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Relationships between cigarette filter ventilation levels, biomarkers of exposure (BOE) and potential harm (BOPH), and harm perceptions were examined.

Filter ventilation levels in cigarette brands were merged with Wave 1 (2013-2014) Population Assessment of Tobacco Use and Health study. Data were restricted to smokers who reported a usual brand and not regular users of other tobacco products. BOEs included nicotine, tobacco-specific nitrosamines, volatile organic compounds (VOC), and polycyclic aromatic hydrocarbons. BOPHs measured inflammation and oxidative stress. Perceived harm was assessed as self-reported risk of one's usual brand compared with other brands.

Filter ventilation ranged from 0.2% to 61.1% (
= 1,503). Adjusted relationships between filter ventilation and BOE or BOPH were nonsignificant except for VOC
-acetyl-S-(phenyl)-L-cysteine (PHMA) and high-sensitivity C-reactive protein (hsCRP). In pairwise comparisons, PHMA was higher in quartile (Q) 4 (4.23 vs. 3.36 pmol/mg;
= 0.0103) and Q3 (4.48 vs. 3.36 pmol/mg;
= 0.0038) versus Q1 of filter ventilation and hsCRP comparisons were nonsignificant. Adjusted odds of perceiving one's own brand as less harmful was 26.87 (95% confidence interval 4.31-167.66), 12.55 (3.01-52.32), and 19.18 (3.87-95.02) times higher in the Q2, Q3, and Q4 of filter ventilation compared with Q1 (
= 0.0037).

Filter ventilation was not associated with BOE or BOPH, yet smokers of higher ventilated cigarettes perceived their brand as less harmful than other brands compared with smokers of lower ventilated cigarettes.

Research to understand the impact of this misperception is needed, and remedial strategies, potentially including a ban on filter ventilation, are recommended.
Research to understand the impact of this misperception is needed, and remedial strategies, potentially including a ban on filter ventilation, are recommended.Esophageal adenocarcinoma is a major cause of cancer-related morbidity and mortality in Western countries. The incidences of esophageal adenocarcinoma and its precursor Barrett's esophagus have increased substantially in the last four decades. Current care guidelines recommend that endoscopy be used for the early detection and monitoring of patients with Barrett's esophagus; however, the efficacy of this approach is unclear. To prevent the increasing morbidity and mortality from esophageal adenocarcinoma, there is a tremendous need for early detection and surveillance biomarker assays that are accurate, low-cost, and clinically feasible to implement. The last decade has seen remarkable advances in the development of minimally invasive molecular biomarkers, an effort led in large part by the Early Detection Research Network (EDRN). Advances in multi-omics analysis, the development of swallowable cytology collection devices, and emerging technology have led to promising assays that are likely to be implemented into clinical care in the next decade. In this review, an updated overview of the molecular pathology of Barrett's esophagus and esophageal adenocarcinoma and emerging molecular biomarker assays, as well as the role of EDRN in biomarker discovery and validation, will be discussed.See all articles in this CEBP Focus section, "NCI Early Detection Research Network Making Cancer Detection Possible."Prostate cancer remains the most common non-skin cancer and second leading cause of death among men in the United States. Although progress has been made in diagnosis and risk assessment, many clinical questions remain regarding early identification of prostate cancer and management. The early detection of aggressive disease continues to provide high curative rates if diagnosed in a localized state. Unfortunately, prostate cancer displays significant heterogeneity within the prostate organ and between individual patients making detection and treatment strategies complex. Although prostate cancer is common among men, the majority will not die from prostate cancer, introducing the issue of overtreatment as a major concern in clinical management of the disease. The focus of the future is to identify those at highest risk for aggressive prostate cancer and to develop prevention and screening strategies, as well as discerning the difference in malignant potential of diagnosed tumors. The Prostate Cancer Research Group of the National Cancer Institute's Early Detection Research Network has contributed to the progress in addressing these concerns. This summary is an overview of the activities of the group.See all articles in this CEBP Focus section, "NCI Early Detection Research Network Making Cancer Detection Possible."Lung cancer is the leading worldwide cause of cancer mortality, as it is often detected at an advanced stage. Since 2011, low-dose CT scan-based screening has promised a 20% reduction in lung cancer mortality. However, effectiveness of screening has been limited by eligibility only for a high-risk population of heavy smokers and a large number of false positives generated by CT. Biomarkers have tremendous potential to improve early detection of lung cancer by refining lung cancer risk, stratifying positive CT scans, and categorizing intermediate-risk pulmonary nodules. Three biomarker tests (Early CDT-Lung, Nodify XL2, Percepta) have undergone extensive validation and are available to the clinician. The authors discuss these tests, with their clinical applicability and limitations, current ongoing evaluation, and future directions for biomarkers in lung cancer screening and detection.See all articles in this CEBP Focus section, "NCI Early Detection Research Network Making Cancer Detection Possible."
Evidence-based breast cancer treatment guidelines recommend the most appropriate course of therapy based on tumor characteristics and extent of disease. Evaluating the multilevel factors associated with guideline discordance is critical to identifying strategies to eliminate breast cancer survival disparities.

We identified females diagnosed with a first primary, stage I-III breast cancer between the ages of 20-69 years of age from the population-based Seattle-Puget Sound Surveillance, Epidemiology, and End Results registry. Participants completed a survey about social support, utilization of patient support services, hypothesized barriers to care, and initiation of breast cancer treatment. We used logistic regression to estimate odds ratios and 95% confidence intervals (CI).

Among 1,390 participants, 10% reported guideline-discordant care. In analyses adjusted for patient-level sociodemographic factors, individuals who did not have someone to go with them to appointments or drive them home (OR 1.96; 95% CI, 1.09-3.59) and those who had problems talking to their doctors or their staff (OR 2.03; 95% CI, 1.13-3.64) were more likely to be guideline discordant than those with social support or without such problems, respectively. Use of patient support services was associated with a 43% lower odds of guideline discordance (OR 0.57; 95% CI, 0.36-0.88).

Although guideline discordance in this cohort of early-stage breast cancer survivors diagnosed <70 years of age was low, instrumental social support, patient support services, and communication with doctors and their staff emerged as potential multilevel intervention targets for improving breast cancer care delivery.

This study supports extending the reach of interventions designed to improve guideline concordance.
This study supports extending the reach of interventions designed to improve guideline concordance.
Although immune checkpoint blockade is effective for several malignancies, a substantial number of patients remain refractory to treatment. SBI-0640756 manufacturer The future of immunotherapy will be a personalized approach adapted to each patient's cancer-immune interactions in the tumor microenvironment (TME) to prevent suppression of antitumor immune responses. To demonstrate the feasibility of this kind of approach, we developed combination therapy for a preclinical model guided by deep immunophenotyping of the TME.

Gastric cancer cell lines YTN2 and YTN16 were subcutaneously inoculated into C57BL/6 mice. YTN2 spontaneously regresses, while YTN16 grows progressively. Bulk RNA-Seq, single-cell RNA-Seq (scRNA-Seq) and flow cytometry were performed to investigate the immunological differences in the TME of these tumors.

Bulk RNA-Seq demonstrated that YTN16 tumor cells produced CCL20 and that CD8
T cell responses were impaired in these tumors relative to YTN2. We have developed a vertical flow array chip (VFAC) for targeted ade together with anti-PD-1 mAb therapy eradicated these YTN16 tumors. Thus, the deep immunological phenotyping can guide immunotherapy for the tailored treatment of each individual patient's tumor.
suppression of neoantigen-specific CD8+ T cells which was responsible for the lack of tumor rejection. IL-17 blockade together with anti-PD-1 mAb therapy eradicated these YTN16 tumors. Thus, the deep immunological phenotyping can guide immunotherapy for the tailored treatment of each individual patient's tumor.
Immune checkpoint inhibitors that target the programmed cell death protein 1 (PD-1) receptor induce a response in only a subgroup of patients with metastatic melanoma. Previous research suggests that transforming growth factor beta signaling and a collagen-rich peritumoral stroma (tumor fibrosis), may negatively interfere with the interaction between T cells and tumor cells and thereby contribute to resistance mechanisms by immune-exclusion, while increased tumor infiltration of M1-like macrophages enhances T cell activity. Hence, the current study aimed to assess the relationship between blood-based markers of collagen or vimentin turnover (reflecting M1 macrophage activity) and clinical outcome in patients with metastatic melanoma after PD-1 inhibition.

Patients with metastatic melanoma who were treated with anti-PD-1 monotherapy between May 2016 and March 2019 were included in a prospective observational study. N-terminal pro-peptide of type III collagen (PRO-C3) cross-linked N-terminal pro-peptides ofomponents to predict immunotherapy response.
Skin cancers are known for their strong immunogenicity, which may contribute to a high treatment efficacy of immune checkpoint inhibition (ICI). However, a considerable proportion of patients with skin cancer is immuno-compromised by concomitant diseases. Due to their previous exclusion from clinical trials, the ICI treatment efficacy is poorly investigated in these patients. The present study analyzed the ICI treatment outcome in advanced patients with skin cancer with a concomitant hematological malignancy.

This retrospective multicenter study included patients who were treated with ICI for locally advanced or metastatic melanoma (MM), cutaneous squamous cell carcinoma (cSCC), or Merkel cell carcinoma (MCC), and had a previous diagnosis of a hematological malignancy irrespective of disease activity or need of therapy at ICI treatment start. Comparator patient cohorts without concomitant hematological malignancy were extracted from the prospective multicenter skin cancer registry ADOREG. Treatment outcomrts without hematological malignancy (n=392) revealed no relevant differences in ICI therapy outcome for MM and MCC, but a significantly reduced PFS for cSCC (p=0.002).

ICI therapy showed efficacy in advanced patients with skin cancer with a concomitant hematological malignancy. Compared with patients without hematological malignancy, the observed ICI therapy outcome was impaired in cSCC, but not in MM or MCC patients.
ICI therapy showed efficacy in advanced patients with skin cancer with a concomitant hematological malignancy. Compared with patients without hematological malignancy, the observed ICI therapy outcome was impaired in cSCC, but not in MM or MCC patients.
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