cancer

Erratum: The Immune Landscape of Cancer (Immunity (2018) 48(4) (812–830.e14), (S1074761318301213), (10.1016/j.immuni.2018.03.023))

(Immunity 48, 812–830.e1–e14; April 17, 2018) In the originally published version of this article, the authors neglected to include Younes Mokrab and Aaron M. Newman as co-authors and misspelled the names of authors Charles S. Rabkin and Ilya Shmulevich. The author names have been corrected here and online. In addition, the concluding sentence of the subsection “Immune Signature Compilation” in the Method Details in the original published article was deemed unclear because it did not specify differences among the gene set scoring methods.

Hypoxia Dictates Metabolic Rewiring of Tumors: Implications for Chemoresistance

Hypoxia is a condition commonly observed in the core of solid tumors. The hypoxia-inducible factors (HIF) act as hypoxia sensors that orchestrate a coordinated response increasing the pro-survival and pro-invasive phenotype of cancer cells, and determine a broad metabolic rewiring. These events favor tumor progression and chemoresistance.

Nutlin-3a enhances natural killer cell-mediated killing of neuroblastoma by restoring p53-dependent expression of ligands for NKG2D and DNAM-1 receptors

In this study, we explored whether Nutlin-3a, a well-known nontoxic small-molecule compound antagonizing the inhibitory interaction of MDM2 with the tumor suppressor p53, may restore ligands for natural killer (NK) cell-activating receptors (NK-ARs) on neuroblastoma (NB) cells to enhance the NK cell-mediated killing. NB cell lines were treated with Nutlin-3a, and the expression of ligands for NKG2D and DNAM-1 NK-ARs and the NB susceptibility to NK cells were evaluated. Adoptive transfer of human NK cells in a xenograft NB-bearing NSG murine model was assessed.

Nanotechnology-based strategies to develop new anticancer therapies

The blooming of nanotechnology has made available a limitless landscape of solutions responding to crucial issues in many fields and, nowadays, a wide choice of nanotechnology-based strategies can be adopted to circumvent the limitations of conventional therapies for cancer. Herein, the current stage of nanotechnological applications for cancer management is summarized encompassing the core nanomaterials as well as the available chemical–physical approaches for their surface functionalization and drug ligands as possible therapeutic agents.

Design and functional validation of a mutant variant of the lncRNA HOTAIR to counteract Snail function in Epithelial-to-Mesenchymal Transition

HOTAIR is a lncRNA overexpressed in several epithelial cancers and strongly correlated with invasion. This lncRNA was proven a pivotal element of the epithelial-mesenchymal transition (EMT), a trans-differentiation process triggering metastasis. Snail, master inducer of EMT, requires HOTAIR to recruit EZH2 on specific epithelial target genes (i.e., HNF4α, E-cadherin and HNF1α) and cause their repression. Here we designed a HOTAIR deletion mutant form, named HOTAIR-sbid, including the putative Snail-binding domain but depleted of the EZH2 binding domain.

What cancer patients actually know regarding medical cannabis? A cross-sectional survey with a critical analysis of the current attitudes

Background: In Italy medical cannabis is a prescription drug since 1998. Even though it could not be considered a therapy as such, it is indicated as a symptomatic treatment also in cancer patients, to cure iatrogenic nausea/vomiting and chronic pain. Patients and methods: We conducted a knowledge survey about medical cannabis among cancer patients referred to two outpatient cancer care centers and a home care service. Results: From February to April 2018, 232 patient were enrolled; 210 patients were on active disease-oriented treatment (90.5%), while 22 (9.5%) not.

Preliminary results of a counselling programme for fertility preservation in female cancer patients: The experience of the GEMME DORMIENTI network

Objective: To describe a population of patients referred for fertility preservation (FP), how to efficiently provide FP care, and how FP care changed over time. Methods: This longitudinal observational study enrolled 281 female cancer patients referred between 2013 and 2016 to the non-profit organisation Gemme Dormienti ONLUS (GD) for FP care. All patients underwent the same battery of instrumental and laboratory diagnostic tests. GnRHa therapy was started at least seven days before CTh treatment.

https://researchopenworld.com/covid-19-and-oncological-health-workers-psychological-reactions-and-interventions/#

Stress of Working in Oncology
Oncology is a medicine area of high psychic investment. Working
with cancer patients is a source of human and professional satisfaction
but can involve high emotional costs [1,2]. High levels of burnout and
compassion fatigue are reported by about 32% of oncologists [3,4] this
percentage rises to 70% among people under 40 years [5]. High levels
are also found among nursing staff with marked levels of emotional
exhaustion [6]. Repeated exposure to suffering and loss, to the side

Another side of the association between body mass index (BMI) and clinical outcomes of cancer patients receiving programmed cell death protein-1 (PD-1)/ Programmed cell death-ligand 1 (PD-L1) checkpoint inhibitors: A multicentre analysis of immune-re

Background: Several studies have found an association between higher body mass index (BMI) and improved clinical outcomes in cancer patients receiving programmed cell death protein-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) checkpoint inhibitors. In a previous study, we found that overweight/obese patients were significantly more likely to experience any grade immune-related adverse events (irAEs) compared to non-overweight patients.

Identification and Targeting of Stem Cell-Activated Pathways in Cancer Therapy

The hierarchical organization and heterogeneity that are present within malignancies have been recently attributed to stem cell-like subset of tumor cells. Cancer Stem Cells (CSCs) have gained an exclusive interest as they are identified to push tumor growth and seed metastasis and are responsible for therapy failure and tumor resistance [1]. The molecular mechanism that drives the CSC population

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