Active clinical trials for "Nasopharyngeal Neoplasms"

The purpose of this study is to collect outcomes information to see what effects photon/proton beam radiation has on nasopharynx cancer.

The objectives of this clinical study are threefold: To compare the benefits in cancer control and survival obtained from adding induction-concurrent chemotherapy to radiation with those from adding concurrent-adjuvant chemotherapy to radiation. To test whether replacing fluorouracil with Xeloda in combining with cisplatin (PF or PX, respectively) in the chemotherapy plan will maintain or improve further the chemotherapy benefits while reducing the duration of hospital stay. To see if accelerated fractionation radiotherapy can improve the outcome of patients as compared with conventional fractionation radiotherapy.

In an effort to identify genetic factors linked to the development of nasopharyngeal cancer (NPC), the researchers identified and sampled 2,394 individuals from Taiwanese families in which two or more relatives had been diagnosed with NPC. Serum from these individuals was tested for three anti-Epstein-Barr virus (EPV) antibodies associated with elevated risk of NPC. Results indicate that apparently healthy individuals from high-risk families have a nearly threefold elevation in their EBV antibody prevalence compared with the general population. However, the clinical implications of this finding are not yet understood. To clarify the implications, the 2,394 unaffected individuals from the multiplex family study will be invited to participate in the current study. Approximately 1,600 individuals are expected to participate. Participants will have an ear, nose, and throat examination to determine if they have occult or symptomatic NPC. Their levels of EBV antibody at the time of initial recruitment will be correlated with NPC detection in the period between initial recruitment and the present study. Participants will also be asked to complete a brief risk factor questionnaire and to donate blood, saliva, a nasopharyngeal swab, nasopharyngeal tissue, and urine for future studies. Currently, no accepted clinical management protocol exists for screening unaffected members from families at high risk of NPC development. Results from this study have the potential to significantly impact the clinical management and follow-up of individuals with a family history of NPC.

Colorectal cancer (CRC) is a leading cause for cancer related mortality in the western world with a lifetime risk of 6%. Etiology is complex, while genetic background significantly affects the risk. Around one third of all genetic disorders as well as most cases of Familial Adenomatous Polyposis (FAP) and a large proportion of all sporadic CRC cases occur as a result of premature nonsense mutations (creating a stop codon) in an individual's adenomatous polyposis coli (APC) gene. Nonsense mutations are single-point alterations in the DNA that prematurely halt the protein translation process, producing a shortened, nonfunctional protein. In many of these cases, if the cell can be 'persuaded' to ignore the premature stop codon signal, the resulting protein may be able to ameliorate or stop the disease. Recently, members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and in different mice models. The aim of this project is to determine the ability of the macrolide antibiotic-Azithromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP and to tests its effect on adenoma number and size and on desmoid tumors in these patients. The future goal is to maximize the effect of stop-codon suppressors on APC while minimizing side effects. In this study the investigators will select FAP patients which carry APC nonsense mutations, treat them with Azithromycin PO for 4-6 months and examine colonic and duodenal adenomas as well as abdominal desmoid tumors, that will be documented before during and after treatment. In parallel, investigators will test polyp, adenoma and desmoid tissue samples as well as blood samples from these patients for changes in expression levels of the APC protein and related oncogenic markers. Suppression of nonsense mutations within the APC gene should be of benefit for patients suffering from FAP, attenuated FAP or multiple adenomas and for patients with advanced or diffuse CRC. Furthermore, given the rapid progress being made in the identification of different nonsense mutations in human genes that lead to mostly non-curable disease, the identification of clinically approved compounds that suppress nonsense mutations and that can be administered long-term without significant side effects would open new venues in the treatment of genetic human diseases that arise from pre-mature stop codons in important coding sequences. Immediate goal: establish the ability of Azithromycin to read-through APC nonsense mutation in FAP patients. The read-through effect of Azithromycin will be clinically tested by counting and measuring the number and size of both colonic and duodenal adenomas before and over treatment and by measuring the size of known desmoid tumors. Samples of the adenomas and desmoid tumors will be tested by western blot, immunofluorescence and immunohistochemistry for restoration of APC expression and changes in oncogenic markers. These experiments should be conducted within 6 month. Long term objective: Determine the lowest dose of Azithromycin that can inhibit growth of colonic neoplasia and CRC in patients expressing a truncated APC protein due to nonsense mutations. Examine the ability of a panel of additional macrolide antibiotics to induce APC nonsense mutation suppression using in-vitro methods. Investigators will focus on macrolide antibiotics that are currently in clinical use and are administrated for long terms. These objectives should take around 4 month and will be conducted in parallel.

Colorectal cancer (CRC) is a leading cause for cancer related mortality in the western world with a lifetime risk of 6%. Etiology is complex, while genetic background significantly affects the risk. Around one third of all genetic disorders as well as most cases of Familial Adenomatous Polyposis (FAP) and a large proportion of all sporadic CRC cases occur as a result of premature nonsense mutations (creating a stop codon) in an individual's adenomatous polyposis coli (APC) gene. Nonsense mutations are single-point alterations in the DNA that prematurely halt the protein translation process, producing a shortened, nonfunctional protein. In many of these cases, if the cell can be 'persuaded' to ignore the premature stop codon signal, the resulting protein may be able to ameliorate or stop the disease. Recently, members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and in different mice models. The aim of this project is to determine the ability of the macrolide antibiotic-erythromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP and to tests its effect on adenoma number and size and on desmoid tumors in these patients. The future goal is to maximize the effect of stop-codon suppressors on APC while minimizing side effects. In this study investigators will select FAP patients which carry APC nonsense mutations, treat them with erythromycin PO for 4-6 months and examine colonic and duodenal adenomas as well as abdominal desmoid tumors, that will be documented before during and after treatment. In parallel, investigators will test polyp, adenoma and desmoid tissue samples as well as blood samples from these patients for changes in expression levels of the APC protein and related oncogenic markers. Suppression of nonsense mutations within the APC gene should be of benefit for patients suffering from FAP, attenuated FAP or multiple adenomas and for patients with advanced or diffuse CRC. Furthermore, given the rapid progress being made in the identification of different nonsense mutations in human genes that lead to mostly un-curable disease, the identification of clinically approved compounds that suppress nonsense mutations and that can be administered long-term without significant side effects would open new venues in the treatment of genetic human diseases that arise from pre-mature stop codons in important coding sequences. Immediate goal: establish the ability of erythromycin to read-through APC nonsense mutation in FAP patients. The read-through effect of erythromycin will be clinically tested by counting and measuring the number and size of both colonic and duodenal adenomas before and over treatment and by measuring the size of known desmoid tumors. Samples of the adenomas and desmoid tumors will be tested by western blot, immunofluorescence and immunohistochemistry for restoration of APC expression and changes in oncogenic markers. These experiments should be conducted within 6 month. Long term objective: Determine the lowest dose of erythromycin that can inhibit growth of colonic neoplasia and CRC in patients expressing a truncated APC protein due to nonsense mutations. Examine the ability of a panel of additional macrolide antibiotics to induce APC nonsense mutation suppression using in-vitro methods. Investigators will focus on macrolide antibiotics that are currently in clinical use and are administrated for long terms. These objectives should take around 6 month and will be conducted in parallel.

The purpose of this study is to evaluate the efficacy and safety of recombinant human endostatin（continuously-pumped）combined with chemoradiotherapy in patients with advanced squamous cell carcinoma of the head and neck. The patients will be randomized to concurrent radiotherapy (CRT) arm and CRT + Endostar arm. All patients will receive one cycles of induction chemotherapy, intensity modulated radiation therapy (IMRT) with weekly cisplatin and 3 cycles of chemotherapy after IMRT. Treatment cycles will be repeated every 21 days for a maximum of 4 cycles. In CRT + Endostar arm, Endostar will be continuously intravenous pumped (7.5 mg/m2) for 14 days (d1-d14) during chemotherapy and for 5 days/week (d-5-d-1, d3-d7, d10-d14, d17-d21) during IMRT.

Observe and compare the chrono-chemotherapy IMRT and conventional chemotherapy and intensity modulated radiotherapy term efficacy of the treatment of locally advanced nasopharyngeal carcinoma. Evaluation chrono-chemotherapy IMRT and conventional chemotherapy and intensity modulated radiotherapy in locally advanced nasopharyngeal carcinoma safety and tolerability. 3）observing the adverse reaction and effects of two groups,expected chrono-chemotherapy group can achieve lower toxicity, improve the curative effect, for the treatment of nasopharyngeal carcinoma provides a more reasonable way.

This study is carried out to find out the safety and recommended dose of CD137L-DC-EBV-VAX in nasopharyngeal cancer. CD137L-DC-EBV-VAX is a product made from one of our own immune system cells (dendritic cell, DC). Dendritic cells are immune cells that help to stimulate our body's T lymphocytes to fight cancer by presenting specific proteins from the cancer cells. The investigators have developed in the laboratory a highly effective dendritic cell which is primed to activate T cells with the Epstein-Barr virus (EBV) proteins. It is hoped that this will stir an immune response to recognize NPC cells and kill them as part of body's immune surveillance system.

Nimotuzumab is an IgG1 humanized monoclonal antibody that recognized an epitope located in the extra cellular domain of the human epidermal growth factor receptor (EGFR). Clinical trials are ongoing globally to evaluate nimotuzumab in different indications. Nimotuzumab has been granted approval for use in squamous cell carcinoma of head and neck (SCCHN), glioma and nasopharyngeal cancer in different countries. The Clinical efficacy has been shown in adult with head and neck cancer. The study assessed the clinical efficacy, and safety of the combination of Nimotuzumab administered concomitantly with chemotherapy and radiotherapy in patients with advanced nasopharyngeal cancer.

This is a registry-based observational study assessing clinical outcomes in FAP patients receiving celecoxib compared with historical/concurrent registry patients who have not received celecoxib. Both retrospective and prospective data will be utilized. No sampling methods apply.