Cancer via Alexandros G.Sfakianakis on Inoreader

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Cancer via Alexandros G.Sfakianakis on Inoreader

Long non-coding RNA FER1L4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer
1:17:59 AM Ben Yue, Bo Sun, Chenchen Liu, Senlin Zhao, Dongyuan Zhang, Fudong Yu, Dongwang Yan

Summary

Novel long non-coding RNA Fer-1-like protein 4 (FER1L4) has been confirmed play crucial regulatory roles in tumor progression. It exerts impact on tumor suppression and functions as a competing endogenous RNA (ceRNA) by sponging miR-106a-5p in gastric cancer. However, its clinical significances in colon cancer are completely unknown. The aim of this study was to annotate the role of FER1L4 and its clinical value in colon cancer. Results showed that aberrant expression of FER1L4 and miR-106a-5p in colon cancer tissues. In addition, significant negative correlation between FER1L4 and miR-106a-5p expression levels was observed. Among the colon cancer cell lines, FER1L4 levels were relatively lower with concurrent high levels of miR-106a-5p. Restoration of FER1L4 decreased the expression of miR-106a-5p, and had a significant influence on colon cancer cell proliferation, migration and invasion. The FER1L4 expression was correlated with depth of tumor invasion, lymph node metastasis, vascular invasion, and clinical stage. Moreover, striking differences in overall survival (OS) and disease-free survival (DFS) were observed when the cases with both low FER1L4 expression and high miR-106a-5p expression compared with cases with high FER1L4 expression and low miR-106a-5p expression. Circulating FER1L4 and miR-106a-5p levels were decreased and increased respectively in colon cancer patients after surgery. Our findings indicated that FER1L4 could exert tumor suppressive impact on colon cancer, which at least in part, by suppressing miR-106a-5p expression, and depletion of FER1L4, alone, or combined with overexpression of miR-106a-5p, is predictive of poor prognosis in colon cancer and may play a crucial role in cancer prevention and treatment.

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iPS cell technology for dissecting the cancer epigenome
1:17:59 AM Katsunori Semi, Yasuhiro Yamada

Abstract

Cancer arises through the accumulations of both genetic and epigenetic alterations. Although the causal role of genetic mutations on cancer development has been established in vivo, similar evidence for epigenetic alterations is limited. Moreover, mutual interactions between genetic mutations and epigenetic alterations remain unclear. Cellular reprogramming technology can be used to actively modify the epigenome without affecting the underlying genomic sequences. Here we introduce recent studies that utilized this property for cancer research. We propose that just as it has potential for regenerative medicine and disease modeling, cell reprogramming could also be a powerful tool for dissecting the role of the cancer epigenome on the development and maintenance of cancer cells.

This article is protected by copyright. All rights reserved.



Carboplatin therapeutic monitoring in preterm and full-term neonates
Wednesday, July 29, 2015 10:30 PM Gareth J. Veal, Julie Errington, James Hayden, David Hobin, Dermot Murphy, Rachel M. Dommett, Deborah A. Tweddle, Helen Jenkinson, Susan Picton
Administration of the most appropriate dose of chemotherapy to neonates is particularly challenging and frequently not standardised based on any scientific rationale. We report the clinical utility of carboplatin therapeutic drug monitoring in preterm and full-term neonates within the first month of life.


A review of breast cancer awareness among women in India: Cancer literate or awareness deficit?
Wednesday, July 29, 2015 10:30 PM A. Gupta, K. Shridhar, P.K. Dhillon
Breast cancer is the most common female cancer worldwide including India, where advanced stages at diagnosis, and rising incidence and mortality rates, make it essential to understand cancer literacy in women. We conducted a literature review to evaluate the awareness levels of risk factors for breast cancer among Indian women and health professionals.


Featuring the special issue editor: Assistant Professor Alexandros G. Georgakilas
Wednesday, July 29, 2015 10:09 PM Alexandros G. Georgakilas
. SYSTEMIC EFFECTS. Radiation biology. Carcinogenesis. Complex DNA Damage. DNA Repair. Radiation effects


Inhibition of CDK4/6 as a novel therapeutic option for neuroblastoma
Wednesday, July 29, 2015 9:42 PM Ali Rihani
Background: Neuroblastoma is a neural crest-derived tumor and is the most common cancer in children less than 1 year of age. We hypothesized that aberrations in genes that control the cell cycle could play an important role in the pathogenesis of neuroblastoma and could provide a tractable therapeutic target. Methods: In this study, we screened 131 genes involved in cell cycle regulation at different levels by analyzing the effect of siRNA-mediated gene silencing on the proliferation of neuroblastoma cells. Results: Marked reductions in neuroblastoma cellular proliferation were recorded after knockdown of CCND1 or PLK1. We next showed that pharmacological inhibition of cyclin D1 dependent kinases 4/6 (CDK4/6) with PD 0332991 (palbociclib) reduced the growth of neuroblastoma cell lines, induced G1 cell cycle arrest, and inhibited the cyclin D1-Rb pathway. Conclusion: Selective inhibition of CDK4/6 using palbociclib may provide a new therapeutic option for treating neuroblastoma.


Featuring the special issue editor: Assistant Professor Alexandros G. Georgakilas
Wednesday, July 29, 2015 9:38 PM Alexandros G. Georgakilas
. SYSTEMIC EFFECTS. Radiation biology. Carcinogenesis. Complex DNA Damage. DNA Repair. Radiation effects


Prostate cancer is five different diseases
Wednesday, July 29, 2015 8:36 PM
Scientists have for the first time identified that there are five distinct types of prostate cancer and found a way to distinguish between them, according to a study published in EBioMedicine. The findings could have important implications for how...


Impact of delays in initiating postoperative chemoradiation while determining the MGMT promoter-methylation statuses of patients with primary glioblastoma
Wednesday, July 29, 2015 8:20 PM Sebastian Adeberg
Background: The benefits of new innovations in glioblastoma therapies should not be curtailed as a result of delays in commencement of radiation therapy, caused by clinical circumstances as well as diagnostic procedures. This study evaluates whether delays in chemo-radiotherapy after surgery, while determining O6-methylguanine-DNA-methyltransferase (MGMT) promoter status, affect the survival rates of patients with glioblastoma (GBM). Methods: Our sample comprised 50 GBM patients in a retrospective analysis of three prospective studies that focused on combined radiotherapy and required MGMT promoter-status testing as inclusion criteria. Results were compared with a reference group of 127 favourable GBM cases (Karnofsky performance-status scale???70), in which the patients underwent standard postoperative chemo-radiotherapy with temozolomide. Survival time was calculated using the Kaplan-Meier method, and a multivariate analysis of the delays between surgical and radiotherapy procedures was performed using the Cox regression model. Results: The study group's median overall survival time was 16.2 months (with a range of 2 to 56 months), versus the reference group's survival time of 18.2 months (with a range of 1 to 92 months) (p?=?0.64). The delay between surgery and radiotherapy was increased by 8 days in the study patients (p?<?0.001), with a median delay of 35 days (range: 18-49 days) corresponding to the typical 27-day delay (range: 5-98 days) for those in the reference group. Univariate and multivariate analyses did not show any negative association between survival time and delaying radiation therapy to determine MGMT-promoter status; commencement of radiation therapy sooner than 24 days after surgery was the threshold for significantly decreased overall survival (p?=?0.01) and progression-free (p?=?0.03) survival. Conclusion: Delaying postoperative chemoradiation for GBM patients-carried out in order to determine MGMT-promoter status-did not have a negative impact on survival time. Indeed, the data of the present study shows that initiating radiation therapy sooner than 24 days after surgery has a negative impact on progression and survival.


Population-based SEER trend analysis of overall and cancer-specific survival in 5138 patients with gastrointestinal stromal tumor
Wednesday, July 29, 2015 8:20 PM Ulrich Güller
Background: The objective of the present population-based analysis was to assess survival patterns in patients with resected and metastatic GIST. Methods: Patients with histologically proven GIST were extracted from the Surveillance, Epidemiology and End Results (SEER) database from 1998 through 2011. Survival was determined applying Kaplan-Meier-estimates and multivariable Cox-regression analyses. The impact of size and mitotic count on survival was assessed with a generalized receiver-operating characteristic-analysis. Results: Overall, 5138 patients were included. Median age was 62 years (range: 18-101 years), 47.3 % were female, 68.8 % Caucasians. GIST location was in the stomach in 58.7 % and small bowel in 31.2 %. Lymph node and distant metastases were found in 5.1 and 18.0 %, respectively. For non-metastatic GIST, three-year overall survival increased from 68.5 % (95 % CI: 58.8-79.8 %) in 1998 to 88.6 % (95 % CI: 85.3-92.0 %) in 2008, cancer-specific survival from 75.3 % (95 % CI: 66.1-85.9 %) in 1998 to 92.2 % (95 % CI: 89.4-95.1 %) in 2008. For metastatic GIST, three-year overall survival increased from 15.0 % (95 % CI: 5.3-42.6 %) in 1998 to 54.7 % (95 % CI: 44.4-67.3 %) in 2008, cancer-specific survival from 15.0 % (95 % CI: 5.3-42.6 %) in 1998 to 61.9 % (95 % CI: 51.4-74.5 %) in 2008 (all P Trend ?<?0.05). Conclusions: This is the first SEER trend analysis assessing outcomes in a large cohort of GIST patients over a 11-year time period. The analysis provides compelling evidence of a statistically significant and clinically relevant increase in overall and cancer-specific survival from 1998 to 2008, both for resected as well as metastatic GIST.


Transforming growth factor-? signaling pathway cross-talking with ER? signaling pathway on regulating the growth of uterine leiomyoma activated by phenolic environmental estrogens in vitro
Wednesday, July 29, 2015 7:20 PM

Abstract

The aim of this paper is to study the participation of transforming growth factor-? (TGF-?) signaling pathway in mediating the growth of human uterine leiomyoma (UL) activated by phenolic environmental estrogens (EEs), via the interaction between TGF-? and ER signaling pathways. The UL cells were prepared by primary culture and subculture methods. To validate the role of TGF-?3 (5 ng/ml) for the viability of human uterine leiomyoma cells, CCK-8 assay was performed in each of five treatment groups including E2 group (E2 109 mol/l), BPA group (bisphenol A 10 ?mol/l), NP group (nonylphenol 32 ?mol/l), OP group (octylphenol 8 ?mol/l), or control group (DMSO only). Subsequently, qRT-PCR was applied to detect mRNA expressions of ER? and c-fos, while western blot assay was used to test the expressions of p-Smad3, SnoN, and c-fos proteins in all settings mentioned above; the expressions were compared among different groups, and also in settings with and without synchronous treatment of ICI 182,780. Primarily cultured UL cells were successfully established. Compared with the control group, there were statistically significant increases in the proliferation rate of the UL cells in all EE groups or treated with TGF-?3 only (p?<?0.05). Nevertheless, a slight decrease in proliferation rate of UL was detected in coexistence with TGF-?3 in all EE groups (p?>?0.05). Interestingly, mRNA expressions of ER? and c-fos reduced in the setting of coexistence of TGF-?3 and EEs compared to isolated EE treatment (p?<?0.05). Compared with the control group, the expression of p-Smad3 and c-fos proteins significantly decreased (p?<?0.05) in each of E2, BPA, NP, and OP group, and the expression of SnoN protein also significantly reduced only in BPA and NP groups (p?<?0.05), followed by TGF-?3 treatment. When adding ICI 182,780, the expression of p-Smad3 protein significantly increased in OP group (p?<?0.05), but slightly increased in E2, BPA, NP, and OP groups (p?>?0.05). However, compared with the control group, the expressions of SnoN and c-fos proteins significantly decreased (p?<?0.05) after adding ICI182,780. Moreover, there was a significant statistical difference in the expression of p-Smad3, SnoN, and c-fos proteins between pre- and post-treatment of ICI 182,780 in all groups (p?<?0.05). The ER? signaling pathway and TGF-? signaling pathway have different roles in the control of UL cell proliferation. The phenolic EEs can be a promoter of UL cell proliferation, which is mediated by ER? signaling pathway and its cross-talking with TGF-? signaling pathway. Both less exposure to EEs and blockade of TGF signaling pathway are necessary strategies to prevent UL.



NYU's Bluestone Center Receives a $369,250 High Priority, Short Term Project Award from NIDCR to Study Oral Cancer Pain
Wednesday, July 29, 2015 3:29 PM Oral Cancer Foundation News Team - A
Source: www.nyu.edu/news Author: Christopher James   Drs. Yamano and Schmidt have developed a novel non-viral gene delivery method, and the proposed studies are designed to test whether this could be used to treat cancer pain effectively and safely. Up to 90% of cancer patients suffer from pain, with oral cancer ranked consistently as one of [.]


Fibroblast growth factor receptor signaling in hereditary and neoplastic disease: biologic and clinical implications
Wednesday, July 29, 2015 2:47 PM

Abstract

Fibroblast growth factors (FGFs) and their receptors (FGFRs) are transmembrane growth factor receptors with wide tissue distribution. FGF/FGFR signaling is involved in neoplastic behavior and also development, differentiation, growth, and survival. FGFR germline mutations (activating) can cause skeletal disorders, primarily dwarfism (generally mutations in FGFR3), and craniofacial malformation syndromes (usually mutations in FGFR1 and FGFR2); intriguingly, some of these activating FGFR mutations are also seen in human cancers. FGF/FGFR aberrations reported in cancers are mainly thought to be gain-of-function changes, and several cancers have high frequencies of FGFR alterations, including breast, bladder, or squamous cell carcinomas (lung and head and neck). FGF ligand aberrations (predominantly gene amplifications) are also frequently seen in cancers, in contrast to hereditary syndromes. There are several pharmacologic agents that have been or are being developed for inhibition of FGFR/FGF signaling. These include both highly selective inhibitors as well as multi-kinase inhibitors. Of note, only four agents (ponatinib, pazopanib, regorafenib, and recently lenvatinib) are FDA-approved for use in cancer, although the approval was not based on their activity against FGFR. Perturbations in the FGFR/FGF signaling are present in both inherited and malignant diseases. The development of potent inhibitors targeting FGF/FGFR may provide new tools against disorders caused by FGF/FGFR alterations.



Clinical translation for endometrial cancer stem cells hypothesis
Wednesday, July 29, 2015 2:47 PM

Abstract

Endometrial cancer is the most frequent gynecological malignancy in developed world. Cancer stem cells (CSC) are recognized as a small proportion of cells among the tumor cell population that are capable of self-renewal, aberrant differentiation, and escape homeostasis. This review aims to systematize the existing evidence of CSC of endometrial cancer and its clinical translation. In endometrial cancer, the cancer stem cell hypothesis has been studied in vitro using the isolation of colony forming units, side population with dye efflux capacity, and tumorospheres. The stem cell markers for endometrial cancer do not have uniform characteristics, albeit CD133 and aldehyde dehydrogenase (ALDH) were being associated with CSC phenotype. The application of endometrial CSC on xenograft models proves the tumorigenic capacity of this small group of cells. The metastatic process has been explained due to epithelial-mesenchymal transition (EMT) in which CSC seems to have a critical role. The chemoresistance is characteristic of CSC that in endometrial cancer has been shown in CSC phenotype and associated with CSC markers. The most ambitious potential for CSC is the development of targeted therapies. Its application on endometrial cancer is still poor, being a future perspective for research.



Revisit dietary fiber on colorectal cancer: butyrate and its role on prevention and treatment
Wednesday, July 29, 2015 2:47 PM

Abstract

Colorectal cancer is still a major health problem worldwide. Based on the most recent released data by the World Health Organization GLOBOCAN in 2012, colorectal cancer is the third most prevalent type of cancer in males and the second in females. In 1999, it was published the first report showing evidence of a strong correlation between diet and cancer incidence, being its positive or negative impact intimately linked to dietary patterns. A diet rich in fiber is associated with a low risk of developing colorectal cancer. The fermentation of the dietary fiber by intestinal microflora results in production of butyrate, which plays a plurifunctional role on the colonocytes, and it has also been reported as a chemopreventive agent. However, there are limited studies focusing its anti-cancer potential. Here, we review the recent new insights that focus butyrate and its role in colorectal cancer prevention and treatment, from its synthesis, metabolism, and transport, through its involvement on several cancer-related signaling pathways, to the novel existing approaches for its clinical use.



Persistence of Trichomonas vaginalis serostatus in men over time
Wednesday, July 29, 2015 2:37 PM

Abstract

Purpose

Previous epidemiologic studies have observed positive associations between Trichomonas vaginalis (Tv) serostatus and both prostate cancer (PCa) risk and mortality. However, only a few small older studies have examined Tv antibody persistence over time, all of which were composed mainly of female patients. Therefore, we examined Tv antibody persistence over time, as well as intra-individual variability, among middle- to older-aged men in the Southern Community Cohort Study (SCCS).

Methods

We tested baseline and repeat plasma specimens (collected 1-3 years later) from 248 male participants for Tv antibodies. We used the same enzyme-linked immunosorbent assay as in previous studies of Tv serostatus and PCa.

Results

At baseline, 46 (18.5 %) participants were seropositive for Tv infection. Seventy-six percent of these men were still seropositive 1-3 years later. A similar proportion of men "seroconverted" (4.0 %) as "seroreverted" (4.4 %), all of whom had absorbance values near the cutoff point for seropositivity. Overall, substantial agreement was observed between baseline and repeat serostatus (? = 0.72, 95 % confidence interval 0.60-0.83).

Conclusion

Tv seropositivity was largely persistent between plasma specimens collected 1-3 years apart from middle- to older-aged men. These high levels of persistence are similar to those observed for other sexually transmitted infections frequently investigated in relation to PCa.



Urinary melatonin and risk of ovarian cancer
Wednesday, July 29, 2015 2:37 PM

Abstract

Purpose

Melatonin has anti-carcinogenic properties, including modulation of estradiol production, cell cycle regulation, and promotion of apoptosis. Urinary melatonin has been inversely associated with breast cancer in some studies, but the association with ovarian cancer has not been investigated.

Methods

We measured urinary 6-sulfatoxymelatonin (aMT6s) in nested ovarian cancer case-control studies in the Nurses' Health Study (NHS; n = 100 cases; 199 controls) and NHSII (n = 52 cases; 105 controls); samples were mainly from first morning voids. Controls were matched to cases on year of birth, menopause status, use of menopausal hormone therapy, and urine collection characteristics. We evaluated the association of tertiles of aMT6s, corrected for creatinine concentrations, with risk of ovarian cancer using conditional logistic regression. Models were adjusted for key ovarian cancer risk factors, and we additionally evaluated adjustment for usual sleep duration, snoring, and history of rotating night shift work.

Results

aMT6s was not significantly associated with risk of ovarian cancer. In multivariable models, the odds ratio comparing the highest tertile of aMT6s to the lowest was 0.79, 95 % confidence interval (CI) 0.40-1.56 in the NHS and 2.88, and 95 % CI in the NHSII 0.97-8.52. Additional adjustment for sleep habits and night shift work had little impact on the observed results. We observed no clear association between urinary melatonin and ovarian cancer risk.

Conclusions

These results are consistent with our previous study in which we reported no association between night shift work and ovarian cancer; however, given the small sample size in our study, additional evaluation in larger studies is warranted.



The assumption of radon-induced cancer risk
Wednesday, July 29, 2015 2:37 PM


Red grape chemical may help prevent bowel cancer but less is more
Wednesday, July 29, 2015 2:23 PM
Resveratrol, a chemical found in red grapes, is more effective in smaller doses at preventing bowel cancer in mice than high doses, according to new research published in Science Translational Medicine. Previous research looked at high doses of purified...


Quality of life in head and neck cancer patients
Wednesday, July 29, 2015 2:15 PM
Prof de Abreu Alves talks to ecancertv at IAOO 2015 about the merits of the congress and quality of life challenges needing consideration in head and neck cancer.


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