44 research outputs found
Prophylactic beclomethasone spray to the skin during postoperative radiotherapy of carcinoma breast: A prospective randomized study
Background and Aims: Radiation induced wet desquamation of skin in
carcinoma breast patients is a painful condition. In this study topical
beclomethasone dipropionate spray was used as prophylaxis with the
purpose of reducing risk of the wet desquamation of skin in irradiated
field. Materials and methods: Sixty patients of carcinoma breast were
planned for postoperative loco regional radiotherapy (50 Gy in 25
fraction over five weeks) were prospectively randomized into two groups
(1) steroid group-patients were advised to use beclomethasone
dipropionate spray in irradiated axilla from day one of radiotherapy,
(2) control group-patients were not allowed to use any topical agent in
irradiated area. Radiation induced skin reaction was noted in terms of
erythema, dry desquamation and wet desquamation weekly till end of
prescribed 50Gy dose of the radiation therapy. Statistical Method:
Chi-square test was used to see the statistical significance of the
difference in wet desquamation between two arms of the study.
Chi-square value and P -value was calculated for the difference of wet
desquamation in two study arms. Result: In steroid group 4/30 (13.33%)
patients developed wet desquamation of the axillary skin at the end of
the radiotherapy. For the control group, this figure was 11/30
(36.66%). The difference in wet desquamation of the axillary skin in
the two groups was statistically significant ( P -value= 0.0369).
Conclusion: Topical steroid (beclomethasone dipropionate spray) for
skin during radiotherapy significantly reduces the risk of wet
desquamation of the skin
2-Deoxy-D-Glucose Treatment Induces Ketogenesis, Sustains Mitochondrial Function, and Reduces Pathology in Female Mouse Model of Alzheimer's Disease
Previously, we demonstrated that mitochondrial bioenergetic deficits preceded Alzheimer's disease (AD) pathology in the female triple-transgenic AD (3xTgAD) mouse model. In parallel, 3xTgAD mice exhibited elevated expression of ketogenic markers, indicating a compensatory mechanism for energy production in brain. This compensatory response to generate an alternative fuel source was temporary and diminished with disease progression. To determine whether this compensatory alternative fuel system could be sustained, we investigated the impact of 2-deoxy-D-glucose (2-DG), a compound known to induce ketogenesis, on bioenergetic function and AD pathology burden in brain. 6-month-old female 3xTgAD mice were fed either a regular diet (AIN-93G) or a diet containing 0.04% 2-DG for 7 weeks. 2-DG diet significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, 2-DG treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that 2-DG induced a shift towards a non-amyloidogenic pathway. In addition, 2-DG increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF. Results of these analyses demonstrate that dietary 2-DG treatment increased ketogenesis and ketone metabolism, enhanced mitochondrial bioenergetic capacity, reduced β-amyloid generation and increased mechanisms of β-amyloid clearance. Further, these data link bioenergetic capacity with β-amyloid generation and demonstrate that β-amyloid burden was dynamic and reversible, as 2-DG reduced activation of the amyloidogenic pathway and increased mechanisms of β-amyloid clearance. Collectively, these data provide preclinical evidence for dietary 2-DG as a disease-modifying intervention to delay progression of bioenergetic deficits in brain and associated β-amyloid burden
Antiangiogenic Activity of 2-Deoxy-D-Glucose
During tumor angiogenesis, endothelial cells (ECs) are engaged in a number of energy consuming biological processes, such as proliferation, migration, and capillary formation. Since glucose uptake and metabolism are increased to meet this energy need, the effects of the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) on in vitro and in vivo angiogenesis were investigated.In cell culture, 2-DG inhibited EC growth, induced cytotoxicity, blocked migration, and inhibited actively forming but not established endothelial capillaries. Surprisingly, 2-DG was a better inhibitor of these EC properties than two more efficacious glycolytic inhibitors, 2-fluorodeoxy-D-glucose and oxamate. As an alternative to a glycolytic inhibitory mechanism, we considered 2-DG's ability to interfere with endothelial N-linked glycosylation. 2-DG's effects were reversed by mannose, an N-linked glycosylation precursor, and at relevant concentrations 2-DG also inhibited synthesis of the lipid linked oligosaccharide (LLO) N-glycosylation donor in a mannose-reversible manner. Inhibition of LLO synthesis activated the unfolded protein response (UPR), which resulted in induction of GADD153/CHOP and EC apoptosis (TUNEL assay). Thus, 2-DG's effects on ECs appeared primarily due to inhibition of LLOs synthesis, not glycolysis. 2-DG was then evaluated in two mouse models, inhibiting angiogenesis in both the matrigel plug assay and the LH(BETA)T(AG) transgenic retinoblastoma model.In conclusion, 2-DG inhibits endothelial cell angiogenesis in vitro and in vivo, at concentrations below those affecting tumor cells directly, most likely by interfering with N-linked glycosylation rather than glycolysis. Our data underscore the importance of glucose metabolism on neovascularization, and demonstrate a novel approach for anti-angiogenic strategies
Long term control of a maxillary sinus mucoepidermoid carcinoma with low dose radiation therapy: a case report
Targeting cancer metabolism: a therapeutic window opens
Genetic events in cancer activate signalling pathways that alter cell metabolism. Clinical evidence has linked cell metabolism with cancer outcomes. Together, these observations have raised interest in targeting metabolic enzymes for cancer therapy, but they have also raised concerns that these therapies would have unacceptable effects on normal cells. However, some of the first cancer therapies that were developed target the specific metabolic needs of cancer cells and remain effective agents in the clinic today. Research into how changes in cell metabolism promote tumour growth has accelerated in recent years. This has refocused efforts to target metabolic dependencies of cancer cells as a selective anticancer strategy.Burroughs Wellcome FundSmith Family FoundationStarr Cancer ConsortiumDamon Runyon Cancer Research FoundationNational Institutes of Health (U.S.
An appraisal of radiation therapy techniques for adjuvant and neoadjuvant therapy in gastric cancer
Case Report - Cutaneous Metastasis from Carcinoma of Tonsil
Hematogenous spread from carcinoma of tonsil is an uncommon event and
skin is an extremely rare site of metastasis. We encountered a 40 year
old male patient who initially presented with carcinoma of the tonsil
with T3N2cMO disease and treated by curative radiotherapy. After about
2 years, he developed a skin lesion in the periorbital region which on
cytological examination turned out to be metastasis from tonsillar
carcinoma. The present paper describes this rare case report along with
a brief review of the literature
Economic cost analysis in cancer management and its relevance today
The global cancer burden has shown a distinct shift in the last two
decades and its financial impact can be large, even among patients
living in high resource countries, with comprehensive health insurance
policies. It is hard to imagine its impact on patients of developing
countries where insurance policies exist infrequently and often cost
becomes the greatest barrier in availing cancer treatment. It is
recognized that these costs include the direct cost of disease
treatment and care, indirect costs accrued by the patient and the
family, and economic losses to the society as a whole. Economic cost
analysis or cost-effectiveness analysis has emerged as a basic tool in
the evaluation of health-care practices. To date, these cost data have
been collected only sporadically, even in the most developed countries,
and there is a great need for incorporating economic cost assessment
practices in developing countries, so that patients and their families
can access the care adequately. The current review has been done using
pubmed and medline search with keywords like cancer, cost-analysis,
cost-effectiveness, economic burden, medical cost, etc
Economic cost analysis in cancer management and its relevance today
The global cancer burden has shown a distinct shift in the last two
decades and its financial impact can be large, even among patients
living in high resource countries, with comprehensive health insurance
policies. It is hard to imagine its impact on patients of developing
countries where insurance policies exist infrequently and often cost
becomes the greatest barrier in availing cancer treatment. It is
recognized that these costs include the direct cost of disease
treatment and care, indirect costs accrued by the patient and the
family, and economic losses to the society as a whole. Economic cost
analysis or cost-effectiveness analysis has emerged as a basic tool in
the evaluation of health-care practices. To date, these cost data have
been collected only sporadically, even in the most developed countries,
and there is a great need for incorporating economic cost assessment
practices in developing countries, so that patients and their families
can access the care adequately. The current review has been done using
pubmed and medline search with keywords like cancer, cost-analysis,
cost-effectiveness, economic burden, medical cost, etc