Background: In spite of recent advances in diagnostic and therapeutic measures, the prognosis of hepatocellular carcinoma (HCC) patients remains poor. Therefore, it is crucial to understand what factors are involved in promoting development of HCC. Evidence is accumulating that members of the chemokine receptor family are viewed as promising therapeutic targets in the fight against cancer. More recent studies have revealed that chemokine receptor CXCR7 plays an important role in cancer development. However, little is known about the effect of CXCR7 on the process of HCC cell invasion and angiogenesis. The aim of this study is to investigate the expression of CXCR7 in hepatocellular carcinoma tissues and cell lines and to evaluate the role of CXCR7 in tumor growth, angiogenesis and invasion of HCC cells. Methods: We constructed CXCR7 expressing shRNA, and CXCR7shRNA was subsequently stably transfected into human HCC cells. We evaluated the effect of CXCR7 inhibition on cell invasion, adhesion, VEGF secretion, tube formation and tumor growth. Immunohistochemistry was done to assess the expression of CXCR7 in human hepatocellular carcinoma tissues and CD31 in tumor of mice. We also evaluated the effect of VEGF stimulation on expression of CXCR7. Results: CXCR7 was overexpressed in hepatocellular carcinoma tissues. We showed that high invasive potential HCC cell lines express high levels of CXCR7. In vitro, CXCL12 was found to induce invasion, adhesion, tube formation, and VEGF secretion in SMMC-7721 cells. These biological effects were inhibited by silencing of CXCR7 in SMMC-7721 cells. In addition, we also found that VEGF stimulation can up-regulate CXCR7 expression in SMMC-7721 cells and HUVECs. More importantly, enhanced expression of CXCR7 by VEGF was founctional. In vivo, tumor growth and angiogenesis were suppressed by knockdown of CXCR7 in SMMC-7721 cells. However, silencing of CXCR7 did not affect metastasis of tumor in vivo. Conclusions: Increased CXCR7 expression was found in hepatocellular carcinoma tissues. Knockdown of CXCR7 expression by transfected with CXCR7shRNA significantly inhibits SMMC-7721 cells invasion, adhesion and angiogenesis. Finally, down-regulation of CXCR7 expression lead to a reduction of tumor growth in a xenograft model of HCC. This study provides new insights into the significance of CXCR7 in invasion and angiogenesis of HCC.

Introduction: The efficacy of gefitinib supplementation for breast cancer remains controversial. We conduct a systematic review and meta-analysis to explore the influence of gefitinib supplementation vs placebo on the efficacy of breast cancer. Methods: We have searched PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through February 2019 and included randomized controlled trials assessing the effect of gefitinib supplementation vs placebo on overall response for breast cancer patients. This meta-analysis was performed using the random-effect model. Results: Seven randomized controlled trials involving 927 patients were included in the meta-analysis. Overall, compared with control group for breast cancer, gefitinib supplementation revealed no obvious impact on complete response (risk ration [RR] = 1.19; 95% confidence interval [CI] = 0.58 to 2.44; P = .63), progressive disease (RR = 0.81; 95% CI = 0.59–1.11; P = .18), partial response (RR = 0.67; 95% CI = 0.36–1.25; P = .21), stable disease (RR = 1.02; 95% CI = 0.65–1.60; P = .92), nausea or vomiting (RR = 0.99; 95% CI = 0.73–1.33; P = .93), but was associated with increased incidence of diarrhea (RR = 2.80; 95% CI = 2.23–3.52; P < .00001), decreased incidence of hot flash (RR = 0.53; 95% CI = 0.37–0.78; P = .001), and improved incidence of adverse events (RR = 1.12; 95% CI = 1.05–1.19; P = .0006). Conclusions: Gefitinib supplementation may provide no positive effect on complete response, progressive disease, partial response or stable disease for breast cancer patients, but with the increase in adverse events.

The study explored the impact of pretreatment serum albumin-to-alkaline phosphatase ratio (AAPR) and changes in tumor blood supply on pathological complete response (pCR) in breast cancer (BC) patients following neoadjuvant chemotherapy (NACT). Additionally, a nomogram for predicting pCR was established and validated. The study included BC patients undergoing NACT at Yongchuan Hospital of Chongqing Medical University from January 2019 to October 2023. We analyzed the correlation between pCR and clinicopathological factors, as well as tumor ultrasound features, using chi-square or Fisher's exact test. We developed and validated a nomogram predicting pCR based on regression analysis results. The study included 176 BC patients. Logistic regression analysis identified AAPR [odds ratio (OR) 2.616, 95% confidence interval (CI) 1.140–5.998, P = 0.023], changes in tumor blood supply after two NACT cycles (OR 2.247, 95%CI 1.071–4.716, P = 0.032), tumor histological grade (OR 3.843, 95%CI 1.286–10.659, P = 0.010), and HER2 status (OR 2.776, 95%CI 1.057–7.240, P = 0.038) as independent predictors of pCR after NACT. The nomogram, based on AAPR, changes in tumor blood supply after two NACT cycles, tumor histological grade, and HER2 status, demonstrated a good predictive capability.

Background: Detection of circulating tumor DNA (ctDNA) has attracted growing attention for predicting postoperative breast cancer recurrence; however, the differences between the landmark and surveillance strategies remain unclear. Methods: We systematically searched the PubMed, Cochrane Library, Embase, and Ovid MEDLINE databases for studies published up to April 17, 2025. Effect models were selected based on heterogeneity tests to pool diagnostic indicators, including sensitivity and specificity. Subgroup analyses were conducted according to molecular subtype, detection method, analytical strategy, and disease stage. Results: A total of 17 studies were included in the analysis. The sensitivity and specificity of the landmark strategy were 0.40 (95% CI: 0.22–0.62) and 0.95 (95% CI: 0.81–0.99), respectively. For the surveillance strategy, sensitivity was 0.79 (95% CI: 0.71–0.85) and specificity was 0.98 (95% CI: 0.92–0.99). The surveillance strategy significantly improved sensitivity without a substantial loss of specificity. Among molecular subtypes, triple-negative breast cancer(TNBC) exhibited the best performance under the surveillance strategy. Whole-genome sequencing (WGS), droplet digital PCR (ddPCR), and whole-exome sequencing (WES) all demonstrated high sensitivity within the surveillance framework. Conclusion: ctDNA serves as a highly specific biomarker for predicting postoperative breast cancer recurrence. The surveillance strategy substantially improves its sensitivity; however, the current performance remains below the ideal threshold for clinical implementation. Future research should focus on refining detection strategies and technologies to achieve personalized recurrence risk stratification and guide therapeutic decision-making. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/ , identifier CRD420251056270.

Purpose Explore the impact of pretreatment serum albumin-to-alkaline phosphatase ratio (AAPR) and changes in tumor blood supply on pathological complete response (pCR) in breast cancer(BC) patients following neoadjuvant chemotherapy (NACT). Additionally, establish and validate a nomogram for predicting pCR. Methods Included BC patients undergoing NACT at Yongchuan Hospital of Chongqing Medical University from January 2019 to October 2023. Analyzed the correlation between pCR and clinicopathological factors, as well as tumor ultrasound features, using chi-square or Fisher's exact test. Developed and validated a nomogram predicting pCR based on regression analysis results. Results The study included 176 BC patients, with 38.64% achieving pCR after NACT. Logistic regression analysis identified AAPR [odds ratio (OR): 2.616, 95% confidence interval (CI): 1.140–5.998, P = 0.023], changes in tumor blood supply after two NACT cycles (OR: 2.247, 95%CI: 1.071–4.716, P = 0.032), tumor histological grade (OR: 3.843, 95%CI: 1.286–10.659, P = 0.010), and HER2 status (OR: 2.776, 95%CI: 1.057–7.240, P = 0.038) as independent predictors of pCR after NACT. The nomogram, based on AAPR, changes in tumor blood supply after two NACT cycles, tumor histological grade, and HER2 status, demonstrated a good predictive capability. Conclusion AAPR, changes in tumor blood supply after two NACT cycles, tumor histological grade, and HER2 status independently predicted pCR in BC patients following NACT. The nomogram, based on these positive factors, demonstrated a good predictive ability.