Intensity-modulated radiotherapy with more than 60 Gy improved the survival of inoperable patients with locally advanced esophageal squamous cell carcinoma: A population-based real-world study.

ABSTRACT: Intensity-modulated radiotherapy (IMRT) is widely applied during the treatment of esophageal squamous cell carcinoma (ESCC), but the optimal radiation dose still lacks a consensus. The aim of this study was to explore the optimal radiation dose for inoperable locally advanced ESCC patients treated with IMRT in a real-world clinical setting.A total of 90 inoperable ESCC patients with locally advanced stages of II-IVA treated with IMRT in our institute between February 1, 2014 and June 30, 2019 were included in this retrospective study. Sixty patients had received >60 Gy (high dose group) and 30 patients had received ≤60 Gy (low dose group). The median radiation dose was 66 Gy (range: 61-70 Gy) and 50.2 Gy (range: 40-60 Gy), respectively. Concurrent chemotherapies were platinum-based regimens.The median progression free survival (PFS) and overall survival (OS) of all patients were 7.6 and 14.1 months, respectively. Patients in the high dose group exhibited a significantly better PFS (1-year PFS 34.6% vs 22.8%; 2-year PFS 11.9% vs 0%, P = .008) and OS (1-year OS 57.5% vs 39.5%; 2-year OS 31.4% vs 15.8%, P = .007). The median PFS in the high and low dose groups were 8.1 and 6.1 months, and the median OS were 15.4 and 8.5 months, respectively. Multivariate Cox analysis showed that radiation dose (>60 Gy vs ≤60 Gy) was independently prognostic factor for OS (HR: 0.44; 95% CI: 0.22-0.89; P = .021), but not for PFS (HR: 0.56; 95% CI: 0.31-1.02; P = .058). There was no significant difference in treatment-related toxicities of grade ≥3 between the 2 groups (P = .402).This retrospective study confirmed that higher radiation dose (>60 Gy) resulted in better survival outcomes for inoperable patients with locally advanced ESCC treated with IMRT.

Construction of Nomograms for Predicting Pathological Complete Response and Tumor Shrinkage Size in Breast Cancer.

PURPOSE: Pathological complete response (pCR) is the goal of neoadjuvant chemotherapy (NAC) for the HER2-positive and triple-negative subtypes of breast cancer and is related to survival benefit; however, luminal breast cancer is not sensitive to NAC, and the size of tumor shrinkage is a more meaningful clinical indicator for the luminal breast cancer subtype. We wanted to use a nomogram or formula to develop and implement a series of prediction models for pCR or tumor shrinkage size. PATIENTS AND METHODS: We developed a prediction model in a primary cohort consisting of 498 patients with invasive breast cancer, and the data were gathered from July 2016 to September 2018. The endpoint was pCR and tumor shrinkage size. In the primary cohort, the HER2-positive cohort, and the triple-negative cohort, multivariate logistic regression analysis was used to screen the significant clinical features and clinicopathological features to develop nomograms. In the luminal group, multivariate linear regression analysis was used to test the risk factors that affect tumor shrinkage size. The area under the receiver operating characteristic curve (AUC) and calibration curves were adopted to evaluate and analyze the discrimination and calibration ability of nomograms. Furthermore, we also performed internal validation and independent validation in the primary cohort. RESULTS: ER status, KI67 status, HER2 status, number of NAC cycles, and tumor size were independent predictive factors of pCR in the primary cohort. These indicators had good discrimination and calibration in the primary and validation cohorts (AUC: 0.873, 0.820). The nomogram for HER2-positive and triple-negative breast cancer (TNBC) had an AUC of 0.820 and 0.785, respectively. Both the HER2 positive and TNBC nomogram calibration curves indicated significant agreement. Moreover, the luminal subtype prediction model was Y (tumor shrinkage size) = -0.576 × (age at diagnosis) + 2.158 × (number of NAC cycles) + 0.233 × (pre-NAC tumor size) + 51.662. CONCLUSION: Utilizing this predictive model will enable us to identify patients at high probability for pCR after NAC. Clinicians can stratify these patients and make individualized and personalized recommendations for therapy.

LncRNA DANCR contributes to tumor progression via targetting miR-216a-5p in breast cancer: lncRNA DANCR contributes to tumor progression.

Breast cancer, the most frequently occurring malignant tumor, has high mortality rate, especially triple-negative breast cancer (TNBC). LncRNA-differentiation antagonizing non-protein coding RNA (lncRNA DANCR) has been found that its aberrant expression was associated with tumor progression and it was promising to be a potential target for cancer therapy. The goal of the present study was to explore the biological effects and underlying mechanism of DANCR in breast cancer. Our results showed that DANCR was up-regulated in TNBC tissues and breast cancer cells compared with normal breast tissues and cells, and higher DANCR level suggested poorer prognosis, implying that it was promising to be a novel biomarker used for TNBC diagnosis and prognosis. To better research the functions and mechanism of DANCR on breast cancer cells, we selected two cell lines used for next study: one TNBC cell line-MDA-MB-231 and one ER-positive breast cancer cell line-MCF-7. Further study indicated that DANCR overexpression significantly promoted cell proliferation and invasion in vitro and contributed to tumor growth in vivo To deeply understand its molecular mechanism, miRNA-216a-5p was identified as a target of DANCR by bioinformatic analysis. Experiments demonstrated that miRNA-216a-5p interacted with DANCR and its inhibitor could weaken the influences induced by DANCR knockdown for cancer cells, including cell proliferation and invasion, and the expression of Nanog, SOX2, and OCT4. Therefore, DANCR might act as a tumor promoter by targetting miRNA-216a-5p, which might provide a potential therapy target for breast cancer treatment.