravenous hyperalimentation (IVH). Most patients were adult women and had solid tumors of the genitourinary tract. Contributory factors were: antibiotic therapy (100%), immunosuppressive drugs (75%), abdominal surgery (63%), IVH (50%), neutropenia (38%), and diabetes mellitus (13%). The clinical course was indistinguishable from a severe bacterial infection. However, endotoxic shock was not observed. The infection was rapidly fatal in four patients. In the remaining five patients, the infection was altered favorably by the discontinuation of infected intravenous hyperalimentation catheters. However, tissue invasion by T. glabrata was found in two of these patients who died shortly thereafter from tumor progression. At autopsy, T. glabrata was identified in tissue sections of the lungs, kidneys, and mucosas of the gastrointestinal and genitourinary tracts. In all cases there was tissue necrosis with a minor inflammatory response consisting of mononuclear cells. To our knowledge, this is the single largest series of T. glabrata fungemia ever reported.
Cancer 1976 Oct
PMID:Fungemia due to Torulopsis glabrata in the compromised host. 82 17

BALB/cCrgl, C57BL/Ki, and (C57BL/Ki X DBAf)F1 mice were treated with 7,12-diemthylbenz[a]anthracene (DMBA) or urethan to determine conditions that would induce a high frequency of ductal hyperplasias in the mammary gland. Among virgin BALB/c mice treated with either 3.0 or 4.0 mg DMBA, ductal hyperplasias and mammary tumors were present in 50% and 31% of the mice, respectively. These ductal hyperplasias were characterized by intraluminal epithelial hyperplasia and capped by endbud-like structures that appeared abnormal. Hyperplastic alveolar nodules were not seen. Most mammary tumors were adenocarcinomas rather than the adenocanthomas observed in DMBA-treated, pituitary isograft-bearing BALB/c mice. The predominant mammary lesions in urethan-treated, pituitary isograft-bearing C57BL and (C57BL X DBAf)F1 mice were terminal duct (lobular) hyperplasias characterized by intraluminal epithelial hyperplasia; the urethan-induced mammary tumors were a mixture of adenocarcinomas (36%), adenoacanthomas (5%), and fibroadenomas (59%). The induction by chemical carcinogens of intraductal hyperplasias in a relatively high incidence, with associated mammary neoplasms, provides a system for study of the process of tumor progression in lesions similar to suspected high-risk lesions occurring in human breast cancer.
J Natl Cancer Inst 1976 Aug
PMID:Mammary tumorigenesis in chemical carcinogen-treated mice. IV. Induction of mammary ductal hyperplasias. 82 49

CCNU (1-[2-chloroethyl]-3-cyclohexyl-1-nitrosourea, NSC-79037) was used to treat advanced malignancies in 329 evaluable patients. The treatment dosage was 130 mg/m2 for patients with adequate bone marrow reserve and 100 mg/m2 for those with compromised bone marrow. Oral treatment was repeated at 6-week intervals unless hematologic toxicity intervened. There were four complete responses: two in ovarian cancer, one with small cell carcinoma of the lung, and one with melanoma. Tumor response greater than 50% reduction in tumor size occurred in 39 patients (11.9%) while stable disease (no change or decrease or increase of less than 50% in tumor size) was noted in 152 patients (46.2%). Tumor progression occurred in 130 cases. Melanomas and ovarian and lung cancers had the highest response rates. Bone marrow depression was the major side effect of treatment; there was a significant positive correlation between the severity of leukopenia and thrombocytopenia and tumor response to treatment.
Cancer 1976 Sep
PMID:Treatment of advanced malignancy with CCNU (NSC 79037): a phase II cooperative study with long-term follow up. 95 55

It is proposed that most neoplasms arise from a single cell of origin, and tumor progression results from acquired genetic variability within the original clone allowing sequential selection of more aggressive sublines. Tumor cell populations are apparently more genetically unstable than normal cells, perhaps from activation of specific gene loci in the neoplasm, continued presence of carcinogen, or even nutritional deficiencies within the tumor. The acquired genetic insta0ility and associated selection process, most readily recognized cytogenetically, results in advanced human malignancies being highly individual karyotypically and biologically. Hence, each patient's cancer may require individual specific therapy, and even this may be thwarted by emergence of a genetically variant subline resistant to the treatment. More research should be directed toward understanding and controlling the evolutionary process in tumors before it reaches the late stage usually seen in clinical cancer.
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PMID:The clonal evolution of tumor cell populations. 95 40

Advances in radiation techniques and increased dosage have improved the cure rate of patients with cancer of the cervix to 65 percent. Associated with this increased dosage (betatron, 5,250 r and intracavitary 137-cesium, 4,000 r at point A) has been a serious complication incidence of 10 percent. Major intestinal complications usually become manifest within an 8 to 24 month period following radiation. Few are associated with tumor and the majority are amenable to surgical correction. Rectosigmoid stenosis is a common and frequently unrecognized complication. The 8 to 12 cm. segment of rectosigmoid, with its rigid wall and narrowed lumen, can be recognized on barium examination. The symptoms are those on incomplete obstruction and deterioration, frequently confused with tumor progression. Thirty-one patients have been treated by resection and low anterior anastomosis with relief of symptoms. Rectosigmoid stenosis progressing to necrosis, perforation, or fistula (an additional 29 patients) is treated best by the Hartmann operation as a first stage. This procedure has been less complicated than either colostomy alone or resection and anastomosis. Fifteen patients with low level rectovaginal fistula or stenosis were treated by defunctioning sigmoid colostomy. A loop transverse colostomy was unsatisfactory. Ileorectovaginal fistulas occurred in an additional six patients. Preoperative investigation should establish the presence or absence of an ileal component in all fistulas. Radiation ileitis is rare as an isolated finding but frequently is associated with severe rectosigmoid damage. Surgical treatment is seldom necessary but, if indicated (ten patients), resection appears to be preferable to bypass.
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PMID:Radiation injuries to the bowel associated with the treatment of carcinoma of the cervix. 96 30

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

A rapid method for determining labeling indices in solid tumor specimens, tumor-induced effusions, and tumor-bearing bone marrows was utilized in 116 patients. Of these, 48 patients were studied pre- and postchemotherapy. The magnitude of a significant change in labeling index (LI percent) was determined statistically. Of the 48 patients studied serially, 42 were studied 17 days or less following completion of their chemotherapy. In 26 patients without a significant change in tumor LI percent, there was no subsequent clinical response to chemotherapy. Three additional patients in this group are inevaluable at present. In 11 patients, there was a significant fall in tumor LI percent following chemotherapy. Seven of these had a 50 percent or greater regression of demonstrable disease, one patient had definite tumor effect but the effect was not a partial response and three patients were not evaluable for clinical response. In two patients there was a significant increase in tumor LI percent and the patients had rapid tumor progression and death. Predictions derived from serial study of the LI percent by this method correlate significantly with subsequent behavior of the tumors tested following chemotherapy and may prove clinically useful in making decisions about when or whether to change therapy.
Cancer Res 1975 Jun
PMID:Serial labeling index determination as a predictor of response in human solid tumors. 109 72

The neoplastic progression induced by intratracheal instillation of benzo[a]pyrene (BP) and magnesium oxide (MgO) was compared with that induced by intratracheal instillation of BP and ferric oxide (Fe2O3). BP and MgO produced squamous cell carcinomas and papillomas in the larynx with a latent period as shor as 9 weeks. They also induced many papillomas as well as squamous cell carcinomas and adenocarcinomas in the trachea and a papilloma, squamous cell carcinomas, adenocarcinomas, adenosquamous lesions, and peripheral adenomatoid lesions in the bronchi. They rarely caused tumors in other organs; only a few forestomach papillomas, one melanoma on the dorsal skin, and one ovarian carconoma were seen BP, with Fe2O3 as the carrier, induced a comparable number of histologically similar tumors; however, tumors developed more frequently in the main bronchi. Thus MgO strongly facilitated the tumor-inducing effects of BP, causing tumors in different areas of the respiratory tract, and was as effective as Fe2O3 as a carrier agent in the experimental induction of respiratory tumors.
J Natl Cancer Inst 1975 Apr
PMID:Magnesium oxide as carrier dust in benzo(a)pyrene-induced lung carcino-genesis in Syrian hamsters. 112 16

The effect on tumor progression produced by the injection of VCN-treated tumor cells in dogs with spontaneous mammary tumors was investigated. Untreated dogs of different races and different ages with at least two palpable spontaneous mammary tumors were selected. One of the tumors was left in the animal for further clinical examination whereas the other tumor(s) was (were) excised for preparation of a single-cell suspension by mechanical disintegration and enzymatic digestion with collagenase and trypsin. (1) In the first group, each animal was infected with 2 times 10-7 similarly prepared autologous, mitomycin-treated tumor cells; in 8 out of 12 dogs of this group the tumors progressed while so far 1 dog has died of metastasis. (2) In the second group, each animal received the same number of 2 times 10-7 tumor cells, which were mitomycin- and VCN-treated: 13 out of 15 dogs had a significant regression of their tumors to less than 10% of the original volume; in 1 dog the tumor remained unchanged and in 1 dog it progressed. (3) In the third group, 8 dogs received 1 times 10-8 mitomycin- and VCN-treated tumor cells: the application of this cell dose resulted in an accelerated tumor progression in all 8 dogs, 3 of which have already died of metastasis. The significance of these findings, with respect to potentiation and abrogation of the immunological response and with regard to immunotherapy in man, is discussed.
Int J Cancer 1975 Mar 15
PMID:Regression of spontaneous mammary tumors in dogs after injection of neuraminidase-treated tumor cells. 114 Aug 60

Lymphocytes from disease-free women and women with primary breast carcinoma were comparable vis-a-vis their capacity to inactivate breast tumor cells in vitro. Sera from comparable numbers of women in each of these two groups either blocked, potentiated or left unaffected the anti-tumor-cell cytotoxicity of their lymphoctes. As such, the results cast doubt on the validity of the hypothesis that there is a positive correlation between the presence of humoral blocking factors and in vivo tumor progression.
Int J Cancer 1975 Jun 15
PMID:Immunological studies of women with primary breast carcinoma. 115 Mar 43


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