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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sections of hypernephroid carcinoma from 20 cases were investigated for aldolase isozymes A and B by a mixed aggregation immuno-cytochemical technique, and for the brush border membrane enzymes aminopeptidase and alkaline phosphatase by conventional histochemical techniques. It was found that the cases could be grouped into four types: type 1 (1 case) contained all 4 enzymes; type 2 (7 cases) contained all enzymes except aldolase-B; type 3 (7 cases) possessed aldolase-A and one brush border membrane enzyme; type 4 (5 cases) contained only aldolase-A. The aldolase-A concentration in all tumor cells was higher than that in proximal tubule cells, whereas the concentration of the two brush border enzymes was lower. In cases tydolase-B and/or higher amounts of the brush border enzymes than the surrounding cells. No correlation was observed between clear cell and granular cell hypernephroid carcinomas or the invasiveness or the nuclear polymorphism of the tumors on the one hand with their enzyme type on the other. These histological enzyme analyses suggest that most, if not all, hypernephroid carcinomas are derived from kidney proximal tubule cells and that the tumor cells then progressively lose aldolase-B, and subsequently the brush border enzymes, but at the same time producing more aldolase-A. The presence of the enzyme-rich patches suggest different patterns of proliferation and differentiation among the tumor cell population. Three tumors other than hypernephroid carcinoma were also examined in this way. The results suggest that histoenzymological analyses are of general applicability in studies of tumor progression. They should also be useful for biopsy and aspiration cytology.
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PMID:A classification of tumor development based on an analysis of enzymes in tissue sections of hypernephroid carcinoma in man. 101 98

Variations in DNA synthesis as measured by tritiated-thymidine autoradiography in mammary carcinoma before and during endocrine therapy were studied in patients treated for inoperable or locally recurrent mammary carcinoma. Tumor cells were collected by aspiration biopsy and immediately expelled into the incubating solution. Cell viability was assessed by staining unfixed cells with trypan blue and fixed cells with orecin. To assess viability tritiated-uridine incorporation was used in some experiments. The same cells were identified by each method. Bilateral oophorectomy was done in 4 patients. In the 1 case in which regression followed, a 5-fold decrease in DNA-synthesis was noted 1 week after oophorectomy but at 2 weeks no cells incoporated thymidine. In the 3 patients with tumor progression the fraction of labeled cells was unchanged. For antiestrogen therapy, Tamoxifen (Nolvadex) was used. Serial needle aspirates were collected from 38 patients who received 20 mg of Tamoxifen twice daily. Complete remission followed in 7, incomplete remission in 8, stationary disease in 7, and progression in 16. DNA synthesis fell to very low values after 1-3 weeks and remained low in the 7 cases with complete regression. Tumors showing partial regression showed diminished fractions of 5-phase cells (tritiated-thymidine-labeled cells) after 1-5 weeks. In 1 instance at 72 weeks the S-phase fraction of cells was higher than initial value. Tumor value remained stationary for 40 weeks and then increased. Antiestrogen therapy was stopped at 82 weeks. In those with progressive tumor growth there was high DNA synthesis. Between 20-30% of the cells were replicating DNA. None showed decrease in the fraction of S-phase cells, and 1 showed increase. For estrogen therapy, estradiol valepianate was given im every 2 weeks. Of the 3 patients who received estrogen therapy, 2 of the tumors responded and the DNA-synthesis rapidly decreased until none was measurable after 4 weeks. S-phase values prior to endocrine therapy showed no correlation with the therapeutic response. Tumors that responded showed a decrease in the proportion of S-phase cells during the first 3 weeks. In tumors responding to encocrine therapy the decrease in tritiated-thymidine incorporation was rapid and preceded reduction in tumor size. Data suggest that 2 aspirates should be studied before therapy and repeated after 2-4 weeks in order to include the minimal proportion of S-phase cells. The patients accepted the needle biopsies well. There were no growths of carcinoma at the puncture sites. About 5 weeks must elapse before tumor response can be assessed. Determining hormone receptors in surgically removed carcinoma specimens gives much more rapid indications as to possible response to endocrine therapy.
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PMID:3H-thymidine incorporation into mammary carcinoma cells obtained by needle aspiration before and during endocrine therapy. 106 73

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.
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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.
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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.
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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.
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PMID:Immunological studies of women with primary breast carcinoma. 115 Mar 43

In vitro lymphocyte function was evaluated in 61 patients with different clinical stages of malignant melanoma. Thirty-one of these patients had localized disease, 13 regional metastases, 10 distant lymph node or skin metastases, and 7 visceral metastases. Following immunization, in vitro lymphocyte reactivity to three antigens (diphtheria toxoid, tetanus toxoid and alpha-hemocyanin of Helix pomatia) was studied in the presence of autologous serum, in addition to lymphocyte reactivity to phytohemagglutinin (PHA). The relationship of these tests with the clinical stage and the subsequent course of the disease in a 6 months' observation period was determined. The patients with visceral metastases (7) had a lowered lymphocyte reactivity to PHA compared with controls and the patients with other stages, while they also had a low reactivity to the test antigens (only significantly lowered compared with patients with localized disease). All these patients showed tumor progression or died from metastatic disease. Between the other stages (54 patients) there was no difference in lymphocyte reactivity to the test antigens or PHA. No correlation between lymphocyte reactivity to PHA and the subsequent course of the disease could be demonstrated in these 54 patients. However, lymphocyte reactivity to the test antigens following immunization showed a definite correlation with the subsequent course. Sixty-four percent (9/14) of patients without any lymphocyte reactivity to the three antigens showed tumor recurrence or progression, against 3% (1/40) of patients with positive lymphocyte reactivity to one, two, or three antigens. A suppressive effect of autologous serum on lymphocyte reactivity could be found only in 1 of 20 patients with a low reactivity to PHA or antigens. It is concluded that defects in lymphocyte function are related to subsequent tumor growth in patients with malignant melanoma.
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PMID:Humoral and cell-mediated immune response in patients with malignant melanoma. I. In vitro lymphocyte reactivity to PHA and antigens following immunization. 117 27

Specific biochemical molecules used as potential biologic markers, including modified nucleosides, polyamines, and pyrimidine catabolic end-products, were quantitatively measured in the urine of seven patients with Burkitt's lymphoma before, during, and after one or more courses of therapy. The results of this preliminary study demonstrated that patients with this disease frequently excrete significantly increased amounts oof modified nuceleosides (considered to be derived primarily from transfer ribonucleic acid), polyamines, and beta-aminoisobutyric acid during the course of their disease. With successful treatment and rapid destruction of tumor cells, a concomitant rise in these molecules occurs. Elevations were observed prior to chemotherapy and changes in levels associated with treatment or tumor progression appeared to correlate with disease status and to aid in assessing antitumor response. Periodic follow-up analysis of these molecules may be helfful in appraising relapse or recurrence of the malignancy prior to overt evidence of tumor by existing clincial means.
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PMID:Potential biologic markers in Burkitt's lymphoma. 117 66

To evaluate the prognostic significance of host immunocompetence in urologic cancer patients, the subsequent clinical course of 95 patients was determined a year after skin testing with dinitrochlorobenzene. A close correlation was demonstrated between dinitrochlorobenzene reactivity and prognosis among 38 transitional carcinoma patients. Of 19 patients with impaired reactivity 13 had tumor recurrences and 11 of these died of cancer within 1 year. Only 5 of 19 patients with normal dinitrochlorobenzene reactivity had recurrences and none died during the same interval. Although not statistically significant, similar results were observed among 10 renal cell carcinoma patients of whom 3 of 5 with impaired dinitrochlorobenzene reactivity had tumor recurrences, while 4 of 5 with normal reactivity remained free of tumor. One testis tumor patient with impaired dinitrochlorobenzene reactivity died of cancer, while 3 of 4 with normal reactivity remained free of tumor. Similarly, 1 patient with carcinoma of the penis with impaired dinitrochlorobenzene reactivity died of cancer, while 2 of 3 with normal reactivity remained free of tumor. In contrast, reactivity to dinitrochlorobenzene did not correlate with the clinical course of 38 prostatic carcinoma patients. Ten of 19 patients with normal dinitrochlorobenzene reactivity and 9 of 19 with impaired reactivity were dead or had symptomatic recurrences within 1 year, while 9 of 19 with normal reactivity and 10 of 19 with impaired reactivity were either free of tumor or asymptomatic. However, a trend toward a correlation between dinitrochlorobenzene reactivity and tumor progression was observed among patients not receiving endocrine therapy. The differences with respect to the prognostic significance of host immunocompetence between transitional carcinoma patients and those with prostatic carcinoma may be explained by fundamental differences in the biologic properties of these tumors, especially the endocrine sensitivity of prostatic carcinoma.
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PMID:Prognostic value of host immunocompetence in urologic cancer patients. 119 75

Twenty-eight patients with inoperable or metastatic carcinoma of the lung who failed to respond to conventional chemotherapy and/or radiotherapy were entered in this study. All of them received repeated courses of multiple chemotherapy (cyclophosphamide, 5-fluorouracil, 6-thioguanine, methotrexate, and vincristine) with or without concurrent intravenous heparin anticoagulation. No tumor regression was noted in any of the 14 patients who received the multiple chemotherapy only. On the contrary, tumor progression was seen in all of them, and subsequently 12 died of their disease. The other 14 patients were anticoagulated with heparin, then received the same multiple chemotherapeutics while anticoagulated. Over 50% tumor regression was noted clinically and radiologically, and occasionally demonstrated histologically in 7 of them. Two patients in this group are alive and well for 1 1/2 years. No increase in toxicity or metastases was noted. The 2 patients who had progression of their disease while on the multiple chemotherapy program alone showed tumor regression when they received the same chemotherapy after heparinization.
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PMID:Heparin and chemotherapy in the management of inoperable lung carcinoma. 120 41


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