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chemotherapy/nekros
Länken sparas på Urklipp
Sida 1 från 6239 resultat
Chemotherapy amplifies production of tumor necrosis factor.
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Several chemotherapeutic agents exert cytotoxicity through the generation of reactive oxygen species (ROS), and our laboratory has shown that ROS increase tumor necrosis factor (TNF) production. Therefore, we hypothesized that cis-dichlorodiammine platinum (CDDP), mitomycin-C, and doxorubicin
Prognostic significance of chemotherapy-induced necrosis in osteosarcoma patients receiving pasteurized autografts.
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BACKGROUND
Among various reconstruction methods after wide excision for osteosarcoma, pasteurized autograft is often preferred. While the whole area of the tumor can be assessed for chemotherapy-induced necrosis, one of the important prognostic factors, in other reconstructive techniques, only a
Impact of chemotherapy-induced necrosis on event-free and overall survival after preoperative MAP chemotherapy in patients with primary high-grade localized osteosarcoma
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Aims: To assess the correlation between the histological response to preoperative chemotherapy and event-free survival (EFS) or overall survival (OS) in patients with high-grade localized osteosarcoma.
Methods: Out of 625 patients
Grade of chemotherapy-induced necrosis as a predictor of local and systemic control in 881 patients with non-metastatic osteosarcoma of the extremities treated with neoadjuvant chemotherapy in a single institution.
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To determine whether necrosis induced by pre-operative chemotherapy correlates with the rate of systemic and local relapse, may change the pattern of relapse and/or may modify the chance of success of post-relapse treatments, we evaluated 881 patients with non-metastatic osteosarcoma of the
A rare case of adenoviral fulminant hepatic necrosis after chemotherapy.
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The authors report a rare case of fulminant adenoviral hepatic necrosis occurring after chemotherapy in a patient with a second relapse of acute myeloid leukemia. The literature is reviewed and the role of rapid viral diagnosis in the clinical management of this complication is discussed. A
Prediction of chemotherapy response by PET-CT in osteosarcoma: correlation with histologic necrosis.
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BACKGROUND
The current standard for neoadjuvant chemotherapy (NACT) response evaluation in osteosarcoma is histopathologic necrosis (HN). However, it is accessible only after NACT completion and may get affected by confounding factors. Thus, noninvasive surrogate such as
Following Chemotherapy: Serum Cytokine (Tumor Necrosis Factor, Interleukin-2, Interleukin-11), Immunoglobulin, Complement, Vascular Endothelial Growth Factor Levels, and the Systemic Symptoms like Capillary Leak Syndrome.
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Several problems such as myalgia, arthralgia, fever, dyspnea, generalized edema, and pleural effusion can occur in cancer patients following the chemotherapy, especially at the first cycle of the first chemotherapy treatment. Although it is assumed that some cytokines are associated with the
Percentage tumor necrosis following chemotherapy in neuroblastoma correlates with MYCN status but not survival.
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The percentage of chemotherapy-induced necrosis in primary tumors corresponds with outcome in several childhood malignancies, including high-risk metastatic diseases. In this retrospective pilot study, the authors assessed the importance of postchemotherapy necrosis in high-risk neuroblastoma with a
Ewing's sarcoma: only patients with 100% of necrosis after chemotherapy should be classified as having a good response.
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OBJECTIVE
The purpose of this study was to review a large cohort of patients and further assess the correlation between the histological response to chemotherapy in patients with Ewing's sarcoma with the overall (OS) and event-free survival (EFS).
METHODS
All patients treated for Ewing's sarcoma
Neoadjuvant chemotherapy followed by concurrent chemoradiotherapy versus concurrent chemoradiotherapy alone in nasopharyngeal carcinoma patients with cervical nodal necrosis.
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The effectiveness of neoadjuvant chemotherapy (NACT) followed by concurrent chemoradiotherapy (CCRT) compared with CCRT alone in nasopharyngeal carcinoma (NPC) patients who presented with cervical nodal necrosis (CNN) is unknown. A total of 792 patients with stage T1-4N1-3M0 NPC and presented with
Femoral head necrosis in three patients with relapsed ovarian cancer receiving high-dose chemotherapy followed by autologous peripheral blood stem cell transplantation.
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We report three patients with relapsed ovarian cancer who developed femoral head necrosis requiring endoprosthetic hip surgery 16-35 months after high-dose chemotherapy (HDC) with treosulfan (47 and 56 g/m(2) body-surface area (BSA)) given as 3-25 h infusions and followed by autologous peripheral
Perivesical fat necrosis after adjuvant intravesical chemotherapy.
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OBJECTIVE
To document the presence of extensive transmural and perivesical fat necrosis in a series of radical cystectomies, and associate the surgical and pathological findings with the administration of intravesical chemotherapy.
METHODS
The study comprised 12 patients with pT2+ transitional cell
In vivo induction of gamma interferon and tumor necrosis factor by interleukin-2 infusion following intensive chemotherapy or autologous marrow transplantation.
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Interleukin-2 (IL-2) therapy may improve immune reconstitution and reduce the risk of leukemic relapse in the setting of minimal residual disease by augmenting cytotoxic effector mechanisms directed at residual malignant cells. In addition, IL-2 in vitro promotes the release of cytokines including
Percutaneous tumor ablation: microencapsulated echo-guided interstitial chemotherapy combined with cryosurgery increases necrosis in prostate cancer.
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This study aimed at confirming the increased growth inhibition (GI) of human prostate tumors produced by a intentionally palliative combination treatment of cryochemotherapy, i.e., partial cryoablation (CA) followed by intratumor partial chemotherapy with injection of microencapsulated
Genomic alterations in human malignant glioma cells associate with the cell resistance to the combination treatment with tumor necrosis factor-related apoptosis-inducing ligand and chemotherapy.
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OBJECTIVE
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently under clinical development as a cancer therapeutic agent. Many human malignant glioma cells, however, are resistant to TRAIL treatment. We, therefore, investigated the genomic alterations in TRAIL-resistant
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