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PURPOSE: The role of mobile health (mHealth) technology in cancer care has evolved alongside the rapid development in digital technology. Its use can come with significant potential benefits; however, such use may also be associated with risks. This paper summarizes the latest developments around mHealth use in cancer care presented by a panel of experts at the 2019 Annual Meeting of the Multinational Association of Supportive Care in Cancer. METHODS: Through lectures, case studies, and panel discussions, speakers and participants (including cancer specialist doctors, nurses, and allied health professionals) evaluated current and emerging mHealth methods for supportive care in cancer survivorship. Focus areas and special considerations were agreed upon by consensus. RESULTS: Three focus areas for the use of mHealth in cancer care were identified: activation and support of self-management, exercise oncology, and enablement of survivorship care delivery. In addition to these focus areas, two special considerations were highlighted: technology-enhanced supportive cancer care for disparate populations, and ethical considerations relevant to the use of technology in supportive care. CONCLUSION: mHealth has the potential to revolutionize and transform cancer care delivery. Future research should guide further advances in the use of technology in supportive cancer care and carefully explore the safety, efficacy, cost-effectiveness, and implementation of interventions delivered through mHealth platforms.

Cognitive impairment due to cancer and its therapy is a major concern among cancer patients and survivors. Extracellular vesicle (EVs) composition altered by cancer and chemotherapy may affect neurological processes such as neuroplasticity, potentially impacting the cognitive abilities of cancer patients and survivors. We investigated the EV proteome of breast cancer patients with and without cognitive impairment following anthracycline-based chemotherapy from longitudinally collected plasma. EVs were cup-shaped and positive for Flotillin-1 and TSG-101. We identified 517 differentially expressed EV proteins between the cognitive impaired and non-impaired groups during and post-chemotherapy. The observed decreased expression of p2X purinoceptor, cofilin-1, ADAM 10, and dynamin-1 in the plasma EVs of the cognitive impaired group may suggest alterations in the mechanisms underlying synaptic plasticity. The reduced expression of tight junction proteins among cognitive-impaired patients may imply weakening of the blood-brain barrier. These EV protein signatures may serve as a fingerprint that underscores the mechanisms underlying cognitive impairment in cancer patients and survivors.

Background Cancer-related fatigue (CRF) is a debilitating condition which commonly affects cancer survivors. The management of CRF remains a challenge due to the lack of effective pharmacological interventions. Traditional Chinese medicine (TCM) could be a potential therapeutic option for CRF. The modified Xiang Bei Yang Rong Tang (XBYRT) is a TCM herbal decoction, formulated to improve fatigue symptoms in cancer survivors. This clinical trial aims to evaluate the efficacy and safety of XBYRT in improving CRF and quality of life (QOL) of cancer survivors. Methods This is a single centre, randomized, double-blind, placebo-controlled, parallel trial. Eighty cancer survivors will be recruited and randomized to receive the XBYRT or placebo decoction, in a ratio of 1:1. Participants will consume the XBYRT/placebo decoction daily for 8 weeks and undergo assessments at baseline and 4, 8 and 10 weeks after baseline. The participants will be assessed for patient-reported outcomes (PRO), blood biomarkers and adverse events at each time point. The primary outcome is the overall health and QOL status, at 8 weeks follow-up. The secondary outcomes are the effects of XBYRT on fatigue levels, cancer-related cognitive impairment and QOL, as assessed by PRO. The incidence of adverse events and the effects of the XBYRT decoction on blood biomarkers associated with CRF will also be evaluated. Discussion Efficacy and safety outcomes from this trial will provide important clinical data to guide future large-scale randomized controlled trials, and the evaluation of the objective blood biomarkers can help to delineate the biological mechanisms of CRF. Trial registration number ClinicalTrials.govNCT04104113. Registered on 26 September 2019

This is the first study to determine the minimal clinically important difference (MCID) of the European Organisation of Research and Treatment of Cancer Quality of Life Questionnaire-CIPN twenty-item scale (EORTC QLQ-CIPN20), a validated instrument designed to elicit cancer patients’ experience of symptoms and functional limitations related to chemotherapy-induced peripheral neuropathy. Cancer patients receiving neurotoxic chemotherapy completed EORTC QLQ-CIPN20 and the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity [FACT/GOG-NTX] at baseline, second cycle of chemotherapy (T2, n = 287), and 12 months after chemotherapy (T3, n = 191). Anchor-based approach used the validated FACT/GOG-NTX neurotoxicity (Ntx) subscale to identify optimal MCID cutoff for deterioration. Distribution-based approach used one-third standard deviation (SD), half SD, and one standard error of measurement of the total EORTC QLQ-CIPN20 score. There was a moderate correlation between the change scores of the Ntx subscale and sensory and motor subscales of QLQ-CIPN20 (T2: r = − 0.722, p

Background Many studies have examined specific mutations in patients with resected lung adenocarcinoma across heterogeneous stages, comprising predominantly advanced/metastatic disease, but there is little data regarding the mutation profile of patients with early stage node negative disease. The aim of this study was to identify patterns of mutations in early stage node negative lung adenocarcinoma. Methods A total of 204 patients who underwent resection for stage IB (sixth Ed American Joint Committee on Cancer) lung adenocarcinoma and received no neoadjuvant or adjuvant treatments were identified. Tumors were genotyped using the OncoCarta v1.0 kit (Sequenom, San Diego, CA) on the Sequenom MassARRAY platform. Fluorescence in situ hybridization for ALK rearrangement was also performed. Results A total of 110 (54%) patients' tumors harbored at least one mutation. KRAS, EGFR, PIK3CA, ALK, PDGFRA, AKT1, BRAF, FGFR1, and HRAS mutations were detected in tumors from 77 (37.7%), 29 (14.2%), 9 (4.4%), 2 (1%), 2 (1%), 1 (0.5%), 1 (0.5%), 1 (0.5%), and 1 (0.5%) patients respectively. Synchronous mutations (either comutations or double mutations) were identified in 18 (8.8%) patients. KRAS and PIK3CA mutations were associated with poorly differentiated tumors (p = 0.03; p = 0.02), whereas EGFR mutations were associated with well-differentiated tumors (p = 0.001). Five tumours contained EGFR mutations (one T790M and four exon 20 insertions), which are associated with resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). Conclusions Diverse patterns of mutations are seen in resected node-negative lung adenocarcinoma including an unexpectedly low rate of ALK rearrangement, EGFR mutations associated with resistance to EGFR-TKIs and a high rate of synchronous mutations. These data may influence the design of future adjuvant targeted therapy trials.

Introduction Inhibitors of the epidermal growth factor receptor (EGFR) show impressive response rates in selected lung cancer patients with activating EGFR gene mutations. Newer targeted agents are also in development with a pressing need to accurately identify the presence of ‘actionable’ mutations in patients with this poor prognosis cancer. We describe our experience with a sensitive, high throughput mass spectrometry based assay which detects a panel of 238 specific mutations in 19 oncogenes identified as biologically significant through literature review including KRAS, EGFR, BRAF, PIK3CA, MET, AKT1 and ERBB2. Methods DNA was extracted from resected tumours of 160 patients with lung adenocarcinoma, prepared using the Oncocarta v1.0 kit and processed on the Sequenom compact MassARRAY platform. Results We identified 101 mutations in 160 patients, with eight patients (5%) showing a mutation in two different genes concurrently. KRAS gene mutations were the most prevalent, seen in 40.6% of patients while EGFR mutations were seen in 13.1%. Rarer mutations were detected in PIK3CA (3.8%), MET (3.1%) and AKT1 (1 case only). Conclusions We detected at least one potentially clinically relevant mutation in the tumours of over half of our patients. We suggest this accurate and high throughput method may offer significant advantages over traditional Sanger sequencing.