Abstract. In this review, the advances in the study of breast cancer molecular classifications and the molecular signatures of the luminal subtypes A and B of breast cancer were summarized. Effective clinical outcomes depend mainly on successful preclinical diagnosis and therapeutic decisions. Over the last few years, the ever-expanding investigations focusing on breast cancer diagnosis and the clinical trials have provided accumulating information on the molecular characteristics of breast cancer. Specifically, among the estrogen receptor (ER)-positive types of breast cancer, the luminal subtype A breast cancer has been shown to exhibit good clinical outcomes with endocrine therapy, whereas the luminal subtype B breast cancer represents the more complicated type, diagnostically as well as therapeutically. Furthermore, even in luminal subtype A breast cancer, the resistance to treatment has become the major limitation for endocrine-based therapy. Accumulating molecular data and further clinical trials may enable more accurate diagnostic and therapeutic decisions. The molecular signatures have emerged as a powerful tool for future diagnosis and therapeutic decisions, although currently available data are limited.

Background Epidemiological studies demonstrate associations between obstructive sleep apnea (OSA) and cancer incidence and mortality. The aim of this study was to measure OSA in women with breast (BC) or endometrial cancer (EC) and associations with clinico-pathological tumor variables. Methods and findings In a cross sectional study, women with BC (12 months) or EC (3 months) post-diagnosis were recruited from cancer clinics. We collected demographic, anthropometric data, cancer stage, grade, histopathology and history of cancer treatment and all subjects had in-laboratory polysomnography. Sleepiness was assessed with the Epworth Sleepiness Scale (ESS). We compared anthropometric and polysomnographic data between cancer groups (unpaired t-tests), and assessed relationships between cancer characteristics and OSA variables (Fishers exact test). There were no significant differences between average age (BC:59.6±8.7 years(n = 50); EC:60.3±7.7 years(n = 37)), or ESS score (BC:6.4±4.4; EC 6.8±4.7; mean±SD; all p>0.2), however, BMI was higher in EC (BC: 29.7±7.9kgm-2; EC: 34.2±8.0 kgm-2; p<0.05). BC had longer sleep latency (BC:31.8±32minutes; EC:19.3±17.9 minutes), less Stage 3 sleep (BC:20.0±5.2%; EC:23.6±8.2%) and more REM sleep (BC:21.1±6.9%; EC: 16.6±5.7%), all p<0.05. EC had lower average awake and asleep oxygen saturation levels (BC: 95.6±1.3%; EC: 94.6±1.9% [awake]: BC: 94.8±2.1%; EC: 93.3±2.4% [asleep]; both p<0.05). Apnea-Hypopnea Index (AHI) (BC: 21.2(7.3–36.9) events/hr; EC: 15.7 (10–33.5) events/hour (median (interquartile range)) was not different p = 0.7), however, 58% and 57% of women with BC and EC respectively, had an AHI>15 events/hour. In this small sample size group, no significant associations (all p>0.1) were detected between OSA metrics and clinico-pathological tumor variables. Conclusion In postmenopausal women with breast or endometrial cancer there is high prevalence of OSA, with no association with specific tumor characteristics detected. Recognition of the high prevalence of OSA in women with cancer is important to recognise as it may impact on surgical risk and quality of life.

Background: Cancer patients often describe poor sleep quality and sleep disruption as contributors to poor quality of life (QoL). In a cross-sectional study of post-treatment breast, endometrial, and melanoma cancer patients, we used actigraphy to quantify sleep regularity using the sleep regularity index (SRI), and examined relationships with reported sleep symptoms and QoL.Methods: Participants were recruited post-primary treatment (35 diagnosed with breast cancer, 24 endometrial cancer, and 29 melanoma) and wore an actigraphy device for up to 2 weeks and SRI was calculated. Self-report questionnaires for cancer-related QoL [European Organization for Research and Treatment of Cancer EORTC (QLQ-C30)] were completed. Data were compared using analysis of variance (ANOVA) or Chi-Square tests. Multivariate linear regression analysis was used to determine independent variable predictors for questionnaire-derived data.Results: Age distribution was similar between cohorts. Endometrial and breast cancer cohorts were predominantly female, as expected, and body mass index (BMI) was higher in the endometrial cancer cohort, followed by breast and melanoma. There were no differences between tumor groups in: total sleep time, sleep onset latency, bedtime, and SRI (breast 80.9 ± 8.0, endometrial 80.3 ± 12.2, and melanoma 81.4 ± 7.0) (all p &gt; 0.05). A higher SRI was associated with both better functional and symptom scores, including increased global QoL, better physical functioning, less sleepiness and fatigue, better sleep quality, and associated with less nausea/vomiting, dyspnea, and diarrhea (all p &lt; 0.05).Conclusion: In cancer patients post-treatment, greater sleep regularity is associated with increased global QoL, as well as better physical functioning and fewer cancer related symptoms. Improving sleep regularity may improve QoL for cancer patients.

Specific sleep disorders have been linked to disease progression in different cancers.We hypothesised sleep symptom clusters would differ between cancer types. The aim of this study was to compare sleep symptom clusters in post-treatment melanoma, breast and endometrial cancer patients. Data were collected from 124 breast cancer patients (1 male, 60 ± 15 years, 28.1 ± 6.6 kg/m 2 ), 82 endometrial cancer patients (64.0 ± 12.5 years, 33.5 ± 10.4 kg/m 2 ) and 112 melanoma patients (59 male, 65.0 ± 18.0 years, 29.1 ± 6.6 kg/m 2 ). All patients completed validated questionnaires to assess sleep symptoms, including the Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), and Functional Outcomes of Sleep Questionnaire-10 (FOSQ-10). Snoring, tiredness, observed apneas, age, BMI, and gender data were also collected. Binary values (PSQI, ISI, FOSQ), or continuous variables for sleepiness (ESS) and perceived sleep quality (PSQI), were created and sleep symptom clusters were identified and compared across cancer cohorts. Four distinct sleep symptom clusters were identified: minimally symptomatic (n = 152, 47.7%); insomnia-predominant (n = 87, 24.9%); very sleepy with upper airway symptoms (n = 51, 16.3%), and severely symptomatic with severe dysfunction (n = 34, 11.1%). Breast cancer patients were significantly more likely to be in the insomnia predominant or severely symptomatic with severe dysfunction clusters, whereas

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Purpose Breast-cancer patients frequently report of poor sleep-quality. Although the pathophysiology is unclear, circadian-sleep misalignment is a plausible mechanism. We compared nocturnal melatonin-secretion, a circadian rhythm marker, in post-menopausal, post-treatment (≥12-months) female breast-cancer patients (BCG), with post-menopausal female controls with no history of cancer (CG) Methods We recruited 6 BCG and 10 CG from Westmead Hospital breast-cancer outpatient clinic or hospital-staff community, respectively. Participants completed the Pittsburgh Sleep Quality Index (PSQI; &gt;5 PSQI-score=poor sleep-quality) and ~7 days of home-actigraphy (Philips Actiwatch-2, Philips Respironics, USA) to ascertain habitual bed-time (HBT). Later, participants completed an overnight, in-laboratory study, with saliva sampled (n=13) at regular intervals under strict dim-light conditions (&lt;1 lux). Salivary-melatonin concentrations were quantified via radioimmunoassay (University of Adelaide). We measured 1) clock-time when salivary-melatonin concentrations reached 4pg/mL (melatonin onset-[DLMO-4pg/ml]) and 2) time-interval between HBT and DLMO-4pg/ml (indicates circadian-sleep misalignment-[PAR-DLMO]). Data were expressed as median [interquartile range], and compared using 2-sided Mann Whitney U-tests. p&lt;0.05 was considered significant. Results BCG and CG had similar ages (62.5 [59.5–67.3] vs. 58.5 [54.0–66.3] yrs, respectively; p=0.23). Compared with CG, BCG had higher PSQI-scores (8.50 [5.25–10.75] vs. 4.00 [3.75–5.50] a.u.; p=0.07), but similar HBT (22:49 [21:46-23:38] vs. 22:17 [21:59-22:21] h:min; p=0.26). BCG had later DLMO-4pg/ml (20:46 [20:01-22:03] vs. 18:23 [17:55-20:07] h:min; p=0.03) and shorter PAR-DLMO (1.43 [0.96–2.38] vs. 3.63 [2.18–3.90] hrs; p=0.09), than CG. Conclusion Preliminary data indicate BCG had poorer sleep-quality, delayed melatonin onset, and altered circadian-sleep alignment; compared with CG. We speculate disrupted nocturnal melatonin-secretion potentially influences poor sleep-quality reported by breast-cancer patients.