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Pubmed
Journal: Current medicinal chemistry
October/26/2004
Abstract
Apoptosis (or programmed cell death) is a genetically controlled "cell suicide" pathway which plays an essential role in deleting excess, unwanted or damaged cells during development and tissue homeostasis. Dysregulation of apoptosis contributes to a wide variety of pathological conditions, including AIDS, cardiovascular disease, infectious disease, autoimmunity and neurodegenerative disorders. Resistance to apoptosis is also a common feature in human malignancies, contributing to both the development of cancer and resistance to conventional therapies such as radiation and cytotoxic drugs, which function by activating apoptotic cell death pathways. Bcl-2 is one of the best characterized cell death control proteins; its overexpression confers resistance to a broad range of apoptosis inducers and the cell survival functions of Bcl-2 are activated by translocation in lymphomas and overexpression in many other cancer types. A wealth of experimental data supports the idea that Bcl-2 is an attractive and tractable target for newer molecularly directed anti-cancer strategies, designed to promote cancer cell death. Here we review current understanding of the mechanism of action and importance of Bcl-2 in cancer cells and progress in developing new agents to target this key survival molecule.
Pubmed
Journal: Reproductive biomedicine online
December/29/2002
Abstract
Preimplantation genetic diagnosis (PGD) has recently been offered for couples with an inherited predisposition for late onset disorders. This paper presents the results of PGD for a group of couples at risk for producing children with cancer predisposition. Using a standard IVF procedure, oocytes or embryos were tested for different mutations predisposing to cancer, preselecting and transferring only mutation-free embryos back to the patients. The procedure was performed for patients with predisposition to familial adenomatous polyposis coli (FAP), Von Hippel-Lindau syndrome (VHL), retinoblastoma, Li-Fraumeni syndrome, determined by p53 tumour suppressor gene mutations, neurofibromatosis types I and II and familial posterior fossa brain tumour (hSNF5). Overall, 20 PGD cycles were performed for 10 couples, resulting in preselection and transfer of 40 mutation-free embryos, which resulted in five unaffected clinical pregnancies and four healthy children born by the present time. Despite the controversy of PGD use for late onset disorders, the data demonstrate the usefulness of this approach as the only acceptable option for at-risk couples to avoid the birth of children with an inherited predisposition to cancer, and to have a healthy child.
Pubmed
Journal: Current medicinal chemistry. Anti-cancer agents
July/27/2005
Abstract
The initial report of the therapeutic anticancer properties of a di-nuclear platinum complex in 1988 started a new paradigm in platinum based chemotherapy. Several multi-nuclear platinum complexes have entered clinical trials in recent years, with varying results. This group of charged complexes, consisting of di- and tri-nuclear compounds linked by aliphatic ligands, many with hydrogen bonding functionality, are able to overcome cisplatin and carboplatin resistance in many important human cancer cell lines. The adducts they form with DNA--which are, to some extent, affected by their pre-covalent association--are the reason for their increased cytotoxicity, and are distinctly different from those formed by cisplatin. Multi-nuclear platinum DNA adducts are broadly defined as flexible, non-directional and mainly interstrand cross-links. These complexes are also able to induce conformational changes in DNA, particularly the conversion from B-type to Z- and A-type. While these complexes are much more cytotoxic than cisplatin, they are also highly toxic. The maximum tolerated doses range from 0.006 to 1.1 mg/m(2) which is 10 to 100 fold lower than cisplatin. BBR3464 has shown in vivo activity at its MTD in several pre-clinical and clinical trials; however, recent phase II trials have shown that BBR3464, and other multi-nuclear platinum drugs, did not yield results substantially different from cisplatin, possibly due to their binding and degradation by human plasma proteins. This review will look at the success, and limitations, of multi-nuclear platinum drugs, and discuss their future potential as anti-cancer agents.
Pubmed
Journal: FEBS letters
July/14/2005
Abstract
Endocytosis is a versatile tool to regulate the intensity, localization, half-life and function of signaling complexes (signalosomes) that form in cells upon binding of growth factors, cytokines and morphogens to their cognate receptors. Endocytic adaptors are non-catalytic proteins that assemble effectors and structural components of the endocytic machinery around the trafficking cargo and serve as scaffolds for signalosomes, which in turn modify their location and activity by various post-translational modifications. We discuss how breakdowns in the function of endocytic adaptors might facilitate impairment of tissue homeostasis and consequent tumor development.
Pubmed
Journal: Blood
November/25/1993
Abstract
Interleukin-12 (IL-12) is a heterodimeric 70-kD cytokine that can enhance the activity of cytotoxic effector cells. Although IL-12 shares some functional properties with interleukin-2 (IL-2), it appears to act via a distinct mechanism. In this report, we examined the effects of IL-12 on the cytolytic activity and proliferation of peripheral blood mononuclear cells (PBMC) obtained from patients with malignant disease. PBMC from two groups of patients were evaluated. The first group consisted of 12 individuals with metastatic solid tumors. PBMC from these patients demonstrated a marked defect in their ability to lyse natural killer (NK)-sensitive targets (K562) compared with normal volunteers. Overnight incubation with IL-12 (35 pmol/L) corrected this defect. The effect of 35 pmol/L of IL-12 on cytotoxicity was similar to that of 3 nmol/L of IL-2. In contrast, this concentration of IL-12 had little effect on cytolytic activity against an NK-resistant cell line (COLO 205). When IL-12 was added to PBMC obtained from cancer patients who were being treated with low-dose IL-2 in vivo, a dramatic increase in cytolytic activity against both NK-sensitive and -resistant tumor targets was observed. Unlike IL-2, IL-12 failed to stimulate proliferation of resting PBMC from cancer patients significantly. The second group of patients we studied comprised 13 patients who had recently undergone allogeneic bone marrow transplantation (BMT) for hematologic malignancy. In resting PBMC from these transplant recipients, IL-12 was capable of enhancing cytotoxicity against both NK-sensitive and -resistant tumor targets. Our findings indicate that IL-12 can restore defective NK activity of PBMC from patients with metastatic cancer, as well as enhance cytolytic function of PBMC from patients after allogeneic BMT. The clinical use of IL-12 as an immunomodulator in patients with malignancy merits further consideration.
Pubmed
Journal: Klinische Padiatrie
October/20/1993
Abstract
OBJECTIVE
This study prospectively investigated the outpatient once daily therapy with ceftriaxone alone or if necessary in combination with teicoplanin, in the treatment of infections in children and adolescents with chemotherapy-induced neutropenia or aplastic anemia.
METHODS
42 patients 1-22 years of age suffering from solid tumors, hematological and oncological diseases, with clinical signs of infection, increased serum CRP (> 1 mg/dl) and/or fever above 38.5 degrees C and neutropenia (WBC count and/or ANC < 1 x 10(9)/l) were included in this outpatient based study. One important exclusion criterion was poor clinical condition with symptoms of septic shock.
METHODS
After bacterial, fungal and viral cultures had been obtained, single agent broad spectrum cephalosporin treatment was initiated with ceftriaxone applied once daily in a dose of 80 mg/kg body weight as short infusion over 30 min. Daily examinations included WBC, CRP, physical inspection and reassessment. In case of persistence or increase of fever and CRP, either outpatient management was carried on with teicoplanin added or patients were hospitalized and switched to combination antibiotic regimen.
RESULTS
There were 64 febrile episodes in 42 patients. Single agent once daily broad spectrum cephalosporin was adequate in 43/64 (67%) of infectious episodes in neutropenic patients. For persisting or increased fever or CRP elevation, 9 patients were treated with ceftriaxone and teicoplanin successfully. Thus hospitalized was avoided in 52/64 (81%) of infectious episodes.
Pubmed
Journal: Cytometry
March/13/1995
Abstract
The proliferation associated antigens, Ki-67 and proliferating-cell nuclear antigen (PCNA), have been widely used in studies assessing the growth fraction in human malignancies. It remains unclear, however, whether these markers yield similar assessments of proliferative activity in any given neoplasm. In this study, we compared Ki-67 and PCNA expression in 93 malignant solid neoplasms using bivariate flow cytometric analysis of these antigens and DNA content. The growth fractions measured by Ki-67 and PCNA were compared and correlated with acridine orange (AO) analysis and tumor grade. Our results indicate a significant difference between Ki-67 and PCNA values in neoplasms of low and intermediate grade (P = 0.002); Ki-67 values were significantly lower than those obtained by PCNA in this group. No statistical difference between Ki-67 and PCNA values was found in high grade neoplasms (P = 0.38). Analysis of different cell cycle compartments indicates that the observed difference in the positivity of these markers was due to their differential expression in the G0/1 segment of the cell cycle. We conclude that Ki-67 may better reflect the proliferative activity in solid neoplasms than does PCNA.
Pubmed
Journal: Nature communications
March/31/2014
Abstract
Intravital microscopy has been used extensively to study dynamic processes in the context of a living animal; however, only a limited number of fluorescent probes and mouse models are available. By contrast, many dyes and antibodies exist for the immuno-labelling of fixed tissue. Here we report a method that combines the advantages of histochemistry and in vivo imaging by correlating cryosection labelling with corresponding intravital microscopy images (CLIM). Using CLIM, we find that the presence of CD3(+) T cells correlates with mammary tumour cell migration. When CD4(+) and CD8(+) T-cell subsets are depleted, reduced tumour cell migration is observed. From these data we conclude that CLIM is a powerful tool to correlate intravital microscopy data with cryosection labelling data.
Pubmed
Journal: Drug news & perspectives
January/21/2008
Abstract
One of the major problems related with the curative treatment of cancer patients is resistance against anticancer drugs. This resistance, which may occur from the beginning or is evident only later as an acquired phenomenon, is due to the action of drug transporters. These transmembrane proteins belong to the ATP-binding cassette (ABC) transporters which reduce bioavailability of drugs, but also determine the elimination of xenobiotics into bile, urine and feces. The present review summarizes recent knowledge in this area, highlighting the mechanism of action of these transporters, its clinical significance and its possible modulation. Novel approaches to overcome multidrug resistance include agents which inhibit or circumvent this efflux mechanism. For the latter category developments in nanomedicine may be of consequence. However, in spite of considerable progress in research regarding multidrug resistance, the phase of efficacious clinical use of this knowledge has not been reached yet.
Pubmed
Journal: Molecules and cells
July/16/2012
Abstract
We have previously isolated dieckol, a nutrient polyphenol compound, from the brown alga, Ecklonia cava (Lee et al.,2010a). Dieckol shows both antitumor and antioxidant activity and thus is of special interest for the development of chemopreventive and chemotherapeutic agents against cancer. However, the mechanism by which dieckol exerts its antitumor activity is poorly understood. Here, we show that dieckol, derived from E. cava, inhibits migration and invasion of HT1080 cells by scavenging intracellular reactive oxygen species (ROS). H2O2 or integrin signal-mediated ROS generation increases migration and invasion of HT1080 cells, which correlates with Rac1 activation and increased expression and phosphorylation of focal adhesion kinase (FAK). Rac1 activation is required for ROS generation. Depletion of FAK by siRNA suppresses Rac1-ROS-induced cell migration and invasion. Dieckol treatment attenuated intracellular ROS levels and activation of Rac1 as well as expression and phosphorylation of FAK. Dieckol treatment also decreases complex formation of FAK-Src-p130C as and expression of MMP2, 9, and 13. These results suggest that the Rac1-ROS-linked cascade enhances migration and invasion of HT1080 cells by inducing expression of MMPs through activation of the FAK signaling pathway, whereas dieckol downregulates FAK signaling through scavenging intracellular ROS. This finding provides new insights into the mechanisms by which dieckol is able to suppress human cancer progresssion and metastasis. Therefore, we suggest that dieckol is a potential therapeutic agent for cancer treatment.
Pubmed
Journal: Nederlands tijdschrift voor geneeskunde
April/6/1994
Abstract
OBJECTIVE
To determine the prevalence of use of alternative cancer therapies, as well as the characteristics of the patients who use these therapies, and their experiences with them.
METHODS
Descriptive study.
METHODS
Outpatient departments of several hospitals in North-Holland.
METHODS
In total, 1091 patients were asked to participate in the study; 949 patients agreed (87%): 535 women (56%) and 414 men, with an average age of 62 years. The sample was stratified by diagnosis: 233 breast, 183 lung, 278 stomach/colon cancer and 255 patients with various other cancer diagnoses. A structured face-to-face interview and several written questionnaires were used.
RESULTS
2XOf the 949 patients, 9.4% were currently using an alternative therapy in addition to conventional treatment, and 5.8% had used an alternative treatment in the past but had subsequently stopped. Patients using alternative therapies were relatively younger and more highly educated than patients who chose not to use these therapies. Use of alternative therapies was more frequent among patients undergoing palliative treatment and patients who were actively dealing with the problems surrounding their disease. Only a minority of the patients believed they could be cured by the alternative therapy; the majority hoped it would help to slow the progression of their disease or strengthen their resistance.
CONCLUSIONS
The motivation for seeking alternative treatment more often appears to be fear and uncertainty rather than belief in the efficacy of the treatment. For many patients the use of alternative therapies represents a means of dealing with the anxiety and stress surrounding their disease.
Pubmed
Journal: European journal of cancer & clinical oncology
May/23/1988
Abstract
The quianazoline antifolate N10-propargyl-5,8-dideazafolic acid (ICI 155,387), an inhibitor of thymidylate synthetase (TS), was evaluated for clinical toxicity in a phase I trial. The compound was given once every week as a bolus injection. Fourteen patients with advanced cancer were treated at doses of 10-30 mg/m3. Four patients from the lowest to the highest dose developed severe renal toxicity, detected by a reversible decrease in the Cr-EDTA clearance. Hepatotoxicity was observed with transient elevations of alanine aminotransferase (ALT) in 10 patients and alkaline phosphatase in nine patients. Neither the incidence nor the severity of these toxicities was dose related. Two patients developed feelings of fatigue, which in one patient coincided with a decrease in Cr-EDTA clearance. No myelotoxicity, dermatological, gastrointestinal toxicity or mucositis was seen. No tumour responses due to ICI 155,387 occurred. The severity and the erratic nature of the renal side-effects suggest that this schedule cannot be recommended for further development of this compound in Phase II trials.
Pubmed
Journal: Annals of the New York Academy of Sciences
June/26/1988
Abstract
Our laboratories have been testing the basic concept that the age-dependent deterioration of the molecular components of living systems may be due in part to the biochemical effects of active oxygen species. The dysdifferentiation hypothesis of aging and cancer (DHAC) as well as the membrane hypothesis of aging (MHA) are discussed and compared to each other. These two hypotheses consider cellular mechanisms through which free radical-induced alterations may lead to the aging process. DHAC emphasizes the importance of the instability of the differentiated state of cells and how active oxygen species may interact with the genetic apparatus of cells, leading to improper gene regulation. The evidence supporting this hypothesis includes an age-dependent increase in the expression of specific genes that normally are expected to be repressed. Such evidence now includes the c-myc oncogene as well as an age-dependent decrease in the average methylation level of the entire genome in liver tissue of mice. The central concept of DHAC is that aging is a result of gene regulatory instability and that lifespan is governed by mechanisms acting to stabilize proper gene regulation. MHA is based on the concept that all cellular components are exposed to free-radical attacks, and that the damaging efficiency of the radicals is density-dependent. Compact structures like membranes are consequently more susceptible to damage than cytosolic components. In addition, the cell plasma membrane is exposed to another damaging effect called residual heat damage, which is due to the depolarization-induced discharge of the membrane during the action potential. MHA predicts that a key process of normal differentiation as well as aging is a continuous, age-dependent loss of the passive permeability of the cell membrane for potassium and probably also for water. This is due to a constant difference between the rates of damage and replacement of the membrane components and results in a gradual dehydration of the intracellular mass from the embryonic state to the aging state. The increasing intracellular density will eventually become rate-limiting for many different cellular functions, resulting in the cessation of growth and the beginning of aging. MHA also predicts an overall decrease of gene expression and protein turnover rate during aging. Pharmacological interventions on the cell membrane have supported the validity of MHA and have indicated specific mechanisms of how aging and dysdifferentiation may occur.
Pubmed
Journal: Oncology (Williston Park, N.Y.)
July/19/1994
Abstract
The ability to provide subcutaneous infusions in the home has had a major impact on patient care. The main indication for this approach in the cancer population is the need for prolonged parenteral administration of an opioid drug. Successful administration begins with proactive consideration of patient selection; choice of pump, drug, mode of infusion, and dosing schedule; the resources of the family and community health-care system; and cost and insurance coverage. Long-term management requires ongoing liaison among the hospital pain management team, home care infusion agency, and community physicians and nurses.
Pubmed
Journal: Cancer research
January/8/2012
Abstract
Cancer progression results from the accumulation of genetic and epigenetic alterations that provide tumor cells with a selective advantage. The consecutive cycles of mutations, selections, and clonal expansions generate, over time, descendant cells with increasing malignant properties. Although this conception of tumor development rests on solid experimental foundations, it has also raised several persisting questions. Does the succession of mutations dictate the progression of each cancer type or does the disturbance of an invariant set of regulatory circuits govern tumor evolution regardless of the linear order of genetic events? Is the ability of malignant cells to disseminate and spawn metastasis a property acquired at late stages of tumor development or is the proclivity to metastasize implanted early during cancer formation? Considering these issues, we elaborate here on the concept of co-option that refers to the emergence of novel functions from ancestral characters during episodes of organismal evolution. As discussed in this Perspective, co-option seems to be a key mechanism propelling the molecular engine that drives malignant transformation. Hence, this notion may constitute a unifying principle that connects a large body of experimental results to clinical observations.
Pubmed
Journal: Breast cancer (Tokyo, Japan)
April/25/2007
Abstract
This article reviews recent topics in health outcomes research. First, we discuss the concept and importance of 'subjective' assessment of quality of life (QOL), and introduce new guidance, by the respective medical product regulatory authorities in Europe and the United States, for labeling claims of medical products that are assessed for outcomes related to QOL. Second, we address the application of item response theory (IRT) in developing and assessing QOL measures to compensate for several drawbacks of the classical psychometric approach, which has been commonly used to verify the reliability and validity of QOL instruments. Third, the relevance and determination of the minimally clinically important difference (MID) of QOL scores is discussed. Finally, we address the so-called 'response shift' which may affect the reliability of analysis results of QOL scores in longitudinal studies such as randomized clinical trials.
Pubmed
Journal: Advances in enzyme regulation
September/29/2009
Pubmed
Journal: Biosensors & bioelectronics
September/29/2009
Abstract
In this paper, a highly sensitive, reagentless, electrochemical strategy is reported for the detection of a cancer biomarker-Vascular Endothelial Growth Factor (VEGF). Disc shaped carbon fiber microelectrodes were used as the immunosensor platform. Ferrocene monocarboxylic acid labeled anti-VEGF was covalently immobilized on the microelectrode surface using a Jeffamine cross-linker. The formation of immunocomplexes leads to a decrease in the electrochemical signal of ferrocene monocarboxylic acid owing to increased spatial blocking of microelectrode surface. These signal changes enable quantitative detection of VEGF in solution. Voltammetric measurements were conducted to evaluate the interfacial immunoreactions and to quantitatively detect VEGF biomarker. The proposed immunosensing strategy allows a rapid and sensitive means of VEGF analysis with a limit of detection of about 38 pg/mL. This opens up the possibility of employing these electrodes for various single cell analysis and clinical applications. Further, experimental conditions such as concentration of the immobilized antibodies and incubation period were optimized. Following this, the stability and specificity of the immunosensors were also evaluated.
Pubmed
Journal: International journal of cancer
March/26/1989
Abstract
In accordance with a previous analysis of US cancer mortality, this report also indicates that cancer mortality in the FRG over the last 3 decades (1952-1985) has not shown any decline commencing in a given period and prevailing in all age groups. If present, such effects could have been interpreted as a manifestation of improvements associated with cancer treatment. The absence of such an effect, derived by using data up to 1985 and age-specific mortality rates, supports the view expressed in the US analysis that improvements in cancer treatment are unlikely to have an impact on overall cancer mortality statistics and that efforts toward prevention may be more rewarding.
Pubmed
Journal: The Journal of nutrition
August/4/1986
Authors
Pubmed
Journal: Cancer research
April/11/2007
Abstract
Chloroethylureas (CEU) are soft alkylating agents that covalently bind to beta-tubulin (betaTAC) and affect microtubule polymerization dynamics. Herein, we report the identification of a CEU subset and its corresponding oxazolines, which induce cell growth inhibition, apoptosis, and microtubule disruption without alkylating beta-tubulin (N-betaTAC). Both betaTAC and N-betaTAC trigger the collapse of mitochondrial potential (DeltaPsi(m)) and modulate reactive oxygen species levels, following activation of intrinsic caspase-8 and caspase-9. Experiments using human fibrosarcoma HT1080 respiratory-deficient cells (rho(0)) and uncoupler of the mitochondrial respiratory chain (MRC) showed that betaTAC and N-betaTAC impaired the MRC. rho(0) cells displayed an increased sensitivity toward N-betaTAC as compared with rho(+) cells but, in contrast, were resistant to betaTAC or classic chemotherapeutics, such as paclitaxel. Oxazoline-195 (OXA-195), an N-betaTAC derivative, triggered massive swelling of isolated mitochondria. This effect was insensitive to cyclosporin A and to Bcl-2 addition. In contrast, adenine nucleotide translocator (ANT) antagonists, bongkrekic acid or atractyloside, diminished swelling induced by OXA-195. The antiproliferative activities of the N-betaTACs CEU-025 and OXA-152 were markedly decreased in the presence of atractyloside. Conversely, pretreatment with cyclosporin A enhanced growth inhibition induced by betaTAC and N-betaTAC. One of the proteins alkylated by N-betaTAC was identified as the voltage-dependent anion channel isoform-1, an ANT partner. Our results suggest that betaTAC and N-betaTAC, despite their common ability to affect the microtubule network, trigger different cytotoxic mechanisms in cancer cells. The role of mitochondria in these mechanisms and the potential of N-betaTAC as a new therapeutic approach for targeting hypoxia-resistant cells are discussed.
Pubmed
Journal: Cancer
May/16/1985
Abstract
The association of radiotherapy (RT) and chemotherapy (CT) constitutes one of the main avenues for research in therapeutic oncology. This association has two aims: (1) increase in control rate of primary tumor (this requires either the potentiation of one of the two modalities by the other or the additivity of their effect on tumor cells without a parallel increase in the toxic effects on critical normal tissues); (2) spatial cooperation (RT being used for the control of the primary tumor or of the sanctuaries, and CT for the control of the disseminated disease). In these two strategies, RT and CT should be given up to full doses in order to be effective. The main risk is an increase in the number and severity of the early and late side effects. To circumvent this problem, two possibilities are being explored: (1) use of drugs without serious toxic effects on those critical tissues which are included in the irradiated volume; and (2) avoidance of concomitant administration and introduction of a sufficiently long-time gap between the completion of one modality and initiation of the other. However, in such sequential treatment, a delay of CT until after the completion of RT, or an interruption of CT cycle during the course of RT, allows the occult metastases to increase in size; a similar delay in initiation of RT is also detrimental, as drugs are often not effective on bulky tumors. Moreover, under CT, the cells which are resistant to the cytotoxic drugs may disseminate and initiate chemoresistant metastases. Taking these disadvantages into account, a treatment protocol was proposed in 1980 in which CT and RT are given alternately, without undue delay. Chemotherapy is started with the usual scheduling of one cycle every month. Radiotherapy courses are interdigitated between CT cycles. Each course is initiated 1 week after interrupting CT and continued until 1 week before beginning the subsequent cycle of chemotherapy, and so on until completion of RT. Such split-course RT should have an effect on a tumor comparable to that of a conventional fractionation. This protocol has been used on 24 patients with non-Hodgkin's lymphoma (NHL) of diffuse histology, and 63 patients with small cell carcinoma of the lung. The 2-year relapse-free survivals are promising (in clinical stage II NHL of diffuse histology, 75%; and in small cell lung carcinomas, 33%).(ABSTRACT TRUNCATED AT 400 WORDS)
Pubmed
Journal: Current pain and headache reports
August/3/2014
Abstract
Cancer pain is a well-documented and prevalent healthcare problem, with current treatment strategies often failing to achieve acceptable efficacy. One of the major difficulties in treating cancer pain owes to the complex interplay between the cancer microenvironment, cancer therapy, and the body's own responses to these biochemical changes. A better understanding of the molecular pathways of nociception that are activated during cancer progression and treatment is necessary for better pain management and increased quality of life. This article reviews the current research that implicates oxidative stress as an important target for attenuating cancer pain. Sources of oxidative stress are first established, followed by a discussion of the various pathways that are affected by oxidative stress and that ultimately cause cancer pain.
Pubmed
Journal: Journal of cancer survivorship : research and practice
January/29/2015
Abstract
OBJECTIVE
The purpose of the study was to validate the Taiwanese version of the Physical Activity Scale for the Elderly (PASE-T) and to assess physical activity in Taiwanese cancer survivors.
METHODS
One hundred twenty-seven cancer survivors participated in this study. Instruments consisted of the PASE-T, the Taiwanese version of the MD Anderson Symptom Inventory (MDASI-T), Karnofsky performance status (KPS), and actigraph. Reliability was assessed by calculating the test-retest reliability. The validity was assessed by the content validity, criterion-related validity, convergent validity, and known-group validity.
RESULTS
The test-retest reliability of PASE-T was 0.90 over a 2-week interval, based on a sample of 30 patients. The content validity index was very acceptable at 0.91. Convergent validity was demonstrated by its significant association with MDASI-T scores (symptom severity: r = -0.23, p = 0.001; symptom interference: r = -0.21, p = 0.001) and KPS scores (r = 0.59, p < 0.001). Criterion-related validity was established by a significant relationship to the actigraph total counts per minute (r = 0.64, p < 0.001). Known-group validity was established by its ability to detect significant differences according to a patient's performance status. Moreover, KPS (β = 0.37), fatigue (β = -0.32), and age (β = -0.20) were significant predictors of physical activity (R(2) = 0.46).
CONCLUSIONS
The PASE-T is a reliable and valid instrument for measurement of physical activity among cancer survivors in Taiwan.
CONCLUSIONS
This scale could be a useful measure of physical activity in cancer survivors and subsequently facilitate the quality of oncology care.
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