Masses In Cancer Patients Research Articles

Xanthogranulomatous Ureteritis: A Diagnostic Challenge in a Patient with Bladder Cancer.

Xanthogranulomatous ureteritis is a very rare process characterized by the presence of foamy histiocytes in a background of chronic active inflammation affecting the ureteral wall. Herein, we describe a case of a 64-year-old man with bladder cancer affecting the left posterolateral wall of the bladder. Radiologically, there was a suspicion of multifocal involvement of the ureteral wall. The patient underwent a radical cystectomy with bilateral pelvic lymphadenectomy and a laparoscopic left nephroureterectomy. Histopathologic examination of the radical cystectomy revealed an invasive high-grade urothelial carcinoma. The wall of the left ureter was replaced by abundant foamy histocytes and a mixed inflammatory infiltrate with lymphocytes and plasma cells consistent with xanthogranulomatous ureteritis. In this report, we highlight the importance of awareness of this benign process when observing a ureteral mass in cancer patients.

Effect of Ketogenic Diets on Cardio-Metabolic Outcomes in Cancer Patients: A Systematic Review and Meta-Analysis of Controlled Clinical Trials

In this systematic review and meta-analysis of clinical controlled trials (CCTs) we aimed to investigate the efficacy of KDs as an adjuvant therapy on cardiometabolic outcomes in patient with cancer compared to conventional non-ketogenic diets. Only CCTs involving cancer patients that were assigned to either a KD or a standard diet control group were selected. Two reviewers independently extracted the data, and a meta-analysis was performed using a random effects model to estimate weighted mean differences (WMDs) and confidence intervals (CIs) in body composition, metabolite, lipid profile, liver and kidney function parameters and quality of life. This meta-analysis showed a significant reduction in body weight (WMD= −2.99 kg; 95% CI: −4.67, −1.31; and P < 0.001), BMI (WMD= −1.08 kg/m2; 95% CI: −1.81, −0.34; P ≤ 0.002) and fat mass (WMD= −1.48 kg; 95% CI: −2.56, −0.40; and P = 0.007) by a KD. KDs significantly decreased glucose (WMD= −5.22 mg/dl; 95% CI: −9.0, −1.44; and P = 0.007), IGF-1 (WMD= −17.52 ng/ml; 95% CI: −20.24, −14.8; and P ˂0.001) and triglyceride (WMD= −24.46 mg/dl; 95% CI: −43.96, −4.95; and P = 0.014) levels. Furthermore, KDs induced ketosis by increasing β-hydroxybutyrate (WMD= 0.56 mmol/l; 95% CI: 0.37, 0.75; and P < 0.001). There were non-significant pooled effects of KDs on improving insulin, C-reactive protein and cholesterol levels and kidney and liver function. Emotional functioning was even increased significantly in the KD compared to the SD groups. In summary we found that KDs result in a greater reduction in glucose, IGF-1, triglycerides, body weight, BMI, and fat mass in cancer patients compared to traditional non-ketogenic diets and improved emotional functioning. The quality of evidence in the meta-analysis was moderate according to the Nutrigrade assessment.

Effects of omega-3 supplementation on lean body mass in cancer patients: a systematic review and meta-analysis.

Omega-3 fatty acids are bioactive nutrients with the potential to preserve lean body mass in individuals with cancer. This study aimed to review the literature on randomized clinical trials that evaluated the effects of omega-3 supplementation on lean body mass in cancer patients. As secondary objectives, we evaluated the effects of omega-3 supplementation on body mass index (BMI) and body weight. We conducted a systematic review and meta-analysis in the following databases: Pubmed, LILACS, Scielo, Scopus, Web of Science, Cochrane, and Embase. It included randomized clinical trials that investigated the effects of omega-3 supplementation on lean body mass in cancer patients. Observational studies, animal experiments, studies carried out with healthy humans, and non-randomized clinical trials were excluded. We utilized the Cochrane scale to assess the quality of the studies. A meta-analysis was carried out to evaluate the effect of omega-3 on lean body mass, BMI, and body weight. Fourteen studies were included, of which four showed significant results from omega-3 supplementation for lean body mass. In the meta-analysis, omega-3 fatty acids increased lean body mass by 0.17 kg compared to placebo, but without significant differences between the groups [SMD: 0.17; CI 95%: -0.01, 0.35; I2 = 41%]. For body weight, omega-3 showed a statistically significant effect [SMD: 0.26; CI 95%: 0.06, 0.45; I2 = 46%], whereas for BMI the results were not significant. This systematic review and meta-analysis showed no statistically significant effect from omega-3 on lean body mass and BMI. On the other hand, there was a statistical significance for body weight.

Efficacy of resistance training during adjuvant chemotherapy and radiation therapy in cancer care: a systematic review and meta-analysis.

To determine the effect of resistance training during adjuvant chemotherapy and radiation therapy in cancer patients on measures of lean mass and muscle strength. Secondary aims were to analyse the prescription and tolerability of supervised resistance training in this population. EMBASE, Medline, CINAHL, Cochrane Library and Web of Science were searched from inception until 29 March 2021. Eligible randomised controlled trials (RCTs) examining supervised resistance training > 6 weeks duration during adjuvant chemotherapy and/or radiation therapy in cancer patients with objective measurement of muscle strength and/or lean mass were included. The meta-analysis was performed using Revman 5.4. A total of 1910 participants from 20 articles were included (mean age: 54 years, SD = 10) and the majority were female (76.5%). Resistance training was associated with a significant increase in upper body strength (standardised mean difference (SMD) = 0.57, 95% CI 0.36 to 0.79, I2 = 64%, P < 0.0001), lower body strength (SMD = 0.58, 95% CI 0.18 to 0.98, I2 = 91%, P = 0.005), grip strength (mean difference (MD) = 1.32, 95% CI 0.37 to 2.27, I2 = 0%, P < 0.01) and lean mass (SMD = 0.23, 95% CI 0.03 to 0.42, I2 = 0%, P = 0.02). A P value of < 0.05 was considered statistically significant. The quality of the studies included was moderate to high with low risk of bias as per the PEDro scale. Resistance training is an effective adjunct therapy to improve muscle strength and lean mass in cancer patients undergoing chemotherapy and/or radiation therapy. CRD42020180643.

Muscle hypertrophy in cancer patients and survivors via strength training. A meta-analysis and meta-regression.

Muscle wasting has a negative effect on treatment toxicity and cancer prognosis. Resistance training appears to be a promising approach to counteract the loss of muscle mass. Pubmed, Cochrane Library, SportDiscus and CINAHL. Randomized controlled resistance training trials with cancer survivros where eligible if lean body mass (LBM) or muscle mass were assessed. A total of 34 trials were included into the primary analysis. Compared to the control individuals, the intervention groups show a superiority in LBM of 0.85 kg (95 % CI = 0.26-1.43, p = .004). Isolated, the participants in the intervention groups show an increase in LBM of 0.51 kg (95 % CI = -0.05-1.06, p = .072); the control groups displayed a decrease of -0.59 kg (95 % CI= -1.04 to 0.06, p = .078). Supervision displayed an mediating role. Resistance training can counteract the loss of muscle mass in cancer patients. Especially in a supervised setting.

Structural Transcatheter Cardiac Interventions in the Cardio-Oncology Population

Modern cancer therapies have resulted in prolonged survival and decreased mortality for many types of cancer. Consequently, cancer patients with concomitant cardiovascular disease (CVD) present prior to diagnosis of cancer, resulting from various forms of cancer therapy, or developing after cancer remission are at higher risk for development of cardiovascular-associated morbidity and mortality. Management of CVD, particularly structural heart disease, in this patient population is challenging and associated with elevated surgical risk. Minimally invasive transcatheter procedures have emerged as lower risk treatment modalities that have been shown to be safe and efficacious. This review will evaluate the current literature on percutaneous management of aortic stenosis (AS), mitral regurgitation (MR), tricuspid regurgitation (TR), and intracardiac thrombus (ICTE) or masses in cancer patients. Multiple cohort- and registry-based studies have demonstrated safe and efficacious implementation of transcatheter interventions for the management of severe AS and MR in cancer patients. The development of transcatheter interventions for severe TR is promising and may also be considered for this high-risk patient population. Interestingly, management of ICTE and cardiac masses has also been achieved with a novel transcatheter approach. While a multidisciplinary heart team approach is necessary to properly manage cancer patients with structural heart disease and ICTE, more robust registry-based and prospective clinical trials are required to meet the needs of a rapidly growing cardio-oncology patient population.

Abstract MP131: The CDK2-FOXO1 Axis Mediates Doxorubicin-induced Cardiomyocyte Apoptosis and Atrophy

Recent clinical investigations indicate that anthracycline-based chemotherapy induces early declines in heart mass in cancer patients. A decline in heart mass can be caused by a decrease in cardiac cell number due to exaggerated cell death, and/or a reduction in cell size via atrophy. Our previous study reveals that the anthracycline doxorubicin (DOX) induces apoptotic death of cardiomyocytes through activation of cyclin-dependent kinase 2 (CDK2). However, the signaling pathway downstream of CDK2 remains to be characterized. In addition, it is unclear whether the same pathway also mediates cardiac atrophy. Here we demonstrated that DOX exposure induced CDK2-dependent phosphorylation of forkhead box O1 (FOXO1) at S249, leading to transcription of its pro-apoptotic target gene Bim. In cultured cardiomyocytes, treatment with the small molecule FOXO1 inhibitor AS1842856, or transfection with FOXO1-specific siRNAs protected against DOX-induced apoptosis and mitochondrial damage. Oral administration of AS1842856 in mice hindered apoptosis and prevented DOX-induced decline in left ventricular systolic function. Intriguingly, pharmacologic inhibition of FOXO1 also attenuated DOX-induced cardiac atrophy, likely due to repression of MuRF1, a pro-atrophic FOXO1 target gene. In conclusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyocyte apoptosis and atrophy. Our results identify FOXO1 as a promising drug target for DOX-induced cardiotoxicity. FOXO1 inhibitors may represent a novel class of therapeutics for cardioprotection during chemotherapy.

The Impact of Protein Supplementation Targeted at Improving Muscle Mass on Strength in Cancer Patients: A Scoping Review.

Deterioration of muscle strength during cancer results in functional limitation, poor quality of life and reduced survival. The indirect effects on muscle strength of nutritional interventions based on protein and amino acid derivatives targeted at improving muscle mass are poorly documented. A scoping review was performed to examine the available evidence on the effects of proteins, amino acids and their derivatives on muscle strength in adult cancer patients. Pubmed and Scopus databases were searched to identify research articles published in the last 10 years. Fourteen studies met the inclusion criteria, showing that changes in muscle strength following protein or amino acid supplementation are generally concordant with those in muscle mass in cancer patients. Administration of both energy and proteins in the presence of reduced oral intakes results in more robust effects on both muscle strength and mass. It is not clear whether this is due to the correction of the energy deficit or to an interaction between proteins and other macronutrients. The optimal mixture, type, and dose of amino acid/protein supplementation alone or in combination with other anabolic strategies should be determined to provide the best nutritional approach in cancer.

Asprosin is associated with anorexia and body fat mass in cancer patients.

Increasing evidence suggests that many adipokines are involved in cancer-related anorexia and cachexia syndrome (CACS), although the underlying mechanism remains to be clarify. Asprosin is a new peptide hormone mainly secreted by white adipose tissues that can increase appetite and body weight. In this cross-sectional study, we tested whether asprosin may intervene in the development of CACS. The fasting plasma asprosin levels were determined via enzyme-linked immune-sorbent assay. Anorexia was determined using the anorexia/cachexia subscale (A/CS) of the functional assessment of anorexia/cachexia therapy (FAACT) questionnaire. The body composition was assessed using bioelectrical impedance analysis. The association of plasma asprosin with anorexia, cachexia, and nutritional status was analyzed. One hundred twenty treatment-naïve patients with pathological confirmed gastrointestinal or lung cancer and 14 mild gastritis patients were recruited. We found no significant difference in asprosin levels between subgroups of patients by age, sex, cancer types or stage. Correlation analysis suggested that asprosin levels were positively associated with body fat mass (r = 0.248, p = 0.043). No correlations were found between asprosin levels and hemoglobin, white blood cell count, blood platelet count, albumin, C-reactive protein, glucose, cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, body mass index, body fat percentage, protein, skeletal muscle, muscle mass, lean body mass, and basal metabolic rate. Furthermore, asprosin levels were not significantly different between patients with or without cachexia. However, patients with anorexia had significantly lower asprosin levels compared with patients without anorexia. No significant difference in asprosin levels between gastritis and gastric cancer patients. Similarly, no significant change of asprosin levels occurred postoperatively in 10 gastric cancer patients. Patients with anorexia had significantly lower asprosin levels compared with patients without anorexia. We therefore speculated that asprosin might intervene in the development of cancer anorexia and serve as a potential therapeutic target.

Creatinine-to-cystatin C ratio and bioelectrical impedance analysis for the assessement of low lean body mass in cancer patients: Comparison to L3-computed tomography scan.

Lean body mass (LBM) is an important prognostic factor in patients with cancer. Although the L3-computed tomography (CT) scan is considered a reference method for assessment, a convenient and easily available method for longitudinal follow-up is required. Although bioelectrical impedance analysis (BIA) is widely used, its accuracy is questioned; plasma creatinine-to-cystatin C (CC) ratio could be an attractive alternative. The aim of this study was to evaluate the ability of the CC ratio and BIA to detect myopenia in patients with cancer compared with the use of the CT scan as a standard. Patients with any kind of cancer had body composition evaluation by CT scan, BIA, and CC. Statistical analysis included correlation test, Bland-Altman, and receiver operating characteristic curve analysis. Forty-four patients (14 women) were included. Of the participants, 59% had myopenia on CT scan. Both BIA LBM and CC ratio were well correlated with CT scan LBM (r=0.763 and 0.648, respectively) but concordance analysis revealed a 3-kg constant bias toward BIA compared with CT scan. In terms of ability to detect myopenia, areas under the curve (AUC) for BIA were 0.675 and 0.388 for men and women, respectively. For CC ratio, AUCs were 0.813 and 0.673. This study demonstrated that LBM assessed by the CC ratio or BIA is well correlated with that determined by L3-CT scan. The ability of the CC ratio to detect myopenia was better than that of BIA. Findings from the present study demonstrated that CC ratio can be conveniently used in patients with cancer as a reliable biomarker of muscularity.

MicroRNAs as potential therapeutic targets for muscle wasting during cancer cachexia

Muscle wasting in cancer cachexia remains an unmet clinical need due to lack of effective therapies associated with the complexity of the disease. Here, we discuss microRNAs, robust regulators of the expression of multiple genes, only recently characterized in cancer cachexia in humans and their therapeutic potential for muscle wasting. Changes in microRNAs in muscle of cancer patients have been demonstrated for the first time and these are associated with dysregulated signalling networks during muscle wasting. These data, together with studies in animal models, indicate that microRNAs are attractive therapeutic candidates for maintaining muscle mass, both during and following cancer treatment ultimately improving patient outcomes. Cancer cachexia is a complex metabolic condition associated with muscle wasting. Maintenance of muscle mass in cancer patients can improve their response to therapy and prognosis. microRNAs, which can act as oncogenes or tumour suppressors, are also dysregulated in muscle of cachexia patients. Studies in animal models of muscle wasting have demonstrated that microRNAs regulate muscle mass and strength. With more microRNA-based therapeutics in clinical trials and first RNA drugs approved, microRNAs present an attractive novel therapeutic avenue for maintaining muscle homeostasis in cachexia patients to improve their prognosis.

May an adrenal incidentaloma change its nature?

Up to 70% of adrenal masses detected in patients affected by extra-adrenal malignancy are metastatic lesions. Therefore, detection of an adrenal mass in patients with active or previous malignancy requires a careful differential diagnostic workup. 18F-Fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) is increasingly being used to determine the malignant potential of adrenal lesions. We report the case of a 64-year-old man who had a single adrenal metastasis due to non-small-cell lung carcinoma developing on a pre-existing benign adrenal lesion. This metastasis occurred in a phase of perceived oncological remission and was detected thanks to 18F-FDG-PET/CT showing a focal adrenal uptake. Contrast-enhanced computed tomography (CT), performed as part of oncological follow-up, and MRI with chemical shift sequences did not lead to the correct diagnosis. The patient underwent laparoscopic adrenalectomy and the pathological evaluation confirmed a lung carcinoma metastasis. The present case highlights the peculiarity of the follow-up of adrenal masses in cancer patients and the primary role of 18F-FDG-PET/CT in the management of such patients.

Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2–mediated activation of forkhead box O1

Recent clinical investigations indicate that anthracycline-based chemotherapies induce early decline in heart mass in cancer patients. Heart mass decline may be caused by a decrease in cardiac cell number because of increased cell death or by a reduction in cell size because of atrophy. We previously reported that an anthracycline, doxorubicin (DOX), induces apoptotic death of cardiomyocytes by activating cyclin-dependent kinase 2 (CDK2). However, the signaling pathway downstream of CDK2 remains to be characterized, and it is also unclear whether the same pathway mediates cardiac atrophy. Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2-interacting mediator of cell death (Bim). In cultured cardiomyocytes, treatment with the FOXO1 inhibitor AS1842856 or transfection with FOXO1-specific siRNAs protected against DOX-induced apoptosis and mitochondrial damage. Oral administration of AS1842856 in mice abrogated apoptosis and prevented DOX-induced cardiac dysfunction. Intriguingly, pharmacological FOXO1 inhibition also attenuated DOX-induced cardiac atrophy, likely because of repression of muscle RING finger 1 (MuRF1), a proatrophic FOXO1 target gene. In conclusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyocyte apoptosis and atrophy. Our results identify FOXO1 as a promising drug target for managing DOX-induced cardiotoxicity. We propose that FOXO1 inhibitors may have potential as cardioprotective therapeutic agents during cancer chemotherapy.

Impact of regular enteral feeding via jejunostomy during neo-adjuvant chemotherapy on body composition in patients with oesophageal cancer.

BACKGROUNDMalnourishment and sarcopenia are well documented phenomena in oesophageal cancer. Patients undergoing neo-adjuvant chemotherapy prior to oesophagectomy have complex nutritional needs.AIMTo examine the effect of regular nutritional support via feeding jejunostomy on overall body composition in patients undergoing neo-adjuvant chemotherapy prior to oesophagectomy for oesophageal cancer.METHODSRetrospective data were collected for 15 patients before and after neo-adjuvant chemotherapy. All patients had feeding jejunostomies inserted at staging laparoscopy prior to neo-adjuvant chemotherapy and underwent regular jejunostomy feeding. Changes in body composition were determined by analysis of computed tomography imaging.RESULTSPatient age was 61.3 ± 12.8 years, and 73% of patients were male. The time between start of chemotherapy and surgery was 107 ± 21.6 d. There was no change in weight (74.5 ± 14.1 kg to 74.8 ± 13.1 kg) and body mass index (26.0 ± 3.8 kg/m2 to 26.1 ± 3.4 kg/m2). Body composition analysis revealed a statistically significant decrease in lumbar skeletal muscle index despite regular feeding (45.8 ± 8.0 cm2/m2 to 43.5 ± 7.3 cm2/m2; P = 0.045). The proportion of sarcopenic patients increased (33.3% to 60%). Six patients (40%) experienced dose-limiting toxicity during chemotherapy.CONCLUSIONRegular jejunostomy feeding during neo-adjuvant chemotherapy can maintain weight and adipose tissue. Feeding alone is not sufficient to maintain muscle mass. Further insight into the underlying processes causing reduced muscle mass in cancer patients may help to provide targeted interventions.

IL-8 Released from Human Pancreatic Cancer and Tumor-Associated Stromal Cells Signals through a CXCR2-ERK1/2 Axis to Induce Muscle Atrophy.

Tumor-derived cytokines are known to drive the catabolism of host tissues, including skeletal muscle. However, our understanding of the specific cytokines that initiate this process remains incomplete. In the current study, we conducted multiplex analyte profiling of cytokines in conditioned medium (CM) collected from human pancreatic cancer (PC) cells, human tumor-associated stromal (TAS) cells, and their co-culture. Of the factors identified, interleukin-8 (IL-8) is released at high levels from PC cells and PC/TAS co-culture and has previously been associated with low muscle mass in cancer patients. We, therefore, treated C2C12 myotubes with IL-8 which led to the activation of ERK1/2, STAT, and Smad signaling, and induced myotube atrophy. Moreover, the treatment of mice with IL-8 also induced significant muscle wasting, confirming the in vivo relevance of IL-8 on muscle. Mechanistically, IL-8-induced myotube atrophy is inhibited by treatment with the CXCR2 antagonist, SB225002, or by treatment with the ERK1/2 inhibitor, U0126. We further demonstrate that this axis mediates muscle atrophy induced by pancreatic cancer cell CM, as neutralization of IL-8 or treatment with SB225002 or U0126 significantly inhibit CM-induced myotube atrophy. Thus, these data support a key role of IL-8 released from human PC cells in initiating atrophy of muscle cells via CXCR2-ERK1/2.

437P - Correlation between bio-impedance analysis and abdominal CT scan to diagnose decreased muscle mass in adult cancer patients

BackgroundSarcopenia, characterized by a decline of skeletal muscle plus low muscle strength and/or physical performance, has emerged to be an important prognostic factor for advanced cancer patients. Sarcopenia is diagnosed if there is decreased muscle mass and either decreased muscle function or physical activity. The diagnostic tools for evaluating muscle mass in cancer patients was using muscle index derived from abdominal CT scan. However, the practicability of using CT scan for screening decreased muscle mass has been questioned. Until know there is limited data diagnostic value of Bio-impedance analysis (BIA) in cancer patients. The aim of this study is to know the correlation between BIA and abdominal CT scan to diagnose decreased muscle mass in cancer patients. MethodsThis cross-sectional study included adult cancer patients who underwent abdominal CT scans in purpose for diagnostic. BIA was performed in the same day when CT-scan was performed. CT-scans was analyzed using special software. BIA was performed using standing-posture 2-electrode BIA device BC-418 (BIA, Tanita Corp, Tokyo, Japan). Height adjusted appendicular skeletal muscle mass (ASM) was calculated from BIA. Height adjusted skeletal muscle Index (SMI) was performed from a single cross-sectional CT image (slice) at third lumbar (L3) for abdominal skeletal muscle area. We calculated Pearson’s r correlation coefficient between two parameters. ResultsA total of 39 patients were included. Twenty-eight (71.8%) patients were female. The mean of age was 51.18 +13.83 years old. Several type of cancer such as breast, lung, gastrointestinal and genitourinary cancer were included. Eleven (28.2%) patients were in advanced stage. Mean of height adjusted BIA was 6.60 + 0.98 kg/m2. Mean of height adjusted muscle mass was 42.25 + 7.57 cm2/m2. BIA and CT-derived muscle were moderately correlated (r = 0.72, p < 0.001). ConclusionsThis study showed that BIA- and CT-derived muscle mass was moderately correlated in adult cancer patients. Further research is needed to confirm this result. Legal entity responsible for the studyThe authors. FundingHas not received any funding. DisclosureAll authors have declared no conflicts of interest.

Multiplatform Urinary Metabolomics Profiling to Discriminate Cachectic from Non-Cachectic Colorectal Cancer Patients: Pilot Results from the ColoCare Study.

Cachexia is a multifactorial syndrome that is characterized by loss of skeletal muscle mass in cancer patients. The biological pathways involved remain poorly characterized. Here, we compare urinary metabolic profiles in newly diagnosed colorectal cancer patients (stage I–IV) from the ColoCare Study in Heidelberg, Germany. Patients were classified as cachectic (n = 16), pre-cachectic (n = 13), or non-cachectic (n = 23) based on standard criteria on weight loss over time at two time points. Urine samples were collected pre-surgery, and 6 and 12 months thereafter. Fat and muscle mass area were assessed utilizing computed tomography scans at the time of surgery. N = 152 compounds were detected using untargeted metabolomics with gas chromatography–mass spectrometry and n = 154 features with proton nuclear magnetic resonance spectroscopy. Thirty-four metabolites were overlapping across platforms. We calculated differences across groups and performed discriminant and overrepresentation enrichment analysis. We observed a trend for 32 compounds that were nominally significantly different across groups, although not statistically significant after adjustment for multiple testing. Nineteen compounds could be identified, including acetone, hydroquinone, and glycine. Comparing cachectic to non-cachectic patients, higher levels of metabolites such as acetone (Fold change (FC) = 3.17; p = 0.02) and arginine (FC = 0.33; p = 0.04) were observed. The two top pathways identified were glycerol phosphate shuttle metabolism and glycine and serine metabolism pathways. Larger subsequent studies are needed to replicate and validate these results.

Allantoin reduces cell death induced by cisplatin: possible implications for tumor lysis syndrome management.

Massive lysis of tumor mass in cancer patients under chemotherapy regimens generates high levels of uric acid, leading to what is known as tumor lysis syndrome (TLS). Rasburicase, a recombinant urate oxidase, converts urate to allantoin, which is readily excreted by the kidneys. Even though there is a high production of allantoin from urate in cancer patients following rasburicase treatment, there are no studies on how allantoin excess could interfere with chemotherapy. We have evaluated allantoin interference with cisplatin efficiency on the lung cancer cell line H460 in vitro. The cells were treated with cisplatin (33µM), with or without allantoin, for 48h, in the presence or absence of UV light, and N-acetyl-L-cysteine (NAC) for 24h. Cell viability, cell cycle, ROS production, apoptosis and immunoblot assays were performed. We showed that allantoin reduced the apoptosis induced by cisplatin in the H460 cell line. However, the activity of carboplatin and oxaliplatin, betulinic acid, TIBA, UV and H2O2 was not affected by allantoin. NMR spectroscopy showed that allantoin reduces cisplatin activity through direct interaction with cisplatin.

MDCT combined parameters in characterization of adrenal masses in cancer patients; A prospective study in South Egypt Cancer Institute

MDCT combined parameters in characterization of adrenal masses in cancer patients; A prospective study in South Egypt Cancer Institute

Analysis of three methods of nutritional screening in oncologic patients

malnutrition is one of the complications that appears most frequently in oncological patients and causes serious consequences such as loss of lean mass. to know which nutritional screening method is most useful in predicting the loss of lean mass in cancer patients. a descriptive study was carried out evaluating three methods of nutritional screening, Malnutrition Screening Tool (MST), Malnutrition Universal Screening (MUST) and Nutritional Risk Screening (NRS-2002), in oncological patients undergoing radiotherapy treatment. Each method was analyzed by ROC curves with AUC calculation. loss of lean mass is present in 48.73% of the patients. Of them, 29.44% present a loss of lean mass between 0-2%; 10.66% of patients, between 2-5%; and 8.13% of patients present a loss of lean mass > 5%. The results show that when taking a loss of lean mass > 5% as a cut-off point, the MST method has a higher AUC than the one presented by the MUST and the NRS-2002 (0.596, CI: 0.444-0.747), with significant statistics (p = 0.041). In addition, it presents high sensitivity and positive and negative predictive value. MST is a more valid nutritional screening method than MUST and NRS-2002 to predict the loss of lean mass > 5% in oncological patients undergoing radiotherapy treatment. Its routine use is recommended in patients under radiotherapy treatment.