umor differentiation status were independent factors that have statistically significant influences on clinical outcomes of IMA patients.

Our study provided genomic insights into Chinese surgically resected lung IMA. We also identified several genomic features that may serve as potential biomarkers on postoperative recurrence in IMA patients with stage III disease.

Our study provided genomic insights into Chinese surgically resected lung IMA. We also identified several genomic features that may serve as potential biomarkers on postoperative recurrence in IMA patients with stage III disease.

To investigate dosimetry of submandibular glands on xerostomia after intensity-modulated radiotherapy for nasopharyngeal carcinoma (NPC).

From September 2015 to March 2016, 195 NPC patients were investigated. Xerostomia was evaluated at 12 months after treatment

the RTOG/EORTC system. The least absolute shrinkage and selection operator regression model was used to optimize feature selection for grades 2-3 xerostomia. Multivariable logistic regression analysis was applied to build a predicting model incorporating the feature selected in the least absolute shrinkage and selection operator regression model. Discrimination, calibration, and clinical usefulness of the predicting model were assessed using the C-index, calibration plot, and decision curve analysis.

The V30 of the parotid glands was selected based on the least absolute shrinkage and selection operator regression. The nomogram displayed good discrimination with a C-index of 0.698 (95% confidence interval [CI] 0.626-0.771) and good calibration (model 1). Addition of the dosimetric parameters including the mean dose to the submandibular glands, V50 of the submandibular glands, and volume of the submandibular glands to the model 1 failed to show incremental prognostic value (model 2). The model 2 showed a C-index of 0.704 (95% CI 0.632-0.776). Decision curve analysis demonstrated that the model 1 was clinically useful when intervention was decided at the possibility threshold of > 20%. Within this range, net benefit was comparable between the model 1 and model 2.

PGv30 was a major predictive factor of grades 2-3 xerostomia for NPC. In contrast, the mean dose to the submandibular glands, V50 of the submandibular glands, and volume of the submandibular glands were not independent predictive factors.

PGv30 was a major predictive factor of grades 2-3 xerostomia for NPC. In contrast, the mean dose to the submandibular glands, V50 of the submandibular glands, and volume of the submandibular glands were not independent predictive factors.The use of high dose ascorbate infusions in cancer patients is widespread, but without evidence of efficacy. Several mechanisms whereby ascorbate could affect tumor progression have been proposed, including (i) the localized generation of cytotoxic quantities of H2O2; (ii) ascorbate-dependent activation of the 2-oxoglutarate-dependent dioxygenases that control the hypoxia-inducible factors (HIFs) and that are responsible for the demethylation of DNA and histones; (iii) increased oxidative stress induced by dehydroascorbic acid. We hypothesize that the dysfunctional vasculature of solid tumors results in compromised delivery of ascorbate to poorly perfused regions of the tumor and that this ascorbate deficit acts as an additional driver of the hypoxic response via upregulation of HIFs. Using a randomized “therapeutic window of opportunity” clinical study design we aimed to determine whether ascorbate infusions affected tumor ascorbate content and tumor biology. Patients with colon cancer were randomized to receive infusions of up to 1 g/kg ascorbate for 4 days before surgical resection (n = 9) or to not receive infusions (n = 6). Ascorbate was measured in plasma, erythrocytes, tumor and histologically normal mucosa at diagnostic colonoscopy and at surgery. Protein markers of tumor hypoxia or DNA damage were monitored in resected tissue. Plasma ascorbate reached millimolar levels following infusion and returned to micromolar levels over 24 h. Pre-infusion plasma ascorbate increased from 38 ± 10 µM to 241 ± 33 µM (p

ANZCTR Trial ID ACTRN12615001277538 (https//www.anzctr.org.au/).

ANZCTR Trial ID ACTRN12615001277538 (https//www.anzctr.org.au/).The field of cancer survivorship has significantly advanced person-centered care throughout the cancer continuum. Within cancer survivorship, the last decade has seen remarkable growth in the investigation of prehabilitation comprising pre-treatment interventions to prevent or attenuate the burden of oncologic therapies. While the majority of evidence remains in the surgical setting, prehabilitation is being adapted to target modifiable risk factors that predict poor treatment outcomes in patients receiving other systemic and localized anti-tumor treatments. Here, we propose a multiphasic approach for prehabilitation across the cancer continuum, as a conceptual framework, to encompass the variability in cancer treatment experiences while adopting the most inclusive definition of the cancer survivor.Development of treatment resistance is a major concern during treatment of cancer, and there is an unmet need for therapeutic strategies with novel modes of action. Polyvinyl alcohol carbazate (PVAC) is a polymer compound with unique biological properties. Herein, we describe the antitumoral effects of PVAC. Three well-established cell lines GIST-T1, B16.F10, and A375 were used to determine the in vitro antitumoral effects of PVAC. SolutolHS15 Assessments included light microscopy, cell viability, cell cycle, and apoptosis assays. In vivo treatment safety and efficacy were characterized in one immunocompetent (B16.F10) mouse model and one athymic nude (MDA-MB-231) mouse model. Excised tumors were measured, weighed, stained for Ki-67, CD3, and histopathologically evaluated. Intact PVAC expressed a non-linear dose-response antitumoral effect in vitro, whereas its separate components, PVA and carbazate, did not display antitumoral effects alone. In vivo, PVAC induced a significant intratumoral CD3+ T-cell recruitment in immunocompetent mice (B16.F10), which was associated with tumor growth inhibition. Although growth inhibition was not significant in athymic mice (MDA-MB-231), histopathological evaluation detected an increase in stromal tissue and leukocyte infiltration. In conclusion, we present evidence for PVAC antitumoral effects both in vitro and in vivo. The mode of action was not elucidated in vitro, but a potential mechanism of in vivo activity was observed, characterized by an increase of immune cells into both immunocompetent and athymic mice. This finding warrants further study to validate its possible role as an immunomodulatory polymeric agent.