Prognosis of immunotherapy for non-small cell lung cancer with CDKN2A loss of function.

Background: Immunotherapy has been widely used to treat non-small cell lung cancer (NSCLC) but is only effective in 20% of patients. Cyclin-dependent kinase inhibitor 2A (CDKN2A) is an important tumor suppressor gene, and its loss of function (LOF) is quite common in NSCLC. Pre-clinical studies suggest CDKN2A LOF promotes immune evasion; however, the results in relation to NSCLC are controversial, and debate continues as to the effect of CDKN2A LOF on immunotherapy. Methods: In this study, we collected the data of 49 CDKN2A LOF and 173 CDKN2A wild-type NSCLC consecutive patients treated by any line of immunotherapy. Through immunohistochemical (IHC) and immunofluorescent (IF) staining, we analyzed the CDKN2A predominant transcription protein p16INK4A in the CDKN2A LOF and CDKN2A wild-type NSCLC patients. Using Kaplan-Meier curves, we also examined the relationship between CDKN2A LOF and immunotherapy. Results: The IHC and IF staining results showed that most CDKN2A LOF patients were p16INK4A negative, while most CDKN2A wild-type patients were p16INK4A positive. In the LOF group, five patients had partial responses, 35 had stable disease, and nine had progressive disease after the first evaluation of immunotherapy. The LOF group had a median progression-free survival (PFS) time of 4.67 months, while the wild-type group had a median PFS time of 8.63 months [hazard ratio (HR): 0.54; 95% confidence interval (CI): 0.38-0.77; P<0.001]. The LOF group had a median overall survival (OS) time of 9.07 months, while the wild-type group had a median OS time of 21.37 months (HR: 0.42; 95% CI: 0.29-0.61; P<0.001). Conclusions: Our study revealed that CDKN2A LOF NSCLC patients treated with immune checkpoint inhibitor (ICI) mono-therapy or combined therapy had a worse prognosis than those with CDKN2A wild-type NSCLC. However, our study also suggested that ICI could work quite effectively in selective CDKN2A LOF patients.

Treatment with palbociclib and tislelizumab for CDKN2A-mutated and PD-L1-positive advanced intrahepatic cholangiocarcinoma: a case report and literature review.

Background: Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver malignancy with a steadily increasing incidence worldwide. ICC has insidious onset, rapid progression, and poor prognosis. More multidisciplinary clinical studies are needed to continuously explore safer and more efficient diagnosis and treatment modes for ICC. Methods and results: A 66-year-old female patient with ICC rapidly developed systemic multiple metastases after surgery, and the first-line two-drug combination chemotherapy was not effective. Due to cyclin-dependent kinase inhibitor 2A mutation and programmed cell death-ligand 1-positive, a partial response and progression-free survival of 9.5 months were achieved after a second-line treatment with cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) combined with immunotherapy. The patient developed thromboembolism 7 months after treatment and died due to disseminated intravascular coagulation. Conclusion: The combination of targeted and immune therapy has revealed a potentially effective regimen for the effective treatment of patients with ICC, which needs to be observed in larger clinical studies. The thromboembolism rates in real-world patients treated with CDK4/6 inhibitors are higher than those reported in clinical trials, and the application of prophylactic anticoagulation in this patient population may be questionable.

WDR12/RAC1 axis promoted proliferation and anti-apoptosis in colorectal cancer cells.

BACKGROUND: WD repeat domain 12 (WDR12) plays a crucial role in the ribosome biogenesis pathway. However, its biological function in colorectal cancer (CRC) remains poorly understood. Therefore, this study aims to investigate the roles of WDR12 in the occurrence and progression of CRC, as well as its underlying mechanisms. METHODS: The expression of WDR12 was assessed through The Cancer Genome Atlas (TCGA) and the Human Protein Atlas (HPA) database. Functional experiments including Celigo assay, MTT assay, and Caspase-3/7 assay were conducted to validate the role of WDR12 in the malignant progression of CRC. Additionally, mRNA chip-sequencing and ingenuity pathway analysis (IPA) were performed to identify the molecular mechanism. RESULTS: WDR12 expression was significantly upregulated in CRC tissues compared to normal colorectal tissues. Knockdown of WDR12 reduced proliferation and promoted apoptosis of CRC cell lines in vitro and in vivo experiments. Furthermore, WDR12 expression had a significantly inverse association with diseases and functions, including cancer, cell cycle, DNA replication, recombination, cellular growth, proliferation and repair, as revealed by IPA analysis of mRNA chip-sequencing data. Moreover, the activation of cell cycle checkpoint kinases proteins in the cell cycle checkpoint control signaling pathway was enriched in the WDR12 knockdown CRC cell lines. Additionally, downregulation of rac family small GTPase 1 (RAC1) occurred upon WDR12 knockdown, thereby facilitating the proliferation and anti-apoptosis of CRC cells. CONCLUSION: Our study demonstrates that the WDR12/RAC1 axis promotes tumor progression in CRC. Therefore, WDR12 may serve as a novel oncogene and a potential target for individualized therapy in CRC. These findings provide an experimental foundation for the clinical development of drugs targeting the WDR12/RAC1 axis.

Bibliometric analysis of global research trends between gut microbiota and pancreatic cancer: from 2004 to 2023.

Background: Pancreatic cancer (PC) is one of the most lethal malignancies of the digestive system and is expected to be the second leading cause of cancer-related death in the United States by 2030. A growing body of evidence suggests that the gut microbiota (GM) is intimately involved in the clinical diagnosis, oncogenic mechanism and treatment of PC. However, no bibliometric analysis of PC and GM has been reported. Methods: The literature on PC and GM was retrieved from the Web of Science Core Collection (WoSCC) database for the period from January 1, 2004 to April 25, 2023. Microsoft Excel 2021, CiteSpace, VOSviewer, Scimago Graphica, Graphpad Prism, Origin, the R package "bibliometrics" and the bibliometric online analysis program were used to visualize the publishing trends and hot spots in this field. Results: A total of 1,449 articles were included, including 918 articles and 531 reviews. Publishing had grown rapidly since 2017, with the 2023 expected to publish 268 articles. Unsurprisingly, the United States ranked highest in terms of number of literatures, H index and average citations. The University of California System was the most active institution, but Harvard University tended to be cited the most on average. The three most influential researchers were Robert M. Hoffman, Zhao Minglei, and Zhang Yong. Cancers had published the most papers, while Nature was the most cited journal. Keyword analysis and theme analysis indicated that "tumor microenvironment," "gemcitabine-resistance," "ductal adenocarcinoma," "gut microbiota" and "diagnosis" will be the hotspots and frontiers of research in the future. Conclusion: In summary, the field is receiving increasing attention. We found that future hotspots of PC/GM research may focus on the mechanism of oncogenesis, flora combination therapy and the exploitation of new predictive biomarkers, which provides effective suggestions and new insights for scholars.

Effect of Occupational Extremely Low-Frequency Electromagnetic Field Exposure on the Thyroid Gland of Workers: A Prospective Study.

OBJECTIVE: The aim of this study was to investigate the biological effects of occupational extremely low-frequency electromagnetic field (ELF-EMF) exposure on the thyroid gland. METHODS: We conducted a prospective analysis of 85 workers (exposure group) exposed to an ELF-EMF (100 µT, 10-100 Hz) produced by the electromagnetic aircraft launch system and followed up on thyroid function indices, immunological indices, and color Doppler images for 3 years. Additionally, 116 healthy volunteers were randomly selected as controls (control group), the thyroid function of whom was compared to the exposure group. RESULTS: No significant difference was observed in thyroid function between the exposure and control groups. During the follow-up of the exposure group, the serum free triiodothyronine (FT3) level was found to slowly decrease and free thyroxine (FT4) level slowly increase with increasing exposure time. However, no significant difference was found in thyroid-stimulating hormone (TSH) over the three years, and no significant difference was observed in the FT3, FT4 and TSH levels between different exposure subgroups. Furthermore, no significant changes were observed in thyroid autoantibody levels and ultrasound images between subgroups or over time. CONCLUSION: Long-term exposure to ELF-EMF may promote thyroid secretion of T4 and inhibit deiodination of T4 to T3. ELF-EMF has no significant effect on thyroid immune function and morphology.

Sequential use of EGFR-tyrosine kinase inhibitors based upon EGFR mutation evolution achieves long-term control in a non-small cell lung cancer patient: a case report.

Tyrosine kinase inhibitor (TKI) has greatly improved the survival of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR)-TKI sensitive mutations. However, TKI resistance constantly occur, although multiple lines of different generations of TKIs are adopted during the progression. For example, in the case when T790M, which is the most common resistance mechanism of first generation TKIs, occurs, alteration to osimertinib (the third generation TKI) could always be effective. Unfortunately, some cases gradually become resistant even to osimertinib leaving limited therapy choice for clinical practitioners. Few cases have been reported in the situation after EGFR tertiary mutations occurred, such as C797S, G724S, etc. Herein, we report the first clinical evidence that sequential therapy with erlotinib, osimertinib, afatinib plus endostar, brigatinib plus cetuximab, almonertinib, almonertinib plus afatinib achieved long-term control in a NSCLC patient demonstrating EGFR 19Del/T790M/G724S/cis-C797Sevolution in response to TKI treatment. EGFR targeted therapy introduced successful management for more than 36 months until now. ctDNA NGS was performed at the time of important clinical event. The EGFR 19Del was discovered in October 2017, and erlotinib was administered for 10 months with PR in the beginning. Then T790M was detected and osimertinib was used for 9 months with SD condition. Subsequently, EGFR G724S was identified in ctDNA with the remaining 19Del and loss of T790M. Afatinib plus endostar was administered and PR was achieved after 1.5 months. PD occurred 6 months later with the emergence of EGFR cis-C797S. Then brigatinib plus cetuximab was chosen and lasted for 4 months with the best response of SD. And then EGFR 19Del and T790M were still detected with loss of G724S and C797S. Almonertinib, another third-generation TKI, was administered for 3 months with SD condition. Finally, 19Del/T790M/G724S/cis-C797S recurred, and whole dose of almonertinib plus afatinib was prescribed until now with a PR at 2 months until now. The side effect was acceptable during the whole period of therapies. Plasma ctDNA NGS provided information of EGFR mutation evolution and inform appropriate therapy regimen during the progression.

Podoplanin is a useful prognostic marker and indicates better differentiation in lung squamous cell cancer patients? A systematic review and meta-analysis.

BACKGROUND: The CSC (cancer stem cell) markers often indicate poor prognosis and more cell invasion or migration of cancer patients. Podoplanin was assumed as a candidate CSC marker and predict poor prognosis among squamous cancers. Whereas, the prognostic value of podoplanin among lung squamous cancer (LUSC) patients remains controversial. METHODS: A search of databases including PubMed, Embase and Web of Science was performed. Eligible articles studying the prognostic significance of podoplanin were selected. Odds ratio and HR (hazard ratio) were used to assess the relationships between podoplanin and clinical characteristics, as well as to quantify its prognostic role. The heterogeneity was estimated by I2 Statistic and P values from sensitivity analysis. Begg's funnel plots were used to estimate possible publication bias. RESULTS: 8 eligible studies containing 725 I-IV LUSC patients were included. Podoplanin expression showed no significant correlations with TNM stage, vascular invasion, lymphatic invasion, lymph node metastasis, pleural metastasis of tumor and gender of patients. However, podoplanin showed significant associations with better differentiation (pooled OR = 2.64, 95% CI 1.53-4.56, P = 0.0005, fixed effect) and better overall survival (HR = 2.14, 95% CI 1.45-3.15, P = 0.0001, fixed effect) and progression-free survival (HR = 1.73, 95% CI: 1.01-2.98, P = 0.05, fixed effect) of LUSC. Funnel plots illustrated no evidence of publication bias in our results. CONCLUSIONS: Podoplanin could be a useful prognostic marker and indicates better differentiation for LUSC patients, and the value of PDPN expression as a marker for cancer stem cells in LUSC should be critically evaluated in future studies.

Prospective comparison of the value of CRASH and CARG toxicity scores in predicting chemotherapy toxicity in geriatric oncology.

Predicting the risk of severe adverse reactions to chemotherapy is of great clinical significance for proper selection of effective and safe treatment for elderly cancer patients. The present study aimed to verify and compare the value of two evaluation models of chemotherapy risk prediction for elderly cancer patients through prospective analysis. The two evaluation models assessed were the Chemotherapy Risk Assessment Scale for High-Age Patients (CRASH) and Cancer Aging Research Group (CARG) toxicity scores. Elderly patients aged ≥70 with cancer were recruited at two participating hospitals in China and completed an assessment prior to starting chemotherapy. CRASH and CARG toxicity scores of each participant were calculated. Chemotherapy-related toxicity was recorded through each cycle of chemotherapy. A total of 106 participants were recruited between September 2015 and August 2018. The CRASH and CARG toxicity scores were positively correlated (r=0.689; P<0.01). Of the participants, 54 (50.9%) participants underwent a grade 3-5 chemotherapy-related toxicity and 21 (19.8%) experienced grade 3-5 nonhematological toxicity in the process of treatment. CRASH and CARG toxicity scores predicted severe chemotherapy-related toxicity and had a high discriminatory value based on receiver operating characteristic curve analysis (area under the curve of 0.772 and 0.760, respectively; P<0.001). The results of the present study indicate that the CRASH and CARG toxicity scores are helpful tools for the prediction of severe chemotherapy-related toxicity, and are recommended for routine oncology practice.

A 5-year follow-up of primary seminal vesicle adenocarcinoma: A case report.

RATIONALE: Primary seminal vesicle adenocarcinoma (PSVA) is an extremely rare malignancy that should be carefully differentiated from cancer originating in the prostate, colon or bladder. Without standard guidelines, radical resection is considered a mainstay treatment, providing the best prognosis. However, as manifestations of PSVA are not detected in early stages, the majority of cases of PSVA are diagnosed at late stages, contributing to poor prognosis. PATIENT CONCERNS: We described the case of a PSVA patient confirmed by histopathology and immunohistochemistry (IHC) staining positive for carbohydrate antigen-125 (CA-125) and negative for prostate specific antigen (PSA). DIAGNOSIS: Primary seminal vesicle adenocarcinoma. INTERVENTIONS: Surgery was carried out at the beginning, however, residual tumor was verified; thus 3 cycles of chemotherapy with a regimen of paclitaxel and cis-platinum were performed, followed by radical pelvic radiotherapy with a dose of 60 Gray in 30 fractions; then, another 3 cycles of the same chemotherapy were carried out. OUTCOMES: At the moment, the patient is still under follow-up and has been disease-free for more than 5 years. LESSONS: Our manuscript describes a patient with PSVA with long-term survival and supplies a successful management strategy for this malignancy.

Outcome of Molecular Targeted Agents Plus Chemotherapy for Second-Line Therapy of Metastatic Colorectal Cancer: A Meta-Analysis of Randomized Trials.

INTRODUCTION: The aim of this study was to evaluate the efficacy and toxicity of molecular targeted agents plus chemotherapy compared with chemotherapy alone as second-line therapy for patients with metastatic colorectal cancer (mCRC). MATERIALS AND METHODS: We identified randomized controlled trials that compared molecular targeted agents plus chemotherapy with chemotherapy alone by searching the PubMed and Embase databases for articles published between January 2000 and September 2015. The outcome measures included progression-free survival, overall survival, objective response rate, and adverse events. Two investigators independently performed the information retrieval, screening, and data extraction. Stata 10.0 software was used to statistically analyze the extracted data. In accordance with our inclusion criteria, 11 trials, with a total of 7440 patients, were included in this meta-analysis through rounds of selection. We divided the biologic agents used into 3 subgroups based on the type of biologic agents-vascular endothelial growth factor (VEGF) inhibitor, epidermal growth factor receptor inhibitor, and other pathway inhibitors. RESULTS: Our results suggested that the regimen of a molecular targeted agent plus chemotherapy had a significant advantage in progression-free survival, overall survival, and objective response rate over chemotherapy alone (hazard ratio, 0.74; 95% confidence interval [CI], 0.70-0.78; hazard ratio, 0.88; 95% CI, 0.83-0.93; risk ratio, 2.24; 95% CI: 1.58-3.17, respectively). However, the rate of grade ≥ 3 adverse events was also higher in the combination therapy arm (risk ratio, 1.25; 95% CI, 1.17-1.33). Subgroup analysis showed that the combination of VEGF inhibitor with chemotherapy had a significant advantage in PFS, OS, and ORR over chemotherapy alone, but there was also a higher risk ratio in adverse events for this combination compared with the control group. CONCLUSION: In conclusion, a molecular targeted agent, especially VEGF inhibitor, plus chemotherapy is a worthwhile combination for patients with metastatic colorectal cancer as second-line therapy. However, more randomized controlled trials on a larger scale are needed for evaluating the value of epidermal growth factor receptor and other pathway inhibitors.

The DACH/EYA/SIX gene network and its role in tumor initiation and progression.

The functional abnormality of developmental genes is a common phenomenon in cancer initiation and progression. The retinal determination gene network (RDGN) is a key signal in Drosophila eye specification, and this conservative pathway is also required for the development of multiple organs in mammalian species. Recent studies demonstrated that aberrant expressions of RDGN components in vertebrates, mainly Dach, Six, and Eya, represent a novel tumor signal. RDGN regulates proliferation, apoptosis, tumor growth and metastasis through interactions with multiple signaling pathways in a co-ordinated fashion; Dach acts as a tumor suppressor, whereas Six and Eya function as oncogenes. Clinical analyses demonstrated that the expression levels of RDGN correlate with tumor stage, metastasis and survival, suggesting that combinational detection of this pathway might be used as a promising biomarker for the stratification of therapy and for the prediction of the prognosis of cancer patients.

DACH1 is a novel predictive and prognostic biomarker in hepatocellular carcinoma as a negative regulator of Wnt/ß-catenin signaling.

The cell fate determination factor Dachshund (DACH1) functions as a novel suppressor in the progression of various neoplasms. Previous study has suggested that hypermethylation of promoter region was responsible for the reduction of DACH1 expression in hepatocellular carcinoma (HCC), and associated with the progression of HCC, but the clinical significance and the exact molecular mechanisms of DACH1 in the progression of HCC remain unclear. In this study, we employed public microarray data analysis and tissue microarrays (TMAs) technologies and showed that DACH1 expression was reduced in HCC even at early stage and associated with the tumor progression. Notably, Kaplan-Meier analysis further indicated DACH1 could be an independent prognostic factor for the overall survival of HCC. Further, mechanistic studies revealed that overexpression of DACH1 inhibited the growth and migration of HCC cell line, which were dependent in part on the inactivation of Wnt pathway via phosphorylation of GSK3ß to suppress ß-catenin. In agreement, the abundance of DACH1 was inversely correlated with several Wnt target genes. Collectively, our study indicated ß-catenin is a novel target of DACH1 in HCC.

Lentivirus-mediated Nox4 shRNA invasion and angiogenesis and enhances radiosensitivity in human glioblastoma.

Radioresistance remains a significant therapeutic obstacle in glioblastoma. Reactive oxygen species (ROS) are associated with multiple cellular functions such as cell proliferation and apoptosis. Nox4 NADPH oxidase is abundantly expressed and has proven to be a major source of ROS production in glioblastoma. Here we investigated the effects of Nox4 on GBM tumor cell invasion, angiogenesis, and radiosensitivity. A lentiviral shRNA vector was utilized to stably knockdown Nox4 in U87MG and U251 glioblastoma cells. ROS production was measured by flow cytometry using the fluorescent probe DCFH-DA. Radiosensitivity was evaluated by clonogenic assay and survival curve was generated. Cell proliferation activity was assessed by a cell counting proliferation assay and invasion/migration potential by Matrigel invasion assay. Tube-like structure formation assay was used to evaluate angiogenesis ability in vitro and VEGF expression was assessed by MTT assay. Nox4 knockdown reduced ROS production significantly and suppressed glioblastoma cells proliferation and invasion and tumor associated angiogenesis and increased their radiosensitivity in vitro. Our results indicate that Nox4 may play a crucial role in tumor invasion, angiogenesis, and radioresistance in glioblastoma. Inhibition of Nox4 by lentivirus-mediated shRNA could be a strategy to overcome radioresistance and then improve its therapeutic efficacy for glioblastoma.

(18)F-FDG PET/CT in Patients with Nodular Pulmonary Amyloidosis: Case Report and Literature Review.

A 62-year-old woman was found to have multiple bilateral pulmonary nodules showing different (18)F-fluorodeoxyglucose (FDG) uptakes on positron-emission tomography/computed tomography (PET/CT). Only the largest nodule in the left lower lobe showed an increased (18)F-FDG uptake on PET/CT. Three nodules were surgically resected from different lobes of the left lung. Two lobes were benign and showed amyloid deposition. The largest nodule in the left lower lobe showed adenocarcinoma and a heavy amyloid deposition. Pulmonary amyloidosis should be added to the differential diagnosis for cases with multiple pulmonary nodules that show different (18)F-FDG uptakes on PET/CT. To the best of our knowledge, this is the second reported case of a lung nodule consisting of adenocarcinoma and amyloid deposition.

Expression of thymidylate synthase predicts clinical outcomes of pemetrexed-containing chemotherapy for non-small-cell lung cancer: a systemic review and meta-analysis.

PURPOSE: Observational and preclinical studies suggested an association between the expression of thymidylate synthase (TS) and clinical effects of pemetrexed-based chemotherapy in non-small-cell lung cancer (NSCLC) patients. However, the predictive value of TS for pemetrexed-containing chemotherapy regimen remained controversial. The aim of the study was to further appraise the association between the expression of TS and clinical efficacy pemetrexed-based chemotherapy in NSCLC patients. METHODS: We searched in MEDLINE (PubMed), EMBASE, and Cochrane Library from January 1945 to May 2013. Two authors independently extracted information from the characteristics of study participants. Primary outcomes included therapeutic response (TR; i.e., complete response + partial response vs. stable disease + progressive disease), progression-free survival (PFS), and overall survival (OS). Relative risk (RR) and hazard ratio (HR) were used for evaluating the risk or hazard. RESULTS: Eight studies were included in the meta-analysis. Better response usually appeared in NSCLC patients with a lower expression of TS [RR = 2.06 95 % confidence intervals (CI) 1.44, 2.96]. There was a significant association between TS expression and outcomes of pemetrexed-based chemotherapy for NSCLC (PFS: HR = 0.63 95 % CI 0.52, 0.76; OS: HR = 0.74, 95 % CI: 0.63, 0.88). In addition, no evidence of publication bias was observed. CONCLUSIONS: This meta-analysis evaluated the predictive value of TS and provided evidence that NSCLC patients with lower TS expression could significantly benefit from pemetrexed-based chemotherapy. This increased level of TS was probably an independent risk factor of potential resistance against pemetrexed.

PTD4-apoptin protein and dacarbazine show a synergistic antitumor effect on B16-F1 melanoma in vitro and in vivo.

PTD4-apoptin protein enters cells and harbors tumor-selective cell death activity. Dacarbazine is the mainstay of treatment for malignant melanoma. In this study, we investigated the cytotoxic effect of PTD4-apoptin protein and/or dacarbazine in mouse B16-F1 and human A875 and SK-MEL-5 melanoma cells in vitro and by means of a mouse B16-F1 melanoma model in vivo. PTD4-apoptin protein inhibits the growth of B16-F1, A875 and SK-MEL-5 melanoma cells in a dose-dependent manner, but not in normal human cell lines WI-38 and L-02. PTD4-apoptin combined with dacarbazine revealed a synergistic cytotoxic effect (coefficient of drug interaction<1) in all three different tumor cell lines. In vivo, PTD4-apoptin protein and dacarbazine alone effectively inhibited the growth of B16-F1 melanoma in C57BL/6 mice. Strikingly, combined PTD4-apoptin/dacarbazine treatment significantly increased the antitumor effect in comparison to the single treatments. As important, a combined PTD4-apoptin/dacarbazine treatment with a 50% reduction of dacarbazine revealed similar antitumor activities, without detectable hematologic side effects. A combined PTD4-apoptin/dacarbazine treatment represents a promising novel efficient and safe anticancer strategy.

Correlation between the expression of aquaporin 1 and hypoxia-inducible factor 1 in breast cancer tissues.

The correlation between aquaporin 1 (AQP1) and hypoxia-inducible factor 1 (HIF 1) in breast cancer tissues was preliminarily studied. In 155 cases of breast cancer, the expression levels of AQP1 were detected by immunohistochemistry in HIF1-positive group or HIF1-negative group, and the correlation between AQP1 and HIF1 was analyzed. The overexpression of AQP1 and HIF1 were observed in 155 cases of breast cancer tissues. The expression level of AQP1 in HIF1-positive group was significantly higher than that in HIF1-negative group. The positive expression rate of AQP1 was 296.55+/-24.67 and 168.37+/-37.53 in HIF1-positive group and HIF1-negative group respectively with the difference being very significant between them (P<0.001). It was concluded that AQP1 was overexpressed in the HIF1-positive group and there were some correlations between AQP1 and HIF1, suggesting they interact each other and regulate the oncogenesis of breast cancer.

[Correlation of aquaporin 1 with hypoxia-inducible factor 1 in breast cancer].

OBJECTIVE: To determinate the correlation of aquaporin 1 (AQP1) and hypoxia-inducible 1 (HIF-1). METHODS: 155 samples of breast cancer obtained during radical mastectomy underwent immunohistochemistry to detect the expression of AQP1 and HIF-1. RESULTS: The positive rates of AQP1 in the HIF1 positive group was 297 +/- 25, significantly higher than that of HIF1 negative group (168 +/- 38, P < 0.001). CONCLUSION: AQP1 is positively correlated with HIF1. The interaction of AQP1 and HIF1 may co-regulate the progress of breast cancer.

Correlation between the Expression of Aquaporin 1 and Hypoxia-inducible Factor 1 in Breast Cancer Tissues / 华中科技大学学报（医学）（英德文版）

The correlation between aquaporin 1 (AQP1) and hypoxia-inducible factor 1 (HIF 1) in breast cancer tissues was preliminarily studied. In 155 cases of breast cancer, the expression levels of AQP1 were detected by immunohistochemisty in HIF1-positive group or HIF1-negative group, and the correlation between AQP1 and HIF1 was analyzed. The overexpression of AQP1 and HIF1 were observed in 155 cases of breast cancer tissues. The expression level of AQP1 in HIF1-positive group was significantly higher than that in HIF1-negative group. The positive expression rate of AQP1 was 296.55±24.67 and 168.37±37.53 in HIF1-positive group and HIF1-negative group respectively with the difference being very significant between them (P<0.001). It was concluded that AQP1 was overexpressed in the HIF1-positive group and there were some correlations between AQP1 and HIF1, suggesting they interact each other and regulate the oncogenesis of breast cancer.