Until better evidence is available for the effects of soy on women from non–soy-consuming countries, it seems reasonable to limit consumption to soyfoods, and to avoid high-dose supplements of processed soy components.
In their Areas of Confusion article, “Management of Relapsed Mantle Cell Lymphoma: Still a Treatment Challenge,” Ruan et al attempt to make the case that the relative merits of different upfront approaches for mantle cell lymphoma (MCL) are difficult to appreciate due to the differences in eligible patient populations and limited randomized data.
Rituximab (Rituxan) is a chimeric IgG1 anti-CD20 monoclonal antibody increasingly used in the treatment of non-Hodgkin’s lymphoma (NHL). Previous in vitro studies have suggested the role of antibody-dependent cellular cytotoxicity (ADCC) and FcgR-positive effector cells (natural killer and macrophage) in the antitumor effects of anti-CD20 antibodies, but the actual mechanism of rituximab action in vivo remains largely unknown. The FCGR3A gene coding for the FcgRIIIa receptor displays a functional dimorphism with either a phenylalanine (FCGR3A-158F) or a valine (FCGR3A-158V) at amino acid 158, with a higher affinity of human IgG1 and increased ADCC for the latter. The aim of this study was thus to determine the influence of this FCGR3A polymorphism on clinical and molecular responses to rituximab.
The role of radiotherapy in combination with chemotherapy in advanced-stage Hodgkin’s disease remains controversial.
Rituximab (Rituxan) is a chimeric IgG1 anti-CD20 monoclonal antibody increasingly used in the treatment of non-Hodgkin’s lymphoma (NHL). Previous in vitro studies have suggested the role of antibody-dependent cellular cytotoxicity (ADCC) and FcgR-positive effector cells (natural killer and macrophage) in the antitumor effects of anti-CD20 antibodies, but the actual mechanism of rituximab action in vivo remains largely unknown. The FCGR3A gene coding for the FcgRIIIa receptor displays a functional dimorphism with either a phenylalanine (FCGR3A-158F) or a valine (FCGR3A-158V) at amino acid 158, with a higher affinity of human IgG1 and increased ADCC for the latter. The aim of this study was thus to determine the influence of this FCGR3A polymorphism on clinical and molecular responses to rituximab.
The cachexia of malignancy is considered mediated through excess production of tumor necrosis factor–alpha and other cytokines. Thalidomide (Thalomid), a sedative/hypnotic, has been shown to inhibit tumor necrosis factor–alpha production.
In this video from the 2015 ONS meeting, Dr. Gwyn talks about nurse practitioners delivering bad news to patients by utilizing the SPIKES protocol.
High-dose therapy (HDT) with peripheral blood stem cell transplantation is a treatment option for patients with advanced follicular, marginal, and mantle cell lymphoma. In this setting, frequent contamination of peripheral blood stem cell harvests by
Our objective was to determine the efficacy of a fludarabine (Fludara)/mitoxantrone (Novantrone) regimen combined with the monoclonal anti-CD20 antibody rituximab (Rituxan) to induce clinical and molecular remissions in patients with relapsed
Lung cancer is estimated to be the second most commonly diagnosed cancer in both men and women in 2006, and the leading cause of cancer mortality. Non-small-cell lung cancer represents the majority of such cases. Most of these patients have locally advanced disease at presentation and are not eligible for curative resection. For the minority of patients who are technically resectable at presentation, lobectomy or pneumonectomy and pathologic mediastinal nodal staging offer the best overall survival. The high rate of comorbid medical illness and poor baseline pulmonary function in this population, however, make many such early-stage patients medically inoperable. For these patients, conventional single-modality radiotherapy has been the primary definitive treatment option, as discussed in part 1 of this article, which appeared in last month's issue. Numerous retrospective reports demonstrate long-term disease-free and overall survival data that are modestly superior to that expected after observation, but both local and distant failure continue to be significant risks. Investigation of radiotherapy dose escalation is ongoing, in an effort to improve local control while maintaining minimal toxicity. Additionally, emerging evidence suggests that new modalities, such as stereotactic radiosurgery and radiofrequency ablation, may also be potentially curative treatment alternatives. These modalities are addressed in part 2.
To support evidence-based clinical guidelines on erythropoietin use for anemia in oncology, we conducted systematic reviews of controlled trials on four patient groups. These were patients with treatment-related anemia; patients with disease-related anemia; patients transplanted with allogeneic hematopoietic stem cells; and those transplanted with autologous hematopoietic stem cells.
Bone renewal is essential for bone strength. During childhood and early adulthood, bone formation prevails over bone resorption, as bones increase in size and strength. Peak bone mass is achieved during the third decade in life, with a higher peak bone mass being protective against osteoporosis later in life.[1] Bone loss is most prominent in women at menopause due to the effects of a natural decline in estrogen levels. However, bone mass begins to decrease with age, and bone loss is most prominent in women at menopause due to the effects of a natural decline in estrogen levels.[2]
In their article, "Trastuzumab and Beyond: New Possibilities for the Treatment of HER2-Positive Breast Cancer," Drs. Morris and Carey provide an excellent summary of therapeutic progress in this disease, and also turn their attention to the challenge now facing us--that of understanding the heterogeneity of HER2-positive breast cancer and mechanisms of resistance to trastuzumab (Herceptin)-based therapy.
The role of radiotherapy in combination with chemotherapy in advanced-stage Hodgkin’s disease remains controversial.
Recent identification of gene mutations responsible for hereditary nonpolyposis colorectal cancer (HNPCC) has made possible the presymptomatic diagnosis of at-risk family members. If DNA testing shows that a family member is a gene carrier, that individual's lifetime cancer risk is approximately 90%. If the test is negative, the family member's cancer risk drops to that of the general population.
We previously reported the efficacy of concurrent cisplatin (Platinol)/etoposide (PE) and radiotherapy in stage IIIB non–small-cell lung cancer in which biopsy confirmation of T4 (noneffusion) or N3 status was required (S9019). In view of the activity of docetaxel (Taxotere) as second-line therapy and potential molecular mechanisms of action favoring taxane sequencing, we designed the present study to maintain a core of concurrent PE/radiotherapy, but to substitute docetaxel consolidation for the two additional cycles of PE.
The antiapoptotic protein bcl-2 is associated with chemotherapy failure in untreated large B-cell lymphomas, and with the recently described poor-prognosis large B-cell lymphoma subtype displaying an activated B-cell genotype (Nature 403:503, 2000).
Focused discussion on the duration of maintenance avelumab for metastatic urothelial carcinoma and considerations for switching therapy.
This study compared the activity and toxicity of fluorouracil (5-FU)/cisplatin with the combination tegafur and uracil (UFT)/cisplatin in the neoadjuvant treatment of locally advanced-stage III or IV (M0)-head and neck
Overexpression by the HER2 gene plays a significant role in breast cancer pathogenesis, and the phenomenon is commonly regarded as a predictor of a poor prognosis. HER2 overexpression has been linked to sensitivity and/or resistance to hormone therapy and chemotherapeutic regimens, including CMF (cyclophosphamide, methotrexate, and fluoro-uracil) and anthracyclines. Studies of patients with advanced disease demonstrate that, despite the association of HER2 overexpression with poor prognosis, the odds of HER2-positive patients responding clinically to taxanes were greater than three times those of HER2-negative patients. Further studies in preclinical models used combination therapy for breast cancer cells that overexpress HER2, and the use of agents that interfere with HER2 function plus paclitaxel (Taxol) resulted in significant antitumor effects. [ONCOLOGY 11(Suppl):43-48, 1997]
We previously reported that “in vivo purging” with rituximab (Rituxan) during stem-cell collection is safe and does not adversely affect engraftment. We now report on our transplant experience with rituximab. From June 1998 to December
At the 2000 Annual Meeting of the American Society of Hematology, we presented the benefits of rituximab (Rituxan) combined with CHOP (cyclophosphamide [Cytoxan, Neosar], doxorubicin HCl, vincristine [Oncovin], prednisone), known as R-CHOP, in comparison with CHOP alone for the treatment of elderly patients with diffuse large B-cell lymphoma (DLCL).
The side effects commonly experienced by patients receiving chemotherapy for the treatment of cancer can challenge many aspects of daily life. Nausea and vomiting, the most common side effects reported by patients, affect the ability to continue with usual life activities and, thus have a pronounced impact on quality of life.
From March 1996 to March 1998, 106 patients with untreated metastatic breast cancer (MBC) were treated with docetaxel (Taxotere) (100 mg/m²) and doxorubicin (75 mg/m²) on an alternating cycle-by-cycle (doxorubicin, docetaxel, doxorubicin, etc) or sequential (four cycles of docetaxel, then four cycles of doxorubicin) basis, every 3 weeks, for a maximum of eight cycles.
This phase II study aimed to evaluate the tolerability and activity of the monoclonal anti-CD20 antibody rituximab (Rituxan) in patients with either untreated or relapsed biopsy-proven extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) type, with measurable or evaluable disease.
In this interview we discuss predictive biomarkers and response to immune checkpoint inhibitors for urothelial tumors, which include tumors of the bladder, ureters, and the renal pelvis.
Radiation therapy (RT) is an important treatment modality for multiple thoracic malignancies. Incidental irradiation of the lungs, which are particularly susceptible to injury, is unavoidable and often dose-limiting. The most radiosensitive subunit of the lung is the alveolar/capillary complex, and RT-induced lung injury is often described as diffuse alveolar damage. Reactive oxygen species generated by RT are directly toxic to parenchymal cells and initiate a cascade of molecular events that alter the cytokine milieu of the microenvironment, creating a self-sustaining cycle of inflammation and chronic oxidative stress. Replacement of normal lung parenchyma by fibrosis is the culminating event. Depending on the dose and volume of lung irradiated, acute radiation pneumonitis may develop, characterized by dry cough and dyspnea. Fibrosis of the lung, which can also cause dyspnea, is the late complication. Imaging studies and pulmonary function tests can be used to quantify the extent of lung injury. While strict dose-volume constraints to minimize the risk of injury are difficult to impose, substantial data support some general guidelines. New modalities such as intensity-modulated radiation therapy and stereotactic body radiation therapy provide new treatment options but also pose new challenges in safely delivering thoracic RT.
The science supporting molecularly targeted therapies for the treatment of patients with solid tumors continues to evolve. Nurses are challenged to understand cell signaling, molecular targeting, and the mechanism of action of targeted agents. Two cell signal transduction pathways regulate the development, proliferation, and metastasis of solid tumors: the human epidermal growth factor (HER) receptor pathway and the vascular endothelial growth factor (VEGF) receptor pathway. Several novel pharmacologic agents with distinct indications and methods of administration target the HER and VEGF molecular pathways.
FDA approval of palliative chemotherapy is largely based on disease-free and overall survival, quality of life, and symptom reduction; the latter should be routinely measured by the treating oncologist. Physician assessments of symptoms underreport symptom severity compared to patient-reported symptom assessments.
One of the potential side effects of chemotherapy is cardiac toxicity. The resulting damage to the heart can range from non–life-threatening events to devastating heart failure. The spectrum of these events can occur almost immediately, during a drug infusion, or as a delayed complication later in the patient’s life. Oncology nurses not only need to be familiar with identifying and intervening in acute cardiac events, but also in some instances will need to monitor for delayed cardiac toxicities during the continuum of the patient’s life.