Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment with multiple fractions per day would be expected to offer a significant therapeutic gain. Clinical benefits from the therapeutic gain, however, depend on the steepness of dose-response curves for the tumor control. We discussed the therapeutic gain factor of hyperfractionation and accelerated fractionation in head and neck cancer and malignant glioma, and also discussed the impacts of this factor on the local control of the tumors.
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PMID:[Therapeutic gain factor of multiple fractions per day]. 319 11

Loss of heterozygosity (LOH) affecting chromosome 9p has been shown to occur frequently in head and neck cancer, glioma, mesothelioma, melanoma, lung cancer, and numerous other tumor types. Chromosome 9p is therefore presumed to contain a tumor suppressor gene or genes. Since esophageal cancer shares characteristics with some of the above tumor types, we performed a detailed examination of 60 patients with squamous cell carcinoma or adenocarcinoma of the esophagus for LOH at loci D9S162, IFNA, D9S171, D9S126, D9S104, D9S165, and D9S163. Multiplex polymerase chain reactions were performed with the inclusion of one radiolabeled nucleotide, and products were electrophoresed on denaturing polyacrylamide gels. Thirty-six of the 60 patients (60%) exhibited LOH at one or more loci on chromosome 9p. Eight of 17 patients (47%) with adenocarcinoma manifested LOH, while 28 of 43 (65%) with squamous cell carcinoma showed LOH. LOH was most frequent at loci D9S171 (19 of 23, or 83%) and D9S165 (24 of 32, or 75%). These data support the hypothesis that a tumor suppressor gene or genes located on this portion of chromosome 9p exert(s) an effect on esophageal cancer development.
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PMID:Frequent loss of heterozygosity on chromosome 9 in adenocarcinoma and squamous cell carcinoma of the esophagus. 795 53

A novel derivative of camptothecin, 9-aminocamptothecin (9-AC), is currently under Phase II evaluation in various cancers. Exceptionally mild toxicities were observed in patients with brain tumors who were treated with anticonvulsants. To investigate a pharmacokinetic interaction between 9-AC and anticonvulsants, and to evaluate the pharmacodynamics of 9-AC, we investigated the clinical pharmacology of 9-AC, administered by a 72-h infusion, in three Phase II studies. Plasma concentrations of total 9-AC (lactone plus carboxylate) at a steady state were measured in 56, 10, and 14 patients with non-small cell lung cancer, malignant glioma, and head and neck cancer, respectively. For lung cancer or glioma patients, 9-AC was infused at 45 (51 patients) or 59 (15 patients) microg/m2/h, and 9-AC was infused at 35.4 microg/m2/h in head and neck cancer patients. All glioma patients had been treated with phenytoin or carbamazepine. 9-AC clearance did not differ among the dosage rates, but differed according to the diseases (P = 0.002). Glioma patients had a higher clearance (1.0-18.0; median, 2.0 liters/h/m2) than lung cancer patients (0.3-5.1; median, 0.9 liters/h/m2). A logistic regression model described the relationship between the 9-AC concentration and the probability of grade 4 neutropenia, which was the main toxicity. Observed incidences of grade 4 neutropenia for patients with model-predicted probability of 0-20%, 20-40%, and 40-100% were 10%, 32%, and 67%, respectively, and corresponded to 9-AC concentration of <54, 54-86, and >86 ng/ml, respectively. Anticonvulsants seem to induce the clearance of 9-AC, and the concentration of 9-AC predicts the probability of grade 4 neutropenia.
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PMID:Pharmacokinetics and pharmacodynamics of 9-aminocamptothecin infused over 72 hours in phase II studies. 1038 15

The biodistribution and pharmacokinetics of (111)In-DTPA-labeled pegylated liposomes (IDLPL) were studied in 17 patients with locally advanced cancers. The patients received 65-107 MBq of IDLPL, and nuclear medicine whole body gamma camera imaging was used to study liposome biodistribution. The t(1/2beta) of IDLPL was 76.1 h. Positive tumor images were obtained in 15 of 17 studies (4 of 5 breast, 5 of 5 head and neck, 3 of 4 bronchus, 2 of 2 glioma, and 1 of 1 cervix cancer). The levels of tumor liposome uptake estimated from regions of interest on gamma camera images were approximately 0.5-3.5% of the injected dose at 72 h. The greatest levels of uptake were seen in the patients with head and neck cancers [33.0 +/- 15.8% ID/kg (percentage of injected dose/kg)]. The uptake in the lung tumors was at an intermediate level (18.3 +/- 5.7% ID/kg), and the breast cancers showed relatively low levels of uptake (5.3 +/- 2.6% ID/kg). These liposome uptake values mirrored the estimated tumor volumes of the various tumor types (36.2 +/- 18.0 cm3 for squamous cell cancer of the head and neck, 114.5 +/- 42.0 cm3 for lung tumors, and 234.7 +/- 101.4 cm3 for breast tumors). In addition, significant localization of the liposomes was seen in the tissues of the reticuloendothelial system (liver, spleen, and bone marrow). One patient with extensive mucocutaneous AIDS-related Kaposi sarcoma was also studied according to a modified protocol, and prominent deposition of the radiolabeled liposomes was demonstrated in these lesions. An additional two patients with resectable head and neck cancer received 26 MBq of IDLPL 48 h before undergoing surgical excision of their tumors. Samples of the tumor, adjacent normal mucosa, muscle, fat, skin, and salivary tissue were obtained at operation. The levels of tumor uptake were 8.8 and 15.9% ID/kg, respectively, with tumor uptake exceeding that in normal mucosa by a mean ratio of 2.3:1, in skin by 3.6:1, in salivary gland by 5.6:1, in muscle by 8.3:1, and in fat by 10.8:1. These data strongly support the development of pegylated liposomal agents for the treatment of solid tumors, particularly those of the head and neck.
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PMID:Effective targeting of solid tumors in patients with locally advanced cancers by radiolabeled pegylated liposomes. 1123 71

Thalidomide, an oral agent with antiangiogenic and immunomodulatory properties, is being investigated extensively in the management of advanced cancer. Multiple studies with large numbers of patients have confirmed that this drug has significant activity in multiple myeloma. Some patients with myelofibrosis or myeodysplatic syndromes may reduce their need for transfusions after thalidomide treatment. The activity of thalidomide in solid tumors is less prominent. Studies in Kaposi's sarcoma, malignant melanoma, renal cell carcinoma and prostate cancer appear more promising especially when thalidomide is combined with biological agents or with chemotherapy. Limited activity was demonstrated in patients with glioma, while thalidomide appears to be inactive in patients with head and neck cancer, breast or ovarian cancer.
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PMID:Thalidomide in cancer medicine. 1527 53

For improving radiotherapy treatment results, altered fractionation (AF) is one of the most important biological factors to modify the conventional fractionation schedule. AF is classified into two categories. One is decreasing in dose-per-fraction and increasing in total dose, so-called hyperfractionation (HF), which expands the difference in radio-sensitivity between tumor and normal tissue. On the other hand, shortening of overall treatment time, so-called accelerated hyperfractionation (AHF), prevents accelerated repopulation of tumor cells during radiotherapy. AF is rarely recognized as a standard therapy despite many reports about its efficacy against various cancers, totally. This is often used for head and neck cancer. However, the problem is that they usually improve local-control, but do not always improve survival. Although AHF is recognized as one of a standard treatment for small cell lung cancer, it is still objectionable and disputable. Besides these, efficacy of AF against non-small cell lung cancer, bladder cancer and malignant glioma, has been reported. However, AF is not considered as a standard treatment. Accompanied with spread out of stereotactic irradiation, dose-fractionation-time relationship becomes to be more important subject, especially hypofractionation, to clarify the new aspect of AF.
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PMID:[Altered fractionation]. 1661 49

Interferon (IFN)-lambdas, including IFN-lambda1, IFN-lambda2, and IFN-lambda3, are a newly described group of cytokines distantly related to the type I IFNs and IL-10 family members. Besides the antiviral activity, IFN-lambdas were reported to inhibit various tumor growths in vitro and in vivo. Herein, we identified IFN-lambda genes from the genome sequences of the human, chimpanzee, macaque, orangutan, mouse, rat and dog, and found that the locations and copy of a specific IFN-lambda varied in different genomes, not just the copy of IFN-lambdas. We found human IFN-lambdas were expressed in fetal retina, fetal brain and T cells by ESTs search. Moreover, IFN-lambdas were also found to express in bladder cancer, blood cancer, breast cancer, glioma, head and neck cancer and lung cancer tissues. Three tumor-related transcriptional factors (steroidogenic factor-1, Wilms tumor 1 and P53) binding sites were identified within the 1.0-kb regions upstream of the transcriptional start site of human IFN-lambdas. Meta-analysis of the prognostic value of IFN-lambda genes in various cancers showed that the expression of IFN-lambdas are indeed related to the cancer prognosis in certain types of cancer. It can be predicted that IFN-lambdas take part in the cancer development by the regulation of expression of IFN-lambdas related to the SF-1, P53 and WT-1.
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PMID:Integrative genomic analyses on interferon-lambdas and their roles in cancer prediction. 2004 42

Interferon (IFN)-lambdas, including INF-lambda1, -lambda2, and -lambda3, are a newly described group of cytokines distantly related to the type I IFNs and IL-10 family members. IFN-lambda1, -lambda2, and -lambda3 bind to the same receptor (known as IL28RA) to exert their antiviral, antitumor and immunomodulatory effects. Here, we identified IL28RA genes from the genome of human, chimpanzee, macaque, orangutan, mouse, horse, rat, dog, chicken, and found that only one IL28RA existed in each genome. All the identified IL28RAs are single-pass type I membrane proteins except chicken IL28RA. They belong to the type II cytokine receptor family and contain one fibronectin type-III domain. We found human IL28RA was expressed in lymphs, testes, lymphoma, teratocarcinoma, pediatric pre-B cell acute lymphoblastic leukemia, germinal center B cells, embryonic stem cells, fetal lung, and also expressed in bladder, blood and breast cancers, glioma, head and neck cancer and lung cancer tissues. Three tumor-related transcriptional factor binding sites (AP-2, c-Jun and P53) were identified within the 1.0-kb regions upstream of the transcriptional start site of human IL28RA. Meta-analysis of the prognostic value of IL28RA genes in various cancers found that the expression of IL28RA was indeed related to the cancer prognosis in certain cancers. The STAT1 binding sites in the promoter region of IL28RA implied a specific mechanism for the amplifying effects of IFN-lambdas. The LyF-1 binding sites in the promoter region of IL28RA imply that IFN-lambdas were involved in the differentiation of early B and T cells.
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PMID:Integrative genomic analyses on IL28RA, the common receptor of interferon-lambda1, -lambda2 and -lambda3. 2037 26

The first BNCT trials took place in the USA in the early 1960's, yet BNCT is still far from mainstream medicine. Nonetheless, in recent years, reported results in the treatment of head and neck cancer and recurrent glioma, coupled with the progress in developing linear accelerators specifically for BNCT applications, have given some optimism to the future of BNCT. This article provides a brief reminder on the ups and downs of the history of BNCT and supports the view that controlled and prospective clinical trials with a modern design will make BNCT an evidence-based treatment modality within the coming decade.
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PMID:Critical review, with an optimistic outlook, on Boron Neutron Capture Therapy (BNCT). 2435 1

Peroxiredoxin (Prx)II belongs to a family of redox-active proteins that use redox-sensitive cysteine in the active site to reduce peroxides. PrxII is induced by various oxidative stimuli and plays an important protective role against oxidative radical damage by reactive oxygen species. PrxII expression levels are correlated with resistance to radiation therapy or certain anti-cancer drugs in radioresistant breast cancer cells, glioblastomas, and head and neck cancer cells as well as in tissue isolated from head and neck patients who do not respond to radiation therapy. Small interfering RNA (siRNA) that inhibits the PrxII gene expression has been shown to partially reverse the radioresistant phenotype in radiation resistant breast cancer cells and sensitizes glioma cells to oxidative stress, highlighting the potential clinical importance of PrxII in radiation resistance in cancer. This article focuses on the role that PrxII may play in chemoresistant breast cancer cells.
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PMID:The role of peroxiredoxin II in chemoresistance of breast cancer cells. 2497 57


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