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1.
Psychooncology ; 31(6): 1041-1049, 2022 06.
Article in English | MEDLINE | ID: mdl-35112424

ABSTRACT

OBJECTIVE: One primary source of psychological distress in patients with cancer and their caregivers is uncertainty. However, the uncertainty trajectory and its relationship between older adults with advanced cancer and their caregivers have rarely been examined. This study describes the uncertainty trajectory in patient-caregiver dyads, explores the effect of geriatric assessment (GA) intervention on trajectory, and examines the interdependent relationship of uncertainty. METHODS: This secondary analysis used longitudinal data from a national cluster-randomized controlled trial examining a GA intervention compared to usual care. Participants completed the modified 9-item Mishel Uncertainty in Illness Scale at enrollment, 4-6 weeks, 3 months, and 6 months. The dyadic growth model and cross-lagged actor-partner interdependence model were used. RESULTS: A total of 397 dyads (patient age M = 76.81 ± SD5.43; caregiver age M = 66.69 ± SD12.52) were included. Both had a trend of decreased uncertainty over time (b = -0.16, p < 0.01). There was a greater decrease in uncertainty among caregivers in the GA group than those in the usual care group (b = -0.46, p = 0.02). For both patients and caregivers, their past uncertainty was a significant predictor of their own current uncertainty (i.e., actor effect, p < 0.01). The individual's past uncertainty was a significant predictor of the other dyad member's current uncertainty (i.e., partner effect, p < 0.05), indicating an interdependent relationship between patient and caregiver uncertainty over time. CONCLUSIONS: Findings suggest patient and caregiver function as a unit with uncertainty levels affecting each other. Future interventions could build on GA to address uncertainty for older patients with advanced cancer and caregivers.


Subject(s)
Caregivers , Neoplasms , Aged , Caregivers/psychology , Geriatric Assessment , Humans , Neoplasms/psychology , Neoplasms/therapy , Quality of Life/psychology , Uncertainty
2.
Ann Hematol ; 92(6): 719-30, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23494203

ABSTRACT

For more than 2,000 years, arsenic and its derivatives have shown medical utility. Owing to the toxicities and potential carcinogenicity of arsenicals, their popularity has fluctuated. The exact mechanism of action of therapeutic arsenic is not well characterized but likely to involve apoptosis, generation of reactive oxygen species, inhibition of intracellular transduction pathways, and cell functions. Arsenic trioxide has received approval for use in patients with relapsed acute promyelocytic leukemia for remission induction. Arsenic has additionally shown activity in a range of solid tumors, myelodysplastic syndrome, multiple myeloma, and in autoimmune diseases. The following is a review of the history of arsenic, its cellular metabolism, pharmacology, genetic basis of disposition, associated toxicities, and clinical efficacy.


Subject(s)
Antineoplastic Agents/therapeutic use , Arsenicals/therapeutic use , Neoplasms/drug therapy , Antineoplastic Agents/adverse effects , Antineoplastic Agents/pharmacology , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Arsenic Poisoning/diagnosis , Arsenic Poisoning/etiology , Arsenic Trioxide , Arsenicals/administration & dosage , Arsenicals/adverse effects , Arsenicals/pharmacology , Biotransformation/genetics , Biotransformation/physiology , Clinical Trials as Topic , Diabetes Mellitus, Type 2/chemically induced , Gastrointestinal Diseases/chemically induced , Gene Expression Regulation/drug effects , Heart Diseases/chemically induced , Humans , Leukemia, Promyelocytic, Acute/drug therapy , Leukocytosis/chemically induced , Metabolic Networks and Pathways/drug effects , Methyltransferases/genetics , Methyltransferases/metabolism , Neoplasms/chemically induced , Oxides/adverse effects , Oxides/therapeutic use , Reactive Oxygen Species/metabolism , Signal Transduction/drug effects , Treatment Outcome
3.
Support Care Cancer ; 20(11): 2865-72, 2012 Nov.
Article in English | MEDLINE | ID: mdl-22421738

ABSTRACT

BACKGROUND: The benefit of adding a vena cava filter to anticoagulation in treating cancer patients with venous thromboembolism remains controversial. We initiated this study as the first prospectively randomized trial to evaluate the addition of a vena cava filter placement to anticoagulation with the factor Xa inhibitor fondaparinux sodium in patients with cancer. METHODS: Sixty-four patients with deep vein thrombosis (86 %) and/or pulmonary embolism (55 %) were randomly assigned to receive anticoagulation with fondaparinux sodium with or without a vena cava filter. Endpoints included rates of complications by treatment arm, recurrent thromboembolism, complete resolution of thromboembolism, and survival rates. RESULTS: No patient had a recurrent deep vein thrombosis; two (3 %) patients had new pulmonary emboli, one in each randomized cohort. Major bleeding occurred in three patients (5 %). Two patients on the vena cava filter arm (7 %) had complications from the filter. Median survivals were 493 days in the anticoagulation only arm and 266 days for anticoagulation + vena cava filter (p < 0.57). Complete resolution of venous thromboembolism occurred in 51 % of patients within 8 weeks of initiating anticoagulation. CONCLUSIONS: No advantage was found for placement of a vena cava filter in addition to anticoagulation with fondaparinux sodium in terms of safety, recurrent thrombosis, recurrent pulmonary embolism, or survival in this prospective randomized trial evaluating anticoagulation plus a vena cava filter in cancer patients. Favorable complete resolution rates of thrombosis were observed on both study arms.


Subject(s)
Anticoagulants/therapeutic use , Polysaccharides/therapeutic use , Vena Cava Filters , Venous Thromboembolism/therapy , Aged , Aged, 80 and over , Anticoagulants/adverse effects , Combined Modality Therapy , Fondaparinux , Hemorrhage/chemically induced , Hemorrhage/epidemiology , Humans , Male , Middle Aged , Neoplasms/complications , Neoplasms/pathology , Polysaccharides/adverse effects , Prospective Studies , Recurrence , Survival Rate , Treatment Outcome , Vena Cava Filters/adverse effects , Venous Thromboembolism/pathology
4.
Clin Occup Environ Med ; 5(1): 117-37, x, 2006.
Article in English | MEDLINE | ID: mdl-16446258

ABSTRACT

Workplace exposures to carcinogens long have been associated with cancers, and corrective measures to limit exposures have resulted in reductions in such cancers and improved worker health. Some exposures are currently of historical interest, and many current or past exposures are associated with conflicting evidence as to causality. We present a brief overview of the effects of exposure to asbestos, tobacco, and other known carcinogens.


Subject(s)
Carcinogens/toxicity , Occupational Diseases/prevention & control , Occupational Exposure/adverse effects , Occupational Health , Smoking/adverse effects , Tobacco Smoke Pollution/adverse effects , Workplace , Asbestos/toxicity , Humans , Metals, Heavy/toxicity
5.
Med Clin North Am ; 88(6): 1655-75, xiii, 2004 Nov.
Article in English | MEDLINE | ID: mdl-15464119

ABSTRACT

Tobacco consumption has been clearly implicated in the causation of many cancer types, with irrefutable evidence to support the association in multiple organ systems. Tobacco cessation leads to reduced cancer risk and improved survival of those under treatment for their already established cancers. As understanding of the mechanisms by which tobacco products cause cancer increases, clinicians may be able to identify those at highest risk for tobacco-related malignancies and allow for more focused interventions toward risk reduction among current tobacco users. This article reviews the carcinogens present in tobacco products, the mechanisms by which tobacco causes cancer, and the various tumor types causally related to tobacco use.


Subject(s)
Neoplasms/etiology , Nicotiana/adverse effects , Smoking/adverse effects , Female , Humans , Male , Neoplasms/physiopathology , Ribonucleotide Reductases/antagonists & inhibitors , Tars/adverse effects , Nicotiana/chemistry , Tobacco Smoke Pollution/adverse effects
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