Single-cell sequencing reveals the immune landscape of breast cancer patients with brain metastasis.

BACKGROUND: Breast cancer has the highest incidence rate of cancer worldwide, and brain metastases (BrM) are among the most malignant cases. While some patients have benefited from immune checkpoint inhibitors (ICIs), the complex anatomical structure of the brain and the heterogeneity of metastatic tumors have made it difficult to characterize the tumor immune microenvironment (TME) of metastatic tumors. METHODS: To address this, we used single-cell RNA sequencing (scRNA-seq) to analyze immune cells in the cerebrospinal fluid (CSF) of BrM patients with breast cancer, thereby providing a comprehensive view of the immune microenvironment landscape of BrM. RESULTS: Based on canonical marker genes, we identified nine cell types, and further identified their subtypes through differential expression gene (DEG) analysis. We compared the changes in cells and functions in the immune microenvironment of patients with different prognoses. Our analysis revealed a series of genes that promote tumor immune function (CCR5, LYZ, IGKC, MS4A1, etc.) and inhibit tumor immune function (SCGB2A2, CD24, etc.). CONCLUSIONS: The scRNA-seq in CSF provides a noninvasive method to describe the TME of breast cancer patients and guide immunotherapy.

IFT20 Confers Paclitaxel Resistance by Triggering ß-arrestin-1 to Modulate ASK1 Signaling in Breast Cancer.

ABSTRACT: System paclitaxel-based chemotherapy is the first-line treatment regimen of defense against breast cancer, but inherent or acquired chemotherapy resistance remains a major obstacle in breast cancer therapy. Elucidating the molecular mechanism of chemoresistance is essential to improve the outcome of patients with breast cancer. Here, we demonstrate that intraflagellar transport 20 (IFT20) is positively associated with shorter relapse-free survival in patients with system paclitaxel-based chemotherapy. High-expressed IFT20 in breast cancer cells increases resistance to cell death upon paclitaxel treatment; in contrast, IFT20 knockdown enhances apoptosis in breast cancer cells in response to paclitaxel. Mechanistically, IFT20 triggers ß-arrestin-1 to bind with apoptosis signal-regulating kinase 1 (ASK1) and promotes the ubiquitination of ASK1 degradation, leading to attenuating ASK1 signaling and its downstream JNK cascades, which helps cells to escape from cell death during paclitaxel treatment. Our results reveal that IFT20 drives paclitaxel resistance through modulating ASK1 signaling and identifies IFT20 as a potential molecular biomarker for predicting the response to paclitaxel therapeutic in breast cancer. IMPLICATIONS: IFT20 drives paclitaxel resistance through modulating ASK1 signaling and IFT20 may act as a potential molecular biomarker for predicting the response to paclitaxel therapeutic in breast cancer.

Immediate versus Delayed Implantation for Single-Tooth Restoration of Maxillary Anterior Teeth: A Comparative Analysis on Efficacy.

Objective: The present research is aimed at determining the efficacy of immediate implantation (II) and delayed implantation (DI) for single-tooth restoration of maxillary anterior teeth. Methods: From February 2019 to June 2020, 80 patients who received single-tooth restoration of maxillary anterior teeth in Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, were included, among which 38 cases with DI restoration were used as the control group (CG), and the remaining 42 cases with II were used as the research group (RG). The complications that occurred were recorded. Besides, subjective satisfaction (Visual Analogue Scale (VAS)), aesthetic effect after anterior teeth trauma restoration (Pink Esthetic Score (PES)), aesthetics of dental hard tissue (White Esthetic Score (WES)), pocket depth assessed by pure titanium periodontal probe, implant stability (Implant Stability Quotient (ISQ)), and oral health-related quality of life (Oral Health Impact Profile- (OHIP-) 14) were evaluated. Attachment height, general look, color, and chewing function were all much higher in RG than in CG, according to the evaluation results. Furthermore, at 3 months, 6 months, and 12 months after surgery, RG had greater PES, WES, ISQ, and OHIP-14 scores, while the periodontal depth was decreased. In both groups of patients, the incidence of complications was similar, with no discernible differences.

TMB and TCR Are Correlated Indicators Predictive of the Efficacy of Neoadjuvant Chemotherapy in Breast Cancer.

Immune characteristics were reported correlated to benefit neoadjuvant chemotherapy (NAC) in breast cancer, yet integration of comprehensive genomic alterations and T-cell receptors (TCR) to predict efficacy of NAC needs further investigation. This study simultaneously analyzed TMB (Tumor Mutation Burden), TCRs, and TILs (tumor infiltrating lymphocyte) in breast cancers receiving NAC was conducted in a prospective cohort (n = 22). The next-generation sequencing technology-based analysis of genomic alterations and TCR repertoire in paired breast cancer samples before and after NAC was conducted in a prospective cohort (n = 22). Fluorescent multiplex immunohistochemistry was used to stain CD4, CD8, PD1, TIM3, and cytokeratins simultaneously in those paired samples. TMB in pretreatment tumor tissues and TCR diversity index are higher in non-pCR patients than in pCR patients (10.6 vs. 2.3; p = 0.043) (2.066 vs. 0.467; p = 0.010). TMB and TCR diversity index had linear correlation (y = 5.587x - 0.881; r = 0.522, p = 0.012). Moreover, infiltrating T cells are significantly at higher presence in pCR versus non-pCR patients. Dynamically, the TMB reduced significantly after therapy in non-pCR patients (p = 0.010) but without TCR index change. The CDR3 peptide AWRSAGNYNEQF is the most highly expressed in pre-NAC samples of pCR patients and in post-NAC samples of non-pCR patients. In addition to pCR, high clonality of TCR and high level of CD8+ expression are associated with disease-free survival (DFS). TCR index and TMB have significant interaction and may guide neo-adjuvant treatment in operable breast cancers. Response to NAC in tumors with high TCR clonality may be attributable to high infiltration and expansion of tumor-specific CD8 positive effector cells.

High SHP2 expression determines the efficacy of PD-1/PD-L1 inhibitors in advanced KRAS mutant non-small cell lung cancer.

BACKGROUND: Src homology region 2 domain-containing phosphatase 2 (SHP2) is a novel target for Kirsten rat sarcoma oncogene (KRAS) mutant cancer. We retrospectively studied the significance of SHP2 in KRAS mutant non-small cell lung cancer (NSCLC) treated with immunotherapy and its relationship with tumor microenvironment (TME). METHODS: Sixty-one advanced KRAS mutant NSCLC patients who underwent immunotherapy were enrolled. Next-generation sequencing (NGS) was used to profile mutation status. The expression of SHP2, phospho-SHP2 (pSHP2), and programmed death ligand 1 (PD-L1) were analyzed by immunohistochemistry (IHC). Quantitative multiplexed immunofluorescence cytochemistry (mIFC) analysis was conducted to describe the TME. RESULTS: SHP2 was heterogeneously expressed in 32 samples in both tumor cells and immune cells and highly expressed (H-score >10) in 25 (78.1%) samples. The expression levels of SHP2 and pSHP2 were positively correlated. Stromal SHP2 (s-SHP2) was higher in tumors with PD-L1 ≥50% versus PD-L1 <50% (p = 0.039). By quantitative mIFC analysis, the expression of s-SHP2 had positive correlation with CD8, CD4, CD68, and PD-L1 levels in stromal area. Patients with high SHP2 expression made up 100.0% of the partial respond (PR) and 80.0% of the stable disease (SD), whereas 50.0% of the progress disease (PD). High SHP2 expression was associated with longer progression-free survival (PFS) and overall survival (OS) (p < 0.001, p = 0.013). Patients with high expression of both SHP2 and PD-L1 had longer PFS (p < 0.001). CONCLUSION: High SHP2 expression could predict the efficacy of immunotherapy and better survival in advanced KRAS mutant NSCLC. SHP2 may function in both tumor cells and immune cells, warranting further study on the potential diverse effects of SHP2 inhibition in TME.

Bibliometrics research on radiomics of lung cancer.

BACKGROUND: Lung cancer is currently the most commonly diagnosed malignant tumor worldwide. Exploring ways to improve the accuracy and timeliness of diagnosis has important clinical significance. Radiomics transforms images into high-dimensional data, and uses deep learning and artificial intelligence to improve the accuracy and efficiency of disease diagnosis. There is an increasing amount of research on radiomics in the diagnosis of lung cancer. This study analyzes the relevant literature in the Science Citation Index Expanded (SCI-E) database to understand the current research status and future development direction of lung cancer radiomics. METHODS: This study is based on the SCI-E database. The first search formula is topic = Lung cancer OR Lung neoplasms (#1), the second search formula is topic = Radiomics (#2), and the third search formula is #1 and #2, that is, literature that meets both the first and second search results. CiteSpace software was used to analyze lung cancer radiomics from the annual distribution of articles, countries, institutions, journals, and authors and keywords. HistCite software was used to visualize the citation chronology of the lung cancer radiomics literature, and Pajek software was used to analyze the main path of the citation chronology. RESULTS: There were a total of 749 publications, of which most were original articles (529, 70.63%) and reviews (109, 14.55%). The citation frequency is 21,676 times, the h-index is 66, and the average number of citations per publication is 28.94. The research mainly comes from the United States of America, China and other countries. The research institutions are mainly medical centers such as Moffitt Cancer Center, Maastricht University and Harvard Medical School. The authors are also mainly from these institutions. The literature was published in many related journals, mainly imaging and oncology journals. Keyword analysis shows that in recent years, research has focused on deep learning and artificial intelligence. CONCLUSIONS: The field of lung cancer radiomics is developing rapidly, and the main focuses of research are deep learning and artificial intelligence.

Quantitative multiplex immunofluorescence analysis identifies infiltrating PD1+ CD8+ and CD8+ T cells as predictive of response to neoadjuvant chemotherapy in breast cancer.

BACKGROUND: This study aimed to explore the potentially predictive role and dynamic changes of immune checkpoints on T cell subsets in patients with breast cancer receiving neoadjuvant chemotherapies. METHODS: Fluorescent multiplex immunohistochemistry (mIHC) was used to stain CD4, CD8, PD1, TIM3, and cytokeratins simultaneously in paired breast cancer samples before and after neoadjuvant therapies (NAT) in a prospective cohort (n = 50). Singleplex IHC was conducted to stain for CD3 in 100 cases with inclusion of extra retrospective 50 cases. Cell levels were correlated with clinicopathological parameters and pathological complete response (pCR). RESULTS: In pretreatment tumors, the percentages of infiltrating CD8+ , PD1+ , PD1+ CD8+ , and the ratio of PD1+ CD8+ /CD8+ cells, were higher in pCR than non-pCR patients in either the stromal or intratumoral area, but PD1+ CD4+ , TIM3+ CD4+ , TIM3+ CD8+ cells and CD4+ /CD8+ ratio was not. Multivariate analyses showed that the percentage of intratumoral CD8+ cells (OR, 1.712; 95% CI: 1.052-2.786; P = 0.030) and stromal PD1+ CD8+ /CD8+ ratio (OR, 1.109; 95% CI: 1.009-1.218; P = 0.032) were significantly associated with pCR. Dynamically, reduction in the percentages of PD1+ , CD8+ and PD1+ CD8+ cells after therapy strongly correlated with pCR. Notably, incremental percentages of PD1+ CD8+ cells, rather than TIM3+ CD8+ , were shown in tumors from non-pCR patients after NAT. CD3 staining confirmed the percentage of T cells were associated with pCR. CONCLUSIONS: PD1+ CD8+ rather than TIM3+ CD8+ cells are main predictive components within tumor-infiltrating T cells in NAT breast cancer patients. Dynamically incremental levels of PD1+ CD8+ cells occurred in non-pCR cases after NAT, suggesting the combination of chemotherapy with PD1 inhibition might benefit these patients. KEY POINTS: SIGNIFICANT FINDINGS OF THE STUDY: PD1+ CD8+ , rather than TIM3+ CD8+ , T cells are the main component to predict the response of neoadjuvant therapies in breast cancer. WHAT THIS STUDY ADDS: Incremental levels of PD1+ CD8+ T cells in non-pCR post-NAT tumors suggest PD1 inhibition might benefit in the neoadjuvant setting.

Cullin7 enhances resistance to trastuzumab therapy in Her2 positive breast cancer via degrading IRS-1 and downregulating IGFBP-3 to activate the PI3K/AKT pathway.

Patients with Her2-positive breast cancer exhibit de novo resistance or develop acquired resistance in less than one year after Her2 targeting treatment, but the mechanism is not fully elucidated. Compensatory pathways such as the IGF-1R/IRS-1 pathway, are activated, leading to aberrant enhanced PI3K/Akt/mTOR pathway activity to attenuate the efficacy of trastuzumab. Cullin7 could participate in the degradation of IRS-1 in a mTOR/S6K dependent manner. Whether Cullin7 participates in trastuzumab resistance needs to be further investigated. Here, we reveals that Cullin7 is overexpressed in trastuzumab-resistant Her2 positive breast cancer cells. Knockdown of Cullin7 reduces degradation of Ser phosphorylation of IRS-1, attenuates activation of the PI3K/AKT pathway, and partly restores trastuzumab sensitivity in trastuzumab-resistant Her2 positive breast cancer cells. IGFBP-3 expression is decreased in trastuzumab-resistant Her2 positive breast cancer cells, which leads to release of the Wnt signaling pathway inhibition and an increase in Cullin7 expression, as mediated by TCF7L2. Overexpression of Cullin7 in Her2-amplified breast cancer tissues has clinical implications because it positively correlates with shorter disease-free survival (DFS) and inadequate response to trastuzumab. Thus, our results suggest a critical role for Cullin7 in response to trastuzumab, which has significant implications for selection of the optimal therapeutic strategy for Her2 positive breast cancers.

Downregulation of miroRNA-141 mediates acquired resistance to trastuzumab and is associated with poor outcome in breast cancer by upregulating the expression of ERBB4.

BACKGROUND: microRNAs are involved in the control of cell growth and apoptosis; they also play an essential role in resistance towards trastuzumab, in breast cancer. The objective of this study was to identify differentially expressed microRNA(s) and explore its therapeutic role in treatment of the disease. METHODS: Real-time polymerase chain reaction (RT-PCR) was performed to identify the virtual microRNA (miRNA) involved in breast cancer cells resistant to trastuzumab. RT-PCR and Western blot analysis were carried out to study the effects of microRNA-141 (miR-141) on ERBB2, ERBB4 and AKT production. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenylterazolium bromide assay and flow cytometry analysis was carried out to examine the effect of miR-141 on cell proliferation and apoptosis via ERBB4. RESULT: According to RT-PCR results, only miR-141 and miR-375 among miR-141, miR-375, miR-16, miR-155, miR-217 and miR-205 were downregulated in trastuzumab-resistant cells. Trastuzumab-resistant cells displayed higher levels of ERBB4 and p-AKT as well as showing a higher growth rate and a lower apoptosis rate. Online software programs were used, which identified ERBB4 as a gene targeted by miR-141 with a highly conserved binding site for miR-141 located within the ERBB4 3'-untranslated region. In trastuzumab-resistant cells, miR-141 and shERBB4 reduced ERBB4 and p-AKT levels; ERBB2 and total AKT levels in miR-141 and shERBB4 groups showed no significant difference. Anti-miR-141 was upregulated ERBB4 and p-AKT levels in parental cell and had no obvious effect on ERBB2 and total AKT levels. Finally, miR-141 upregulated viability of the cells, which was restored by shERBB4, miR-141 and shERBB4 inhibited proliferation, and enhanced apoptosis of trastuzumab-resistant cells. miR-141 inhibitor caused an evident increase in proliferation and an obvious decrease in apoptosis of parental cells. CONCLUSION: Knockdown of miR-141 causes overexpression of ERBB4, which is involved in trastuzumab resistance in breast cancer cells. This study has implications that miR-141 as well as its target, ERBB4, as a potential target for treating trastuzumab-resistant breast cancers.

Long non­coding RNA FOXD2­AS1/miR­150­5p/PFN2 axis regulates breast cancer malignancy and tumorigenesis.

Breast cancer (BC) is a common cancer and leading cause of cancer­associated mortality in women. Abnormal expression of long non­coding RNA FOXD2 adjacent opposite strand RNA 1 (FOXD2­AS1) was associated with the development of a number of tumors. However, whether FOXD2­AS1 is dysregulated in BC and its underlying mechanisms remain unclear. In the present study, it was identified that FOXD2­AS1 expression was upregulated in BC tissue, cell lines and sphere subpopulation. Additionally, the abnormal upregulation of FOXD2­AS1 predicted poor prognosis in patients with BC. Furthermore, downregulation of FOXD2­AS1 decreased cell proliferation, and migratory and invasive abilities in BC cells, and decreased the growth of transplanted tumors in vivo. Downregulation of FOXD2­AS1 decreased the percentage of CD44 antigen+/signal transducer CD24- in breast cancer stem cell (BCSC) cells, and decreased the expression of numerous stem factors, including Nanog, octamer­binding transcription factor 4 (Oct4), and sex determining region Y­box 2 (SOX2), and inhibited the epithelial­mesenchymal transition process. FOXD2­AS1 was identified to be primarily located in the cytoplasm. Using bioinformatics analysis, a reporter gene assay and reverse transcription­polymerase chain reaction assays, it was demonstrated that microRNA (miR)­150­5p was able to bind directly with the 3'­untranslated region of FOXD2­AS1 and PFN2 mRNA. miR­150­5p mimics decreased the cell proliferation, migration and invasion of BC cells. FOXD2­AS1 knockdown significantly inhibited the miR­150­5p inhibitor­induced increase in Nanog, Oct4 and SOX2 expression. The miR­150­5p inhibitor­induced increase in N­cadherin, and decrease in E­cadherin and vimentin was inhibited by FOXD2­AS1 knockdown. Profilin 2 (PFN2) expression was significantly upregulated in BC tissues. Additionally, the abnormal upregulation of PFN2 was associated with poor prognosis in patients with BC. FOXD2­AS1 and PFN2 expression was positively correlated. Collectively, the present results demonstrated the role of the FOXD2­AS1/miR­150­5p/PFN2 axis in the development of BC, and provides novel targets for the treatment of BC, and potential biomarkers for diagnosis and prognosis of BC.

lincRNA­p21 inhibits the progression of non­small cell lung cancer via targeting miR­17­5p.

Non­small­cell lung cancer (NSCLC) is well established as one of the major subtypes of human lung cancer. NSCLC is characterized by a high incidence rate and poor patient prognosis. Previous studies have identified that long intergenic non-coding RNA (lincRNA) serves a key role in the development of tumor and malignant metastasis. However, the majority of the underlying mechanisms for lincRNA deregulation in various diseases, including cancer and diabetes, have not been completely elucidated. In the present study, the deregulation of lincRNA­p21 in NSCLC tumor tissues in comparison to adjacent healthy tissues was examined using reverse transcription­quantitative polymerase chain reaction. Furthermore, the effect of lincRNA­p21 overexpression and knockdown on different NSCLC cell lines was further investigated in vitro. The association between lincRNA­p21 expression and microRNA (miR)­17­5p level in NSCLC tumor cells was also investigated to clarify the underlying mechanism. The influence of miR­17­5p on different NSCLC cell lines A549 and PC9 were also examined in vitro using miR­17­5p mimics and inhibitors. Bioinformatics and luciferase assays were conducted to verify the direct binding sites on lincRNA­p21 for miR­17­5p. The results demonstrated that there was a significant low­expression of lincRNA­p21 in NSCLC tumor tissues, and lincRNA­p21 effectively inhibited the progression of lung cancer cells by suppressing cell proliferation and migration and promoting cell apoptosis. An evident negative association between lincRNA­p21 and miR­17­5p expression was observed, and the inhibitory effect of overexpressed lincRNA­p21 on lung cancer cells was counteracted by miR­17­5p. Bioinformatics and luciferase reporter analysis results confirmed that miR­17­5p is a direct target for lincRNA­p21. The present study provides evidence for lincRNA­p21 to inhibit the progression of NSCLC via direct targeting of a miR­17­5p associated signaling pathway.

Distribution and proportion of M1/M2 macrophages in periodontal tissues in rats with and without periodontitis / 口腔疾病防治

Objective@#To investigate the distribution and proportion of M1/M2 macrophages in the periodontal tissues of rats with and without periodontitis.@*Method@#Twelve Sprague-Dawley rats were randomly divided into a chronic periodontitis group (CP, n = 6) and a periodontal health group (PH, n = 6). The periodontitis model was induced at the first mandibular molar using a stainless steel ligature and was confirmed by histological analysis. M1 macrophages were labeled with inducible nitric oxide synthase (iNOS), and M2 macrophages were labeled with CD163. The distributions of M1 and M2 macrophages in the two groups were determined via immunohistochemistry and immunofluorescence, and the M1/M2 ratios were compared between the two groups.@*Results @#The M1 type macrophage count in the PH group was 12.17 ± 1.40, and the M1 macrophage count in the CP group was 40.00 ± 3.20; there was a statistically significant difference between the two groups (t = 7.96, P＜0.0001). The M2 macrophage count in the PH group was 4.50 ± 1.09, and the M2 type macrophage count in the CP group was 5.33 ± 0.67. There was no statistically significant difference between the two groups (t = 0.65, P = 0.53). The M1/M2 ratio in the CP group was 3.72 ± 1.08, and the M1/M2 ratio in the PH group was 8.31 ± 1.37; there was a statistically significant difference between the two groups (t = 2.63, P= 0.025).@*Conclusion@#During periodontitis, M1 macrophages increased significantly and were widely distributed; they may be involved in the progression of periodontitis and may be closely related to the destruction of the cementum.

Synergistic antitumor activity of pro-apoptotic agent PAC-1 with cisplatinum by the activation of CASP3 in pulmonary adenocarcinoma cell line H1299.

AIM: Evasion of apoptosis is a hallmark of human cancer cells. We sought to explore the potential synergistic antitumor activity and underlying mechanisms of the pro-apoptotic agent PAC-1 plus cisplatinum (Cis) in non-small cell lung cancer (NSCLC) cell lines. METHODS: The adenocarcinoma cell lines H1299, A549, PC9, H1650 and H1975 were used as in vitro models. Colorimetric MTT assays, Western blotting and flow cytometry were used to evaluate the anti-growth effects of PAC-1 and/or Cis and apoptosis status. The activated form of CASP3 (C-CASP3) was assessed by immunofluorescent staining. RESULTS: Single-agent Cis and PAC-1 were able to inhibit the cancer cell growth in certain dose ranges, with IC50 values of 1.9-11.7 and 5.6-14.8 µM, respectively. Sequential Cis→PAC-1 or concurrent Cis + PAC-1, but not PAC-1→Cis combinations showed synergistic effects on cell growth inhibition in H1299 cells (combination index, CI ≤ 0.6). In contrast, other combination modes mostly showed seemingly antagonistic effects (CI > 1.0). Flow cytometric analysis showed that Cis→PAC-1 sequential combination showed strong pro-apoptotic effects in H1299 cells. Western blots showed that in H1299, PC9 and H1975 cells, PAC-1 promoted the C-CASP3, but only in H1299 cells was there a synergistic effect with Cis on the CASP3 activation. CONCLUSIONS: PAC-1 showed anti-tumor activity in NSCLCs in vitro and a synergistic effect with cisplatin in EGFR(wt)KRAS(wt) H1299 cells. Our data suggest a potential treatment approach using cisplatin plus a pro-apoptotic agent acting via CASP3 activation for this subgroup of pulmonary adenocarcinomas.

Altered expression profile of apoptosis-related molecules correlated with clinicopathological factors in non-small-cell lung cancer.

Apoptosis-related molecules can be abnormally expressed in cancers and underscore the hallmark of resisting cell death in cancer cells. This study was aimed to observe the expression patterns of apoptosis-related molecules in lung cancer and paired non-cancerous tissues, and to observe if there is a correlation between the expression of these apoptotic molecules and clinicopathologic parameters. Immunohistochemistry (IHC) was performed to analyze the expression level of CASP3, CASP8, CASP9, PARP1, Cleaved CASP3 (C-CASP3), Cleaved PARP1 (C-PARP1), XIAP, BIRC5 (Survivin) and BCL2 in lung cancer and paired non-cancerous tissues. We found that apoptosis-related molecules CASP3, CASP9, BCL2, BIRC5 and PARP1 are abnormally expressed in lung cancer cells and their expression were correlated with histology. BCL2, BIRC5 and PARP1 are expressed at higher levels in SCC than in non-SCC. C-PARP1 expression might be an independent prognostic factor for NSCLC.

[Effects of tank operation on renal function of crews].

OBJECTIVE: To explore the effects of harmful factors in tank cabins on renal function of tank crews. METHODS: One hundred and fifty two tank crews as the observation group and 37 soldiers without tank environment exposure as control group were selected in the study. α1-microglobulin(α1-MG), ß2-microglobulin(ß2-MG), IgG, N-acetyl-ß-glucosidase (NAG) and urinary albumin excretion rate (UAER) in morning and 24 h urine were measured. RESULTS: Compared to the control group, the levels of α1-MG, ß2-MG, NAG, UAER in observation group were increased significantly (P < 0.05). ß2-MG, NAG, UAER of Soldiers with more than 50 motorized hours in observation group were significantly higher than those of control group (P < 0.05). ß2-MG, NAG and UAER of soldiers divorced from tank occupation more than 3 years decreased to the normal levels. ß2-MG of soldiers divorced from tank occupation more than 10 years was significantly higher than that of 6-10 years group. CONCLUSION: Tank occupational exposure influences the renal function of tank crews but not to a degree of clinical kidney disease. The renal function of crews divorced from tank occupation may recover but dysfunction of renal tubular reabsorption still exists.