New research from @StanfordMed shows that iron nanoparticles may trigger an immune response to cancer… https: //t.co/Hy1jiwqiaE

New research from @StanfordMed shows that iron nanoparticles may trigger an immune response to cancer… https://t.co/Hy1jiwqiaE

from #Cancer-Sfakianakis via simeraentaxei on Inoreader http://twitter.com/ecancer/status/781869997954064384
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New research from @StanfordMed shows that iron nanoparticles may trigger an immune response to cancer… https: //t.co/Hy1jiwqiaE

RT @ESMO_Open : #ESMO16 starts next week! Speak to us at stand 105 & learn about #openaccess & the high-quality medica l research we publish…

RT @ESMO_Open : #ESMO16 starts next week! Speak to us at stand 105 & learn about #openaccess & the high-quality medical research we publish…

from #Cancer-Sfakianakis via simeraentaxei on Inoreader http://twitter.com/ecancer/status/781857529299144704
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RT @ESMO_Open : #ESMO16 starts next week! Speak to us at stand 105 & learn about #openaccess & the high-quality medica l research we publish…

Pri-miR-34b/c rs4938723 polymorphism is associated with the risk of childhood acute lymphoblastic leukemia

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Publication date: Available online 30 September 2016
Source:Cancer Genetics
Author(s): Mohammad Hashemi, Gholamreza Bahari, Majid Naderi, Simin Sadeghi-Bojd, Mohsen Taheri
MicroRNAs (miRNAs), small noncoding regulatory RNAs, are key regulators of gene expression. The impact of Pri-miR-34b/c rs4938723 variant on development of various cancer is still controversial. In the present study, we examined whether a rs4938723 variant located at promoter region of Pri-miR-34b/c is associated with childhood ALL. A total of 110 children with acute lymphoblastic leukemia (ALL) and 120 healthy children were recruited to participate in this study. The rs4938723 variant was genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. The rs4938723 variant decrease the risk of ALL in heterozygous (TC vs OR=0.48, 95%CI=0.28-0.84, p=0.012, TC vs TT), and overdominant (OR=0.51, 95%CI=0.30-0.89, p=0.0.020, TC vs TT+CC): OR=1.32, 95%CI=0.67-2.59, p=0.498; C vs T: OR = 0.99, 95%CI = 0.75- 1.31, p=0.986) inheritance models tested. The C allele significantly decreased the risk of childhood ALL compared to T allele (OR=0.52, 95%CI=0.33-0.83, p=0.006). Our findings proposed an association between Pri-miR-34 b/c rs4938723 variant and risk of childhood ALL development in a sample of Iranian population.

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Pri-miR-34b/c rs4938723 polymorphism is associated with the risk of childhood acute lymphoblastic leukemia

Scientists from @TheCrick discover a ‘genetic switch’ for cancer cell immortality https://t.co/k9C4MDQJRi https://t.co/LJ5DeSfcZS

Scientists from @TheCrick discover a ‘genetic switch’ for cancer cell immortality https://t.co/k9C4MDQJRi https://t.co/LJ5DeSfcZS

from #Cancer-Sfakianakis via simeraentaxei on Inoreader http://twitter.com/ecancer/status/781827223884029953
via IFTTT Medicine by Alexandros G.Sfakianakis,Anapafseos 5 Agios Nikolaos,Crete 72100,Greece,tel :00302841026182 & 00306932607174

Scientists from @TheCrick discover a ‘genetic switch’ for cancer cell immortality https://t.co/k9C4MDQJRi https://t.co/LJ5DeSfcZS

The risk of myocardial infarction with aromatase inhibitors relative to tamoxifen in post-menopausal women with early stage breast cancer

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Publication date: November 2016
Source:European Journal of Cancer, Volume 68
Author(s): Husam Abdel-Qadir, Eitan Amir, Hadas D. Fischer, Longdi Fu, Peter C. Austin, Paula J. Harvey, Paula A. Rochon, Douglas S. Lee, Geoffrey M. Anderson
BackgroundAromatase inhibitors (AIs) may increase cardiovascular risk relative to tamoxifen in post-menopausal women with breast cancer. This risk has not been well-quantified outside of clinical trials.MethodsObservational population-based cohort study of women aged >55 years diagnosed with stage I–III breast cancer between 2005 and 2010. Women treated with AIs or tamoxifen were followed to March 2012. The primary outcome was hospitalisation for myocardial infarction (MI). Cause-specific hazards were compared using tamoxifen as the reference group. Inverse probability of treatment weighting using the propensity score was used to reduce confounding due to measured baseline covariates. Results were confirmed using two cause-specific hazards models. Subgroup analyses included women aged ≥66 years, those with prior ischaemic heart disease, and a ‘lower-risk group’ aged <74 years with stage I–II cancer and no prior ischaemic heart disease.ResultsIn 7409 aromatase inhibitor-treated and 1941 tamoxifen-treated women, the median age was 71 versus 74 years, respectively (p < 0.001). Baseline prevalence of ischaemic heart disease was similar (17.0% versus 16.9%, p = 0.96). Over a mean of 1184 d of follow-up, there were 123 hospitalisations for MI; the cause-specific hazard was higher with AIs (hazard ratio 2.02; 95% confidence interval 1.16–3.53 in the weighted sample). We observed comparable patterns within pre-defined subgroups and when adjusted using cause-specific hazards models.ConclusionAromatase inhibitors are associated with a higher risk of MI compared with tamoxifen. This risk should be accounted for when managing aromatase inhibitor-treated women.

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The risk of myocardial infarction with aromatase inhibitors relative to tamoxifen in post-menopausal women with early stage breast cancer

How strong is the association between IPF and lung cancer? An answer from airway’s DNA

Abstract

Idiopathic pulmonary fibrosis is a chronic progressive disease of lung interstitium of unknown etiology with poor prognosis. In patients with IPF, the incidence of lung cancer is much higher than that in the general population. The identification of noninvasive biomarkers for early diagnosis of IPF is of great relevance in consideration of the management of these patients. Among the noninvasive omic markers, an increasing interest has been directed toward the study of genetic alterations of microsatellites (MAs) in exhaled breath condensate (EBC). The aim of this preliminary study was to investigate the MAs, located in chromosomal regions 8p21.3–q11.1 and 17q11.2–q21, that harbor tumor suppressor genes, in EBC and in the paired whole blood (WB) of IPF patients. Eleven IPF patients were compared with 10 healthy control subjects. All subjects underwent collection of the EBC and WB. The EBC was collected using a condenser. Four microsatellite markers (THRA1, D17S579, D17S250 and D8S137) were used for the analysis of MAs. The EBC-DNA and WB-DNA were amplified by PCR; PCR products were analyzed using the ABI Prism 310 DNA. Microsatellite alterations were found in 58.82 % of EBC-DNA and 12.50 % of WB-DNA in patients with IPF (p < 0.01). None of the healthy subjects exhibited MAs in the studied markers. Our findings suggest that these genetic alterations, studied in EBC, may play an important role in the complex genetic basis of IPF. Since these MAs are frequently detected in cancer, they might explain the higher relative risk of tumorigenesis in this disease.

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How strong is the association between IPF and lung cancer? An answer from airway’s DNA

Low cancer symptom awareness linked to lower chance of survival

In regions where cancer survival is poorer, people on average have lower awareness of cancer symptoms, according to new findings published in the British Journal of Cancer. Researchers also found that general awareness of cancer symptoms varies greatly…

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Low cancer symptom awareness linked to lower chance of survival