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Results for “biologic therapy”

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At least 19 recordsLinked to original sources
PubMed2026

Effect of Time to Start of Biologic Therapy on Treatment Response in Childhood Arthritis: Results From the UCAN CAN-DU Cohort.

OBJECTIVE: To estimate the effect of time from symptom onset to start of biologic treatment on achieving inactive arthritis within six months in a cohort of patients with juvenile idiopathic arthritis (JIA). METHODS: The international UCAN CAN-DU study prospectively enrolled patients with JIA across Canada and the Netherlands. A nested cohort study was performed and biologic-naive patients with nonsystemic JIA were included at the start of biologic therapy. The primary outcome was inactive arthritis at six months. Demographics, disease-related parameters, and treatment response were compared using (non)parametric tests among early (time symptom onset to biologic start: 0-6 months), intermediate (7-12 months), and late (13-24 months) treatment groups. A logistic regression model analyzed the effect of time to biologic start on the response at six months, adjusting for active joint count and physician global assessment. A graphical representation of the model was created. RESULTS: One hundred and thirty children with JIA were included (early: n = 35; intermediate: n = 46; late: n = 49), 66% were female, and the median age at symptom onset was 11.0 years. The proportion of patients that reach inactive arthritis in the early starters (83%) was significantly higher than in late starters (57%). For each month of delay to the start of biologic treatment, the adjusted odds of having active arthritis after six months of therapy was 1.09 (interquartile range: 1.02-1.17, P = 0.009). CONCLUSION: Early start of biologic therapies in patients with JIA was associated with a higher proportion of patients reaching inactive arthritis within six months, suggesting a window of opportunity to control disease activity.

Humans↗
PubMed1992

Perceptions of quality of life and quality of care for patients with cancer receiving biological therapy.

This retrospective, descriptive study was undertaken to identify patient and family perceptions about quality of life (QOL) and quality of care (QOC) after experimental biological therapy. A mail survey that included instruments designed to measure QOL (the Profile of Mood States [POMS] and the Linear Analogue Self-Assessment [Lasa]) and QOC was sent to patients (response rate, 60%) and to relatives of deceased patients (response rate, 70%). Bivariate and multivariate statistics were used to analyze the data. Patients reported a relatively good quality of life, as measured by POMS and LASA scores. The majority of living patients and of family members of deceased patients were positive about the QOC received; relatives were significantly less positive than patients. Four components were significant in respondents' assessment of QOC: adequate symptom control, availability of support services, communication with the medical team, and receiving information about response to treatment. The findings suggest that there is a need to supplement survival data and biomedical outcomes with information about patient and family perceptions about care and treatment.

Adult↗
PubMed1987

Biologic therapy of chronic myelogenous leukemia.

In a study using human IFN-alpha, 36 of 51 patients with chronic phase CML achieved a complete hematologic remission. More significantly, 20 patients showed suppression of Ph-positive metaphases with reappearance of cells with normal karyotype. To date, the authors have treated 44 chronic phase CML patients with recombinant IFN-alpha as their frontline biologic therapy with similar hematologic and cytogenetic responses. Gamma interferon is active against CML but less so than IFN-alpha. Chemotherapy followed by IFN-alpha also shows promise. Interferons have produced only limited responses in terminal phase CML patients.

Blast Crisis↗
PubMed1992

Regional biologic therapy. Hepatic arterial infusion of recombinant human tumor necrosis factor in patients with liver metastases.

Twenty-two chemotherapy-resistant patients with liver metastases received 46 courses of recombinant human tumor necrosis factor (rhTNF) administered by 5-day continuous infusion through percutaneously inserted hepatic arterial catheters. The maximum tolerated daily dose of rhTNF was 150 micrograms/m2. This is six times the maximum tolerated daily dose of rhTNF that could be given systemically (intravenous) on the same schedule. The dose-limiting toxicity resulted in severe, although transient, hypophosphatemia (less than 1.0 mg/dl) associated with myocardial dysfunction. Objective tumor response (partial tumor response or greater) was observed in 2 of 14 patients (14%) with colorectal cancer and lasted as long as 3 months. Three additional minor responses occurred among these patients with colorectal cancer. Plasma carcinoembryonic antigen levels also decreased significantly (greater than 25%) in 7 of the 14 (50%) patients with colorectal cancer. Regional biologic therapy with rhTNF as a sole modality has definite antitumor activity in colorectal cancer metastatic to the liver and warrants additional study in previously untreated patients.

Adult↗
PubMed1991

Biologic therapy and immunotherapy for ovarian cancer.

Ovarian cancer remains an attractive model for evaluation of biologic and immunologic therapies due to the availability of multiple reagents, the development of preclinical murine models, and the intraperitoneal pattern of clinical disease. Recent studies have focused on conjugated monoclonal antibodies, including radioconjugates, immunotoxins, and bispecific antibodies. Other preclinical and clinical studies have been conducted with recombinant cytokines and adoptive cellular immunotherapy for small-volume residual disease. Dose-limiting clinical toxicities have emerged with many of these approaches in the absence of frequent antitumor responses, and new strategies will be required to develop effective therapies in the future.

Animals↗
PubMed2026

Temporal mismatch in allogeneic iPSC therapies: biological risks and implications for clinical translation.

INTRODUCTION: The clinical translation of pluripotent stem cell-derived therapies has entered a new phase following conditional approval of first-in-class allogeneic induced pluripotent stem cell (iPSC)-derived products in Japan. These approvals highlight both the therapeutic promise of iPSC technologies and regulatory challenges associated with evaluating complex cell-based interventions. AREAS COVERED: This report examines the evidentiary basis supporting recent approvals and reviews key biological characteristics of allogeneic iPSC-derived therapies, including pluripotency-associated instability, immunological constraints, and manufacturing-related genomic variability. Drawing on recent clinical studies and relevant experimental literature, we analyze how these multilayered risks evolve over extended time horizons and assess their implications for the interpretation of early-phase clinical data and current regulatory frameworks. EXPERT OPINION: We argue that the central challenge extends beyond limited clinical evidence to a fundamental mismatch between the temporal dynamics of biological risk and the duration of conventional clinical evaluation. As a result, early clinical observations may systematically underestimate long-term risks. Conditional approval pathways should therefore incorporate safeguards aligned with this temporal uncertainty, including long-term follow-up, rigorous post-approval evaluation, and enhanced transparency in biological and manufacturing data. Aligning regulatory design with intrinsic properties of pluripotent stem cell-derived therapies will be essential for ensuring safe and responsible clinical translation.

Humans↗
PubMed1987

Biologic therapy for the treatment of malignant common epithelial tumors of the ovary.

There are a number of strategies to the treatment of gynecologic tumors that involve the use of biologic agents. Biologic agents may be immunologic in nature and act directly on the tumor or to boost an immune response to the tumor, or they may be nonimmune in nature and directly affect the tumor or a physiologic process on which the tumor depends. Although the potential for these agents in the treatment of all gynecologic tumors is great, most of the data to date have been generated in ovarian cancer. Clinical trials of alpha interferon administered intraperitoneally in patients with small volume ovarian cancer have revealed high response rates with acceptable toxicity. The mechanism of the antitumor effect (i.e., direct tumor killing vs. indirect boosting host immune response) has not yet been determined. Clinical trials of intraperitoneal lymphokine-activated killer (LAK) cells plus recombinant interleukin-2 have also been started based upon significant antitumor effects noted in xenogeneic systems. The finding that the peritoneal fluid of interferon-treated patients is rich with monocytes and macrophages has led to the development of a clinical trial using intraperitoneal human monocytes activated with recombinant gamma interferon along with gamma interferon. Monoclonal antibodies have already made a significant impact on the diagnosis of ovarian cancer, and are being brought to clinical trial as therapeutic agents. The OC-125 antigen is shed by ovarian tumor cells and its elevation in the serum of patients with undiagnosed pelvic masses is highly predictive for ovarian neoplasia. Furthermore, its persistence in the serum of patients with ovarian cancer during chemotherapy is nearly always associated with persistent disease. A number of monoclonal antibodies specific for ovarian cancer have been developed. Radiolabeled antibodies administered intralymphatically and intraperitoneally may be able to demonstrate the presence of tumor reliably enough to save some patients from second-look laparotomy. In addition, clinical trials are underway using immunotoxins, antitumor antibodies conjugated to potent plant or bacterial toxins that are effective at killing cells with amazing efficiency. Antibodies conjugated to alpha-emitting radioisotopes like astatine-211 or to radioisotopes emitting gamma or beta waves or Auger electrons are candidates for clinical trial. There is also some interest in attempting to improve the therapeutic index by using antibodies conjugated to cytotoxic chemotherapeutic agents.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1992

Extrapulmonary and pulmonary small-cell carcinoma: tumor biology, therapy, and outcome.

Extrapulmonary small-cell cancer is a distinct clinicopathological entity from small-cell anaplastic carcinoma of the lung. Approximately 1,000 cases have been projected annually in the United States, which represents an overall incidence of between 0.1% and 0.4% of all cancer. Not surprisingly then, little information is available regarding the treatment of this disease, which presents a challenge to the clinician when it is regionally confined. The majority of patients with extrapulmonary small-cell neoplasms have only been treated with local modalities of therapy, surgery, radiation, or a combination of both. Prolonged survival is not infrequent, which is in contrast to the experience for small-cell lung cancer and surprising given our current systemic approach to patients with this disease. This report will summarize the similarities and differences in biology, natural history, and clinical characteristics of patients with extrapulmonary small-cell cancer and small-cell anaplastic carcinoma of the lung. The histogenesis of small-cell cancer is briefly reviewed. A general therapeutic approach to patients with small-cell lung cancer is reported. Lastly, recommendations for therapy of patients with regionally confined extrapulmonary small-cell cancer by primary site are outlined.

Carcinoma, Small Cell↗
PubMed2026

Biologic Therapies for Alleviating Neurodegeneration in Lysosomal Storage Diseases.

Lysosomal storage diseases (LSDs) are a group of rare inherited metabolic disorders characterized by lysosomal dysfunction and progressive accumulation of undegraded substrates, leading to multisystem involvement and, in many cases, severe neurodegeneration. Because the blood-brain barrier (BBB) restricts central nervous system (CNS) access for most therapeutic modalities, neurological manifestations remain the major unmet need across LSDs. In this review, we summarize current and emerging strategies aimed at correcting CNS pathology, including enzyme replacement therapy (ERT), adeno-associated virus (AAV)-mediated gene therapy, allogeneic hematopoietic stem cell transplantation (HSCT), and autologous HSCT with gene-modified hematopoietic stem cells. While ERT provides limited CNS benefits and allogeneic HSCT mitigates neurodegeneration only partially, their overall impact on CNS outcomes remains restricted. Newer approaches, such as BBB-shuttling ERTs, CNS-tropic AAV capsids, and genetically modified autologous hematopoietic stem and progenitor cells capable of sustained supraphysiological enzyme production, offer promising avenues for enhanced CNS delivery and cross-correction. Together, these advances underscore a shift toward integrated therapeutic strategies that combine systemic and CNS-directed interventions, with the potential to transform outcomes for patients with LSDs and other neurodegenerative disorders amenable to cross-correction.

Journal Article↗
PubMed1992

Design of yeast-secreted albumin derivatives for human therapy: biological and antiviral properties of a serum albumin-CD4 genetic conjugate.

Due to its remarkably long half-life, together with its wide in vivo distribution and its lack of enzymatic or immunological functions, human serum albumin (HSA) represents an optimal carrier for therapeutic peptides/proteins aimed at interacting with cellular or molecular components of the vascular and interstitial compartments. As an example, we designed a genetically engineered HSA-CD4 hybrid aimed at specifically blocking the entry of the human immunodeficiency virus into CD4+ cells. In contrast with CD4, HSA-CD4 is correctly processed and efficiently secreted by Kluyveromyces yeasts. In addition, its CD4 moiety exhibits binding and antiviral in vitro properties similar to those of soluble CD4. Finally, the elimination half-life of HSA-CD4 in a rabbit experimental model is comparable to that of control HSA and 140-fold higher than that of soluble CD4. These results indicate that the genetic fusion of bioactive peptides to HSA is a plausible approach toward the design and recovery of secreted therapeutic HSA derivatives with appropriate pharmacokinetic properties.

Animals↗