Additional PD-1 inhibitor improves complete response to induction chemotherapy in locally advanced nasopharyngeal carcinoma.

Purpose: To investigate the treatment response and toxicity of the combination of induction chemotherapy (IC) and PD-1 inhibitor in locally advanced nasopharyngeal carcinoma (LANPC). Methods: Patients with stage III-IVA NPC who received IC or IC + PD-1 inhibitor were included. The chi-square test and multivariate logistic regression analysis were used for statistical analysis. Results: A total of 225 patients were identified, including 193 (85.8%) and 32 (14.2%) who received IC alone and IC + PD-1 inhibitor, respectively. The addition of PD-1 inhibitor to IC significantly improved the tumor response than those treated with IC alone. The complete response (CR), partial response, stable disease, and progressive disease rates of 4.7% vs. 31.3%, 69.4% vs. 62.5%, 24.9% vs. 6.3%, and 1.0% vs. 0% in patients receiving IC alone and IC + PD-1 inhibitor, respectively (P<0.001). The results of the multivariate logistic regression showed that receiving PD-1 inhibitor was an independent predictor influencing the CR rate of patients (odds ratio 9.814, P<0.001). The most common toxicity by using IC and PD-1 inhibitor was hematological toxicity. In terms of non-hematological toxicity, 7 (21.9%) patients experienced thyroid dysfunction and all of them were hyperthyroidism. No grade 5 toxicities were found. In those who received IC and PD-1 inhibitor, the one-year locoregional recurrence-free survival, distant metastasis-free survival, disease-free survival, and overall survival were 100%, 96.9%, 96.9%, and 100%, respectively. Conclusion: The addition of PD-1 inhibitor to IC has promise as an effective treatment approach for LANPC. More studies are expected to provide further insights into the optimal use of this treatment strategy, paving the way for more personalized and effective treatment options for patients with LANPC.

Design, synthesis, and evaluation of novel ferrostatin derivatives for the prevention of HG-induced VEC ferroptosis.

Ferroptosis is a nonapoptotic, iron-catalyzed form of regulated cell death. It has been shown that high glucose (HG) could induce ferroptosis in vascular endothelial cells (VECs), consequently contributing to the development of various diseases. This study synthesized and evaluated a series of novel ferrostatin-1 (Fer-1) derivatives fused with a benzohydrazide moiety to prevent HG-induced VEC ferroptosis. Several promising compounds showed similar or improved inhibitory effects compared to positive control Fer-1. The most effective candidate 12 exhibited better protection against erastin-induced ferroptosis and high glucose-induced ferroptosis in VECs. Mechanistic studies revealed that compound 12 prevented mitochondrial damage, reduced intracellular ROS accumulation, upregulated the expression of GPX4, and decreased the amounts of ferrous ion, LPO and MDA in VECs. However, compound 12 still exhibited undesirable microsomal stability like Fer-1, suggesting the need for further optimization. Overall, the present findings highlight ferroptosis inhibitor 12 as a potential lead compound for treating ferroptosis-associated vascular diseases.

Addition of nimotuzumab to concurrent chemoradiotherapy after induction chemotherapy improves outcomes of patients with locally advanced nasopharyngeal carcinoma.

Purpose: To investigate the survival outcomes and toxicities associated with the addition of nimotuzumab to concurrent chemoradiotherapy (CCRT) in locally advanced nasopharyngeal carcinoma (LANPC) patients who received induction chemotherapy (IC). Methods: Patients with stage III-IVA nasopharyngeal carcinoma who received IC and CCRT between January 2017 and October 2021 were retrospectively included. We aimed to compare the locoregional recurrence-free survival (LRFS), distant metastasis-free survival (DMFS), disease-free survival (DFS), and overall survival (OS) between patients treated with CCRT+nimotuzumab and CCRT alone. Results: We included 411 patients in the analysis. Of these patients, 267 (65.0%) and 144 (35.0%) had CCRT+nimotuzumab and CCRT alone, respectively. Similar LRFS was found between those with and without nimotuzumab (92.9% vs. 92.6%, p = 0.855). The 3-year DMFS was 88.2% and 76.2% in those with and without nimotuzumab (p = 0.002). The 3-year DFS was 83.4% and 70.6% in those with and without nimotuzumab treatment (p = 0.003). The 3-year OS was 92.1% and 81.1% in those with and without nimotuzumab (p = 0.003). The multivariate Cox regression analysis indicated that the addition of nimotuzumab was independently associated with better DMFS (hazard ratio [HR] 0.606, p = 0.049), DFS (HR 0.613, p = 0.028), and OS (HR 0.497, p = 0.019). No significant differences in major toxicities were found between the two treatment arms, including hematologic toxicities, hepatoxicity, nephrotoxicity, gastrointestinal reactions, and mucositis (all p > 0.05). Conclusion: The addition of nimotuzumab to CCRT after IC in LANPC has shown promising results in improving treatment outcomes and acceptable toxicities.

Neoadjuvant therapy with chemotherapy and immune checkpoint inhibitor for laryngeal function preservation in locally advanced hypopharyngeal cancer.

Purpose: To evaluate the efficacy and laryngeal function preservation of neoadjuvant treatment with chemotherapy and immune checkpoint inhibitor for locally advanced hypopharyngeal cancer (LAHPC). Methods: We retrospectively collected LAHPC patients who were diagnosed between February 2022 and June 2023. The patients received a combination of chemotherapy and immune checkpoint inhibitors as the neoadjuvant therapy. The response to treatment, laryngeal function preservation rate, and short-term survival were assessed. Results: A total of 20 patients were included. Of these patients, 17 (85.0%) had stage IVA-B disease. Ten (50%) and four (20%) patients achieved pathological complete response (PCR) and major pathological response (MPR) to the primary tumor, respectively. In addition, 6 patients had incomplete pathological response (IPR). In the neck, 19 patients had node-positive disease before treatment, and only 5 patients (26.4%) had PCR to regional lymph nodes. Pathologically positive lymph nodes were still observed in 14 (73.6%) patients. Significant downgrading on narrow-band imaging assessment in primary tumors was associated with a higher probability of PCR or MPR than those with IPR (92.9% vs. 33.3%, P=0.014). The overall rate of laryngeal preservation was 95.0%. No severe perioperative complications or perioperative death were found. All patients completed the recommended postoperative radiotherapy/chemoradiotherapy. The median follow-up period was 12.1 months. The 1-year progression-free survival and overall survival were 94.1% and 92.9%, respectively. During the follow-up period, all 19 patients who underwent laryngeal preservation surgery had their laryngeal function preserved. Conclusion: The addition of an immune checkpoint inhibitor to neoadjuvant chemotherapy effectively preserves laryngeal function without increasing complications related to surgery and postoperative radiotherapy in LAHPC.

21-gene recurrence score in predicting the outcome of postoperative radiotherapy in T1-2N1 luminal breast cancer after breast-conserving surgery.

BACKGROUND: In those with one to three positive lymph nodes (N1) breast cancer (BC), the 21-gene recurrence score (RS) classification can be referred for decision-making on adjuvant chemotherapy. This study aimed to investigate the effect of RS in predicting the survival benefit of postoperative radiotherapy (PORT) in T1-2N1 BC with estrogen receptor-positive and human epidermal growth factor receptor 2-negative disease after breast-conserving surgery (BCS). METHODS: We included patients with BC and available RS data from the Surveillance, Epidemiology, and End Results Oncotype DX database. The chi-square test, Kaplan-Meier method, propensity score matching (PSM) as well as multivariable Cox proportional hazard analyses were used for statistical analyses. RESULTS: We included 6509 patients in the analysis. Of these patients, 5302 (85.5%) were treated with BCS + PORT, and 207 (15.5%) had BCS alone. There were 1419 (21.8%), 4319 (66.4%), and 771 (11.8%) patients being low-, intermediate-, and high-risk RS, respectively. After PSM, PORT was significantly associated with a 5-year overall survival (OS) advantage (95.1% vs. 90.5%, P < 0.001) compared to those without PORT, which similar breast cancer-specific survival (BCSS) was found between the treatment arms (P = 0.126). The sensitivity analyses showed that PORT was not associated with a better BCSS (P = 0.472) and OS (P = 0.650) than those without PORT in the low-risk RS cohort. However, PORT was associated with a better BCSS (P = 0.031) and OS (P < 0.001) compared to those without PORT in the intermediate/high-risk RS cohorts. CONCLUSIONS: Our study highlights the possible role of the RS in predicting the outcome of PORT in T1-2N1 luminal BC patients undergoing BCS.

HOXC10 promotes esophageal squamous cell carcinoma progression by targeting FOXA3 and indicates poor survival outcome.

Background: Esophageal cancer is one of the most unknown and deadliest cancers in the world. Although recent studies have identified some mutations linked to the development of squamous cell carcinoma of the esophagus (ESCC), the specific role of HomeoboxC10 (HOXC10) in the pathogenesis still requires further investigation. Methods: Agilent mRNA single-channel gene expression was employed to identify genome-wide gene signatures in ESCC. These signatures were also verified using qRT-PCR, immunohistochemical staining as well as Western blot. The biological functions of HOXC10 were further investigated through cellular studies conducted on ESCC cells. Survival analysis was conducted utilizing the Kaplan-Meier method. The GEPIA database and the STRING website were utilized to predict the potential targets that bind to HOXC10. Co-immunoprecipitation assays were performed to investigate the binding interaction between HOXC10 and Forkhead Box A3 (FOXA3). Animal models were established to analyze the effects of HOXC10 silencing on tumorigenesis in vivo. Results: The expression levels of HOXC10 mRNA were found to be upregulated in ESCC. Survival analysis revealed a significant association between abnormally elevated levels of HOXC10 mRNA and an unfavorable prognosis in patients with ESCC. In vitro studies revealed that the knockdown of HOXC10 expression resulted in the inhibition of the proliferation, invasion, and migrating ability of ESCC cells through the upregulation of FOXA3. Furthermore, tumor-bearing mouse models studies demonstrated that HOXC10 through knockdown techniques significantly suppressed ESCC tumor growth. HOXC10 was found to enhance the activation of the MAPK signaling pathway by regulating FOXA3 in ESCC cells. Conclusion: These results support a key role for HOXC10 in the tumorigenesis of ESCC by upregulating FOXA3 via the MAPK pathway and highlight its potential as a promising diagnostic and prognostic marker for ESCC.

ALAD-YOLO:an lightweight and accurate detector for apple leaf diseases.

Suffering from various apple leaf diseases, timely preventive measures are necessary to take. Currently, manual disease discrimination has high workloads, while automated disease detection algorithms face the trade-off between detection accuracy and speed. Therefore, an accurate and lightweight model for apple leaf disease detection based on YOLO-V5s (ALAD-YOLO) is proposed in this paper. An apple leaf disease detection dataset is collected, containing 2,748 images of diseased apple leaves under a complex environment, such as from different shooting angles, during different spans of the day, and under different weather conditions. Moreover, various data augmentation algorithms are applied to improve the model generalization. The model size is compressed by introducing the Mobilenet-V3s basic block, which integrates the coordinate attention (CA) mechanism in the backbone network and replacing the ordinary convolution with group convolution in the Spatial Pyramid Pooling Cross Stage Partial Conv (SPPCSPC) module, depth-wise convolution, and Ghost module in the C3 module in the neck network, while maintaining a high detection accuracy. Experimental results show that ALAD-YOLO balances detection speed and accuracy well, achieving an accuracy of 90.2% (an improvement of 7.9% compared with yolov5s) on the test set and reducing the floating point of operations (FLOPs) to 6.1 G (a decrease of 9.7 G compared with yolov5s). In summary, this paper provides an accurate and efficient detection method for apple leaf disease detection and other related fields.

Recent Advances in Polyoxometalate Based Nanoplatforms Mediated Reactive Oxygen Species Cancer Therapy.

The potential of reactive oxygen species (ROS) cancer therapy in tumor treatment has been greatly enhanced by the introduction of catalytically superior polyoxometalate (POM)-based nanoplatforms, mainly composed of atomic clusters consisting of pre-transition metals and oxygen. These nanoplatforms have unique advantages, such as Fenton activity at neutral pH, induction of cellular ferroptosis instead of just apoptosis, and sensitivity to external field stimulation. However, there are also inevitable challenges such as neutralization of ROS by the antioxidant system of the tumor microenvironment (TME), hypoxia, and limited hydrogen peroxide concentrations. This review article aims to provide an overview of recent research advancements in POM-based nanoplatforms for ROS therapy from the perspective of chemical reactions and biological processes, addressing endogenous and exogenous factors that affect the antitumor efficacy. Endogenous factors include the mechanism of ROS generation by POM, the impact of pH and antioxidant systems on POM, and the various manners of tumor cell death. Exogenous stimuli mainly include light, heat, X-rays, and electricity. The article analyzes the specific mechanisms of action of each influencing factor in the first two sections, concluding with the limitations of the present study and some possible directions for future research.

High expression COL10A1 promotes breast cancer progression and predicts poor prognosis.

Background: As a common malignant disease in females, breast cancer (BCa) causes increasing numbers of cancer-related death. Collagen X alpha 1 chain (COL10A1) plays a critical role in the oncogenesis and progression of malignant tumors. However, a systematic analysis of COL10A1 in BCa has not been conducted. Methods: The COL10A1 expression level and prognostic value in BCa were defined through the Cancer Genome Atlas (TCGA) as well as the Kaplan-Meier plotter data respectively. The expression pattern of COL10A1 was subsequently confirmed on tissue microarray (TMA) by immunochemistry (IHC) staining. Moreover, cellular functional assays which aimed to evaluate cell proliferation, migration, invasion, and apoptosis, were conducted to investigate the oncogenic activity of COL10A1 in BCa. Then, Tumor Immune Estimation Resource (TIMER) was adopted to determine the association between COL10A1 expression and immune cell infiltration. Results: Bioinformatics analysis revealed that COL10A1 was significantly overexpressed and had notable prognostic value, especially for distant metastasis-free survival (DMFS) in BCa. Moreover, IHC analysis of 140 BCa tissues on TMA chips exhibited the overexpression of COL10A1 was correlated to advanced clinical stage, poor overall survival (OS), and worse recurrence-free survival (RFS). Besides, knockdown of COL10A1 remarkably suppressed cell proliferation, migration, and invasion in BCa cells, and notably promoted cell apoptosis as well. Furthermore, COL10A1 was positively associated with immune cell infiltration including B cell, CD8+ T cell, CD4+ T cell, macrophage, neutrophil, and dendritic cell. Conclusion: The results revealed that COL10A1 is a novel oncogene and could serve as a potential prognostic biomarker in BCa. Besides, the downregulation of COL10A1 could inhibit BCa progression, which could be a potential target for BCa therapy.

LINC00630 as a miR-409-3p sponge promotes apoptosis and glycolysis of colon carcinoma cells via regulating HK2.

Long-chain non-coding RNAs (lncRNAs) belong to the family of non-coding RNAs and contain more than 200 nucleotides. They are involved in the growth, apoptosis, and glycolysis of carcinoma cells. A newly discovered lncRNA, LINC00630, has been reported in colon carcinoma. In this study, we found that the expression of LINC00630 was remarkably upregulated in colon carcinoma tissues and cell lines compared with that in adjacent tissues and the NCM-460 cell lines. Knocking out LINC00630 resulted in inhibition of proliferation and glycolysis but increase in apoptosis. In addition, we confirmed the direct interaction between LINC00630 and miR-409-3p in colon carcinoma cells using bioinformatics methods and dual luciferase reporter gene assay. Finally, we demonstrated that LINC00630 could promote cell growth and glycolysis and inhibit apoptosis by functioning as a miR-409-3p sponge, and further regulate hexokinase 2 (HK2) in colon carcinoma cells. Our results confirmed that LINC00630 regulates proliferation, glycolysis, and apoptosis mainly through targeting the miR-409-3p/HK2 axis, which may explain the progression of colon carcinoma and provide a potential target for the treatment of colon carcinoma.

Wnt5a: A promising therapeutic target in ovarian cancer.

Despite the rapid development of novel adjuvant and neoadjuvant chemotherapeutic drugs in recent years, advanced ovarian cancer still lacks effective treatment strategies and remains one of the main causes of death among women. Wnt protein family is widely expressed in a variety of human tissues, and Wnt5a is an important member of the noncanonical Wnt pathway. Wnt5a has been found to induce tumor suppression as well as to function as an oncogene depending upon the specific cancer type. In ovarian cancer, Wnt5a protein expression has been observed to be significantly upregulated and associated with poor prognosis. Researchers found that downregulating Wnt5a expression levels effectively suppresses ovarian cancer cell migration and invasion abilities. We believe that the downregulation of Wnt5a will be an attractive and promising antimetastatic therapeutic approach for the future treatment of patients with advanced ovarian cancer. The present review focuses on the mechanisms and therapeutic potential of Wnt5a as a promising novel therapeutic target for ovarian cancer.

Creation of a Prognostic Risk Prediction Model for Lung Adenocarcinoma Based on Gene Expression, Methylation, and Clinical Characteristics.

BACKGROUND This study aimed to identify important marker genes in lung adenocarcinoma (LACC) and establish a prognostic risk model to predict the risk of LACC in patients. MATERIAL AND METHODS Gene expression and methylation profiles for LACC and clinical information about cases were downloaded from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, respectively. Differentially expressed genes (DEGs) and differentially methylated genes (DMGs) between cancer and control groups were selected through meta-analysis. Pearson coefficient correlation analysis was performed to identify intersections between DEGs and DMGs and a functional analysis was performed on the genes that were correlated. Marker genes and clinical factors significantly related to prognosis were identified using univariate and multivariate Cox regression analyses. Risk prediction models were then created based on the marker genes and clinical factors. RESULTS In total, 1975 DEGs and 2095 DMGs were identified. After comparison, 16 prognosis-related genes (EFNB2, TSPAN7, INPP5A, VAMP2, CALML5, SNAI2, RHOBTB1, CKB, ATF7IP2, RIMS2, RCBTB2, YBX1, RAB27B, NFATC1, TCEAL4, and SLC16A3) were selected from 265 overlapping genes. Four clinical factors (pathologic N [node], pathologic T [tumor], pathologic stage, and new tumor) were associated with prognosis. The prognostic risk prediction models were constructed and validated with other independent datasets. CONCLUSIONS An integrated model that combines clinical factors and gene markers is useful for predicting risk of LACC in patients. The 16 genes that were identified, including EFNB2, TSPAN7, INPP5A, VAMP2, and CALML5, may serve as novel biomarkers for diagnosis of LACC and prediction of disease prognosis.

BRCA1 Is a Novel Prognostic Indicator and Associates with Immune Cell Infiltration in Hepatocellular Carcinoma.

The breast cancer gene 1 (BRCA1) is a tumor suppressor, and mutations or epigenetic inactivation will increase the risk of breast cancer oncogenesis. The current research aimed to explore the relationship between BRCA1 expression, prognosis, and tumor immunity in hepatocellular carcinoma (HCC). In this study, BRCA1 expression was analyzed via multiple online databases and its association with clinical characteristics, prognosis and genetic alterations was identified using the original The Cancer Genome Atlas-liver hepatocellular carcinoma cohorts. DNA methylation sites and their prognostic values were analyzed using MethSurv. The correlations between BRCA1 and immune infiltration were investigated via Tumor Immune Estimation Resource. As results, BRCA1 was significantly upregulated in tumor tissues in multiple HCC cohorts. Besides, high BRCA1 expression was correlated with race, advanced T stage, clinical stage, poor tumor grade, MSI status, and worse prognosis. Notably, BRCA1 expression was positively correlated with infiltration levels of B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells. The current findings imply that BRCA1 is associated with prognosis and immune infiltration, laying foundations for in-depth research on the role of BRCA1 in HCC.

Evaluation of X-Ray Repair Cross-Complementing Family Members as Potential Biomarkers for Predicting Progression and Prognosis in Hepatocellular Carcinoma.

The X-ray repair cross-complementing (XRCC) gene family has been revealed to participate in the carcinogenesis and development of numerous cancers. However, the expression profiles and prognostic values of XRCCs (XRCC1-6) in hepatocellular carcinoma (HCC) have not been explored up to now. The transcriptional levels of XRCCs in primary HCC tissues were analyzed by UALCAN and GEPIA. The relationship between XRCCs expression and HCC clinical characteristics was evaluated using UALCAN. Moreover, the prognostic values of XRCCs expression and mutations in HCC patients were investigated via the GEPIA and cBioPortal, respectively. Last but not least, the functions and pathways of XRCCs in HCC were also predicted by cBioPortal and DVAID. The transcriptional levels of all XRCCs in HCC tissues were notably elevated compared with normal liver tissues. Meanwhile, upregulated XRCCs expression was positively associated with clinical stages and tumor grades of HCC patients. Survival analysis using the GEPIA database revealed that high transcription levels of XRCC2/3/4/5/6 were associated with lower overall survival (OS) and high transcription levels of XRCC1/2/3/6 were correlated with poor disease-free survival (DFS) in HCC patients. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) demonstrated the possible mechanisms of XRCCs and their associated genes participating in the oncogenesis of HCC. Our findings systematically elucidate the expression profiles and distinct prognostic values of XRCCs in HCC, which might provide promising therapeutic targets and novel prognostic biomarkers for HCC patients.

NY-ESO-1 expression in solid tumors predicts prognosis: A systematic review and meta-analysis.

BACKGROUND: New York esophageal squamous cell carcinoma 1 (NY-ESO-1) is a member of the cancer testis antigen family. NY-ESO-1 has documented potential as an effective target for cancer immunotherapy. The prognostic value of NY-ESO-1 expression in solid tumors, however, remains controversial because of inconclusive data. METHODS: For this analysis, the Medline, Embase, and Cochrane Library databases were searched up to February 2018 for studies investigating NY-ESO-1 expression in solid tumors and overall survival (OS), progression-free survival (PFS), or disease-free survival (DFS). Hazard ratios (HRs) with 95% confidence intervals (CIs) were extracted from each study. Pooled HRs and CIs were calculated using the Mantel-Haenszel fixed effects or random effects model. RESULTS: A total of 23 studies were included in the analysis. The combined HR (95% CI) estimates for OS, PFS, and DFS were 1.41 (95% CI: 1.24-1.61; I = 0%), 1.62 (95% CI: 1.42-1.84; I = 17%), and 0.95 (95% CI: 0.56-1.59; I = 57%), respectively. CONCLUSIONS: NY-ESO-1 expression in solid tumors is associated with worse OS and PFS. Studies are still needed to provide more evidence.

Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects against Aß toxicity via attenuating Aß-induced endoplasmic reticulum stress.

BACKGROUND: Extracellular accumulation of amyloid ß-peptide (Aß) is one of pathological hallmarks of Alzheimer's disease (AD) and contributes to the neuronal loss. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER) stress-inducible neurotrophic factor. Many groups, including ours, have proved that MANF rescues neuronal loss in several neurological disorders, such as Parkinson's disease and cerebral ischemia. However, whether MANF exerts its protective effect against Aß neurotoxicity in AD remains unknown. METHODS: In the present study, the characteristic expressions of MANF in Aß1-42-treated neuronal cells as well as in the brains of APP/PS1 transgenic mice were analyzed by immunofluorescence staining, qPCR, and Western blot. The effects of MANF overexpression, MANF knockdown, or recombination human MANF protein (rhMANF) on neuron viability, apoptosis, and the expression of ER stress-related proteins following Aß1-42 exposure were also investigated. RESULTS: The results showed the increased expressions of MANF, as well as ER stress markers immunoglobulin-binding protein (BiP) and C/EBP homologous protein (CHOP), in the brains of the APP/PS1 transgenic mice and Aß1-42-treated neuronal cells. MANF overexpression or rhMANF treatment partially protected against Aß1-42-induced neuronal cell death, associated with marked decrease of cleaved caspase-3, whereas MANF knockdown with siRNA aggravated Aß1-42 cytotoxicity including caspase-3 activation. Further study demonstrated that the expressions of BiP, ATF6, phosphorylated-IRE1, XBP1s, phosphorylated-eIF2α, ATF4, and CHOP were significantly downregulated by MANF overexpression or rhMANF treatment in neuronal cells following Aß1-42 exposure, whereas knockdown of MANF has the opposite effect. CONCLUSIONS: These findings demonstrate that MANF may exert neuroprotective effects against Aß-induced neurotoxicity through attenuating ER stress, suggesting that an applicability of MANF as a therapeutic candidate for AD.

High-dose fulvestrant as third-line endocrine therapy for breast cancer metastasis to the left kidney: A case report and literature review.

RATIONALE: Endocrine therapy plays an important role in the treatment of patients with hormone receptor-positive breast cancer. Renal metastasis of breast cancer is rare in clinical practice. PATIENT CONCERNS: We present here a 54-year-old woman with breast cancer after first line chemotherapy and second line endocrinotherapy (i.e., toremifene & exemestane) failure. DIAGNOSES: The patient was rarely diagnosed breast cancer metastasis to the kidney and a positive hormone status (ER and PR) but was negative for human epidermal factor receptor 2 (HER2). INTERVENTIONS: The patient was treated with a high dose of fulvestrant (SERD; 500 mg) by intramuscular injection once per month. OUTCOMES: The patient's condition significantly improved as measured by a decrease in the renal and pulmonary masses; symptoms including dry cough and blood phlegm also improved. LESSONS: Endocrinotherapy with high-dose fulvestrant may provide benefits for patients with HR+/HER2- advanced breast cancer with renal metastasis after SERMs failure.

High level of FOXC1 expression is associated with poor prognosis in pancreatic ductal adenocarcinoma.

Accumulating evidence for overexpression of FOXC1 in various types of human cancer suggests that it plays a key role in tumor biology. However, little is known about the function of FOXC1 in pancreatic ductal adenocarcinoma (PDA). This study was to investigate the expression profile of FOXC1 in PDA and its clinical significance. We detected the expression profile of FOXC1 mRNA and protein in PDA tissue and in corresponding normal tissue by quantitative reverse-transcriptase polymerase chain reaction and western blotting. Immunohistochemistry was also used in the detection of FOXC1 protein expression. The clinicopathological implications of these proteins were analyzed statistically. Survival analysis was performed to assess prognostic significance. FOXC1 mRNA was overexpressed in PDA tissue when compared with corresponding normal tissue, so was FOXC1 protein. The overexpression of FOXC1 was significantly associated with the degree of clinical stage (p < 0.001), histological differentiation (p = 0.002), and lymph node metastases (p < 0.001). Survival analysis revealed that overexpression of FOXC1 is associated with a poorer prognosis. These observations suggest that FOXC1 plays a key role in PDA and therefore may provide an opportunity for developing a novel therapeutic target as well as a prognostic marker in PDA.

[Caveolin-1: a novel biomarker for prostate cancer].

For lack of the biomarker, early diagnosis of prostate cancer is often difficult. Caveolin-1 (Cav-1) is an important oncogene and a major structural coat protein of caveolae, which is involved in multiple cellular functions including molecular transport, cell adhesion, and signal transduction, as well as in the development and progression of prostate cancer. Cav-1 is secreted as a biologically active molecule that promotes cell survival and angiogenesis within the tumor microenvironment, and is overexpressed in the metastatic and primary sites of human prostate cancer. Secreted Cav-1 can be detected in the peripheral blood, and its expression level has an indicative value in the diagnosis and prognosis of prostate cancer. This review focuses on the structure and biological characteristics of Cav-1 and its correlation with prostate cancer.