Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucagonoma is a rare pancreatic tumor, necrolytic migratory erythema is its distinctive feature and it is often associated with diabetes mellitus, weight loss, anemia, hypoaminoacidemia, glossitis and stomatitis. We reported a case of glucagonoma misdiagnosed as "eczema" and "benign hepatic anginoma" for 3 years. His blood glucagon level was 1,758 ng/L. The results of abdominal B-mode ultrasonography and CT scan were negative, but selected arteriogram showed a tumor mass between the pancreatic body and tail. Before operation, treatment with octreotide and supply of amino acids were given with improvement of the skin lesion. After resection of the tumor from pancreas, necrolytic migratory erythema disapeared, but his blood level of glucagon and amino acids did not improve. It is suggested that any diabetic patient with chronic skin damage should be checked for blood glucagon level. In suspected cases, selected arteriogram will be helpful for location of the tumor. Vigorous resection of the pancreatic tumor should be done as soon as possible, even though there is already metastases.
 ...
PMID:[Report of a case of glucagonoma misdiagnosed as "eczema" and "hepatic angioma" for three years and review of literature]. 764 42

Xeroderma pigmentosum (XP) is a rare genodermatosis characterized by a defect in the repair of DNA damage induced by ultra-violet rays. In black people, XP are much less frequent, only 29 cases have been reported (22 in Africa). Through the study of 5 individual cases of xeroderma pigmentosum in children at Mayotte (Indian Ocean), the authors analyze, a XP literature in order to highlight how this genetic disease is surprisingly frequent in the bantou population. Ocular lesions are precursory symptoms, before skin damage. Neoplasia and death occur frequently in the first decade. Leukoplasia and carcinoma of the tip of the tongue are frequent.
 ...
PMID:[Xeroderma pigmentosum in negroid children. 5 cases in Mahori children]. 770 62

Treatment of HIV and related malignancies with pharmacologic and biologic agents has not appreciably modified the course of disease. Immunologic impairment remains the critical factor in response. We report the long-term results of a single session of low-flow (0.3 L/min) extracorporeal perfusion hyperthermia on 29 men and 2 women with disseminated Kaposi's sarcoma and profound immunologic impairment. Any antiretroviral drug employed by the patient was stopped 72 hours prior to treatment and withheld during the period of follow-up. Core temperature was raised to 42 degrees C and held for 1 hour with extracorporeal perfusion and ex vivo blood heating to 49 degrees C as the means of temperature control. Of 31 patients, 2 died of complications secondary to treatment (cardiac arrhythmia; CNS bleed). There were two cases of intravascular coagulopathy. Pressure point skin damage may occur despite adequate cushioning. At 30 days posttreatment complete or partial regressions were seen in 20/29 of those treated, with regressions persisting in 14/29 of those treated by 120 days posttreatment. At 360 days, 4/29 maintain tumor regressions with 1 in complete remission (at 26 months). The patient in complete remission remains culture-negative and PCR-negative for HIV. CD4+ counts rose from around 250 to, and remain around, 800 in this man. Selected healed lesions were biopsied to demonstrate tumor absence. Patients were selected for treatment if pretreatment testing of the tumor showed regression in vitro with heat exposure. Analysis of the early and midterm failures showed little sustained rise of the CD4+ cells if presenting total CD4+ counts were below 50 and had been at such low levels for extended periods, although other surrogate markers of HIV activity declined (semiquantitative PCR) during this period and is felt to support the hypothesis of apoptosis proposed in this illness. Analysis of the tumors of the few men not responding demonstrated elevated levels of IL-6 as compared to responders (12 vs < 1 pg/ml). At 120 days 29/31 patients remained alive (expected, 20). At 360 days, 21/31 remained alive (expected, 11). In no patient was HIV activity stimulated with heat exposure. CMV retinitis did clear in some patients treated (both techniques), but treatment alone did not prevent later development of retinopathy. EBV parameters were markedly altered in the short term with heat exposure in some patients. Few patients showed herpes simplex activation. Varicella-zoster virus remitted in some patients. There is utility in the use of systemic hyperthermia to control HIV and related malignancy.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Systemic hyperthermia in the treatment of HIV-related disseminated Kaposi's sarcoma. Long-term follow-up of patients treated with low-flow extracorporeal perfusion hyperthermia. 791 57

Benzoporphyrin derivative monoacid ring A (BPD-MA) is a chlorin-like photosensitizer currently in clinical trials for cancer and psoriasis. It has maximal absorption peaks at both 630 and 690 nm and can be activated at both these wavelengths. In vitro phototoxicity tests using the P815 murine mastocytoma cell lines conducted over wavelengths of light between 678 and 700 nm emitted by an argon-ion pumped dye laser showed that equivalent cell kill could be achieved between 682 and 690 nm. Tests on in vivo phototoxicity of normal skin of DBA/2 mice injected with 2 mg/kg of BPD-MA and exposed to light at 125 J/cm2, between 620 and 700 nm, demonstrated peaks of normal skin damage occurring at 630-640 nm and 680-690 nm. In tests carried out with light between 620 and 700 nm, at 10 nm increments, it was seen that light delivered at 680-690 nm caused slightly more damage to normal skin than light delivered at 630-640 nm. When lower doses of light between 675 and 705 nm were tested using smaller increments, it was determined that equivalent skin damage occurred over a range of 680-695 nm. Antitumor efficacy in tumor-bearing DBA/2 mice was tested between 683 and 695 nm. It was found that equivalent antitumor efficacy, determined by assessing tumor-free status at 20 days posttreatment, occurred at wavelengths between 685 and 693 nm.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Wavelength-dependent effects of benzoporphyrin derivative monoacid ring A in vivo and in vitro. 799 65

A treatment regimen for boron neutron capture therapy of malignant melanomas is described using 10B-paraboronophenylalanine as the tumor-targeting compound. As a therapeutic dose, we adopted the maximum tolerable dose for the skin regardless of tumor 10B concentration. In practice, the maximum neutron fluence should be decided prior to starting irradiation. For this purpose, the kinetics of the concentration of 10B in the blood and skin and the skin-to-blood ratios were analyzed in the six patients who received 170 mg/kg of the compound intravenously, and skin concentrations during irradiation were predicted using a standard skin factor curve. This yields a skin concentration at time T based on the blood concentration at time 0. We calculated the maximum tolerable fluence yielding but not exceeding 18 RBE-Gy by assuming that the RBE of 14N(n,p)14C and 10B(n, alpha)7Li reaction for skin damage is 2.5. Actual skin reactions in three of five patients treated with the therapy were, as predicted, within tolerable limits, and we were able to obtain complete tumor regression in four cases. The results indicate that application of our logical approach will be useful for subsequent cases and further development of this therapy.
 ...
PMID:Boron neutron capture therapy of malignant melanoma using 10B-paraboronophenylalanine with special reference to evaluation of radiation dose and damage to the normal skin. 818 19

The effect of irradiation with 30 fractions of 2 Gy in 6 weeks combined with a single dose of 5mg/kg cisplatin was studied in the rhabdomyosarcoma R1H of the rat and tumor response and normal tissue toxicity were assessed for various combinations of radiotherapy and chemotherapy. Cisplatin was given 3 days before, during (after the 5th and after the 10th fraction), or 3 and 17 days after radiotherapy. Five of the 12 tumors treated with cisplatin injected 3 days after radiotherapy were locally controlled (42%; 95% confidence intervals: 14-70%) as compared to 0/10 for radiotherapy alone (0%; 0-21%; p < 0.02). A similar trend was found for cisplatin injected 17 days after irradiation (2/6 local controls; 33%; 0-71%). With cisplatin given 3 days before radiotherapy 1/13 local controls were observed (8%; 0-22%; p < 0.05 when tested vs. cisplatin 3 days after radiotherapy). Tumor cure was dependent upon tumor size at time of cisplatin administration with 7/9 small tumors (< 2 mm3) cured versus only 2/35 cures of larger tumors (> 2 mm3). By contrast, net growth delay and skin damage were the same for combined modality treatment and for irradiation alone. General toxicity as assessed by body weight change was significantly higher for animals treated with cisplatin before or after radiotherapy, whereas cisplatin during radiotherapy showed equal effects as compared to radiotherapy alone. Although for the rhabdomyosarcoma R1H of the rat the combined modality treatment was shown to be more effective than radiotherapy alone when cisplatin was applied after radiotherapy, general toxicity was also higher for this mode of treatment.
 ...
PMID:Combined modality treatment of the rhabdomyosarcoma R1H of the rat: influence of sequence of cisplatin and fractionated irradiation. 841 84

The effect of the corticosteroid fluocinolone acetonide (FA) on skin tumor induction and inflammation by the contact sensitizer dinitrofluorobenzene (DNFB) was examined. This study broadly relates to the question of whether contact sensitizers, as electrophilic chemicals that produce protein adduction, may constitute an environmental cancer hazard. The specific aim of this study was to evaluate the extent to which the immunogenic inflammatory response to DNFB, in contrast to DNFB cytotoxicity, might be responsible for tumor induction. Experiments were conducted on a transgenic (TG.AC) mouse, incorporating a mutated ras oncogene (v-Ha-ras) that responds rapidly and profusely with skin papillomas to tumor promoters as if it were genetically initiated. Various doses and patterns of DNFB and FA were applied to the skin in a 2-week period; DNFB was given four times and FA was given either with the DNFB or daily. The tumor response to DNFB was completed by 8 weeks from the first dose and was consistent with a dose-squared relationship. FA was not tumorigenic alone; when given with DNFB, it caused only a small reduction in inflammation and tumor yield. When given daily, FA increased ulcerative skin damage, inflammation, and the yield tumors. The results suggest that tumorigenesis by DNFB, in the high-dose short-term regimen used here, is mainly due to its cytotoxicity and not contact sensitization.
 ...
PMID:Mechanism of skin tumorigenesis by contact sensitizers: the effect of the corticosteroid fluocinolone acetonide on inflammation and tumor induction by 2,4 dinitro-1-fluorobenzene in the skin of the TG.AC (v-Ha-ras) mouse. 893 May 47

A commonly recognized feature of chronic radiation dermatitis is the presence of mesenchymal cells with large atypical nuclei known as radiation fibroblasts. Little is known about their lineage or potential for neoplastic transformation. To investigate these properties, we examined 16 biopsy specimens in which radiation fibroblasts were present with antisera to mesenchymal determinants (FXIIIa, CD34, HHF-35), a proliferation marker (Ki-67), and a tumor-suppressor protein that is overexpressed in many cancers (p53). Radiation fibroblasts were largely negative for the markers of lineage that we employed - only 2 of 16 specimens showed strong expression of FXIIIa, with weak expression in another case. Scattered radiation fibroblasts expressed CD34 in one case. HHF-35 (muscle specific actin) stained small, dendritic cells in the superficial dermis, but not radiation fibroblasts. P53 was not detected within radiation fibroblasts in any of our cases, but was overexpressed by endothelial cells in 2 cases. Ki-67 stained rare endothelial and interstitial cells but not radiation fibroblasts. Radiation fibroblasts are immunophenotypically distinct from dermal dendrocytes and myofibroblasts. They appear to be non-cycling cells, and do not express high levels of p53 despite their marked nuclear atypia. Their phenotype argues against their possible role as progenitors of atypical fibroxanthoma (AFX) and dermatofibrosarcoma protuberans (DFSP) which are associated with ionizing radiation-induced skin damage.
 ...
PMID:An immunohistochemical analysis of radiation fibroblasts. 919 85

The Epstein-Barr virus (EBV) encoded latent membrane protein of B cell origin, B-LMP1 (B95-8 prototype) and nasopharyngeal carcinoma (NPC) derived C-LMP1 (CAO prototype) were transfected individually in S6C adenocarcinoma cells of ACA (H-2f) origin. We have shown previously that inoculation of B-LMP1 expressing S6C cells led to tumor rejection in pre-immunized, immunocompetent syngeneic ACA mice, whereas the C-LMP1 transfectants were not immunogenic. Furthermore, B-LMP1 but not C-LMP1 expressing S6C cells grew with necrosis and extensive skin damage in non-immunized mice. A study was carried out to determine whether the in vivo growth pattern of S6C cells expressing two different LMP1 isolates could be correlated to any immunomodulatory mechanism. An increased infiltration of CD45+ leukocytes was found in B-LMP1 expressing S6C tumors originating in non-immunized, syngeneic ACA mice. The C-LMP1 expressors, vector transfectants and untransfected parental tumors had significantly lower number of infiltrating leukocytes. The immunoaccessory molecules ICAM-1, B7-1 and MHC Class I and II expression was unaltered in both B- and C-LMP1 transfectants. The data suggest that B-LMP1 but not C-LMP1 induce anti-tumor immune response.
 ...
PMID:Augmentation of leukocyte infiltration in murine tumors expressing B-cell derived but not nasopharyngeal carcinoma derived EBV membrane protein LMP1. 1068 25

Ultraviolet (UV) radiation plays a pivotal role in skin damage and photocarcinogenesis. The basic mechanism of phototoxicity lies in DNA damage, and involves mutation of tumor suppressor genes, oncogenes and genes directly involved in the control of the stability of genome, such as the mismatch repair (MR) genes. The goal of this study was to evaluate the role of p53 and hMSH2 in the UV-related carcinogenetic process. An immunohistochemical study for p53 and hMSH2 was performed in a series of 43 basal cell carcinomas (BCC) and 60 melanomas (MM) from photoexposed areas of head and neck region, comparing the findings with follow-up. A deregulated p53 expression characterized less differentiated, more aggressive BCC (BCC2) but not the well-differentiated ones (BCC1). The hMSH2 protein was present, though expressed at varying levels, in 18 out of 21 BCC1 cases and in 4 out of 22 BCC2. In the remaining 3 cases of BCC1 and 18 cases of BCC2, a complete absence of hMSH2 expression was found, correlating directly with the presence of recurrence and/or death of the disease in case of melanoma (p<0.05). Overall, the expression of hMSH2 correlated inversely with the p53 overexpression (p<0.01). In MM, p53 was found overexpressed in 81.6% of the cases, and this correlated positively with the level of infiltration and with the presence of relapses (p<0.01) or metastasis (p<0.01) and inversely with the disease-free interval (p<0.05). These results are in agreement with the reported association between p53 deregulation and a more aggressive cancer phenotype. The evaluation of the expression of p53 and hMSH2 could improve the management of patients with BCC and MM, and could have a role also in the evaluation of the early cutaneous photo-inducted damage, contributing to the identification of presymptomatic patients predisposed to the development of UV-related new skin tumors, who could become candidates for chemoprevention trials.
 ...
PMID:P53 and hMSH2 expression in basal cell carcinomas and malignant melanomas from photoexposed areas of head and neck region. 1149 35


<< Previous 1 2 3 4 5 6 7 Next >>