BACKGROUND:Breast cancer (BC) is ranked among the most prevalent malignant tumors in the global female population. DLGAP5 is implicated in the progression of various tumors. However, the molecular mechanisms of DLGAP5 involved in BC and TAM interactions remain unclear. METHODS:We investigated the expression and prognostic significance of DLGAP5 in breast cancer (BC) and its association with M2 macrophage infiltration using bioinformatics and experimental methods. DLGAP5 expression was higher in BC cells (MCF-7, MDA-MB-231) than in normal breast epithelial cells (MCF-10 A), as confirmed by qRT-PCR and Western blot. Functional assays showed that DLGAP5 promoted BC cell proliferation, migration, invasion, and anti-apoptotic ability, and increased levels of PCNA, Ki67, and Bax. DLGAP5 also elevated M2 macrophage markers (Arg1, IL-10) and glycolytic enzymes (PGK1, LDHA, PKM2, HK2), and enhanced glycolysis, as indicated by ECAR and OCR measurements. Bioinformatics analysis further supported the link between DLGAP5, glycolysis, and M2 macrophage infiltration. Finally, by establishing an allograft tumor model, the regulatory effect of DLGAP5 knockdown on the malignant progression of BC was validated in vivo. RESULTS:Bioinformatics analysis revealed that the upregulation of DLGAP5, which is linked to poor prognosis in breast cancer (BC), promotes glycolytic reprogramming. This metabolic shift drives macrophage M2 polarization, thereby facilitating BC progression. CONCLUSION:Our work demonstrated that DLGAP5-induced glycolysis reinforces the progression of BC by promoting the polarization of macrophages towards an M2 phenotype. The study can provide a theoretical foundation for BC treatment, pinpointing DLGAP5 as a promising biomarker.

Radiotherapy is a leading treatment intervention for cancer and has been shown to improve the prognosis of patients with malignant tumors. However, there are several side effects associated with radiotherapy that require attention. The present case study describes the case of a patient who underwent breast-conserving surgery after receiving a diagnosis of right-sided breast cancer, following which they received conventional radiation therapy. A skin nodule was found on the right side of the breast 3 years later, which was pathologically confirmed to be a highly differentiated skin squamous cell carcinoma after surgical local excision. The patient presented with poor skin healing 2 months after the operation, and a myocutaneous flap of the descending branches of the thoracodorsal vessels was used to repair the defect and improve the breast shape. Although skin cancer induced by radiotherapy is relatively rare, physicians should remain cautious when treating skin injuries after radiotherapy, and recovery should be closely monitored. For patients with skin nodules after radiotherapy, a biopsy should be performed as early as possible to clarify the diagnosis and to develop appropriate treatment programs. For such skin cancer patients who have received radiotherapy in the past, it is necessary to consider the potential radiotherapy-related skin injuries they may have suffered after previous radiotherapy, the skin flap should be comprehensively evaluated before the operation and an appropriate surgical method should be selected to reduce the necessity of a second operation.

Breast cancer remains a significant global health challenge, with lung metastasis presenting critical barriers to effective treatment and patient survival. This study conducts the first comprehensive bibliometric and visualized analysis of lung metastasis research in breast cancer from 2000 to 2024, illustrating evolving research trends and collaboration patterns in this critical area. Utilizing data from the Web of Science Core Collection, we employed bibliometric tools such as VOSviewer and CiteSpace to assess publication trends, international collaborations, influential institutions, authors, and keyword dynamics. Our findings reveal a steady increase in annual publications, peaking in 2021, with a significant concentration of research emerging from the USA and China, alongside key insights into molecular mechanisms such as epithelial-mesenchymal transition and immunotherapy. Notably, genes like ERBB2 and ESR1 were identified as pivotal in the metastatic process, highlighting potential therapeutic targets. This study not only illuminates the current landscape of breast cancer lung metastasis research but also underscores the necessity for interdisciplinary collaboration to enhance understanding and treatment strategies for this lethal condition.

Background: Celecoxib has gained attention as a potential anti-tumor agent in breast cancer. This study systematically elucidated the therapeutic mechanisms of celecoxib in this malignancy. Methods: The candidate targets of celecoxib and the molecular targets associated with breast cancer were retrieved. The protein-protein interaction (PPI) networks were established. GO and KEGG pathway enrichment analyses were performed. Molecular docking simulations and normal mode analysis (NMA) were used. Results: This study identified 104 candidate targets of celecoxib, 18,389 potential targets implicated in breast cancer, and 95 overlapping targets. GSK3B, CCND1, PTGS2, CDK2, CDK4, and MTOR were identified as key hub proteins in celecoxib's anti-breast cancer activity. These overlapping candidates were associated with protein serine/threonine kinase activity and cyclindependent protein kinase regulator activity and involved in FoxO, prolactin, p53, and PI3K-Akt pathways. Celecoxib exhibited high binding affinity for GSK3B, CDK4, and MTOR, while showing moderate binding affinity for CDK2. Dynamic simulations revealed stable binding, minimal structural perturbations, and system-dependent rigidity profiles of the docked celecoxib-protein complexes. In vitro experimental results showed that celecoxib suppressed cell colony formation, migration, and invasion and enhanced apoptosis in MCF-7 cells by downregulating MTOR. Conclusion: This study suggests that celecoxib may exert anti-cancer effects in breast cancer via multiple targets (e.g., MTOR) and pathways.

Angiogenesis plays a key role in promoting the growth and metastasis of breast tumors. Tumor exosomes (EXs) contribute to angiogenesis in various tumor tissues by transferring their carried RNAs. MiR-423-5p was enriched in multiple tumors and implicated in tumor growth. In this study, we investigated the roles and underlying mechanisms of tumor-derived EXs and their carried miR-423-5p in regulating human umbilical vein endothelial cell (HUVEC) functions. EXs derived from MCF-7 cells (MCF-7 EXs) or with miR-423-5p knockdown (MCF-7 EXsSimiR-423-5p) were collected and incubated with ECs, and then the proliferation, migration, and tube formation abilities of ECs were detected. We found that miR-423-5p was enriched in breast cancer, MCF-7 cell lines and their derived EXs. After coculture with HUVECs, MCF-7 EXs merged into HUVECs and subsequently increased the miR-423-5p expression, proliferation, migration, and tube formation abilities of HUVECs, paralleling the increased EFNA3 and Notch1 expression, which was partially abolished by miR-423-5p knockdown. Altogether, our data suggest that MCF-7 EXs enriched with miR-423-5p promote the angiogenic function of vascular endothelial cells by activating the miR-423-5p/EFNA3/Akt signaling pathway.

Numerous studies have indicated that N6-methyladenosine (m6A) and lncRNAs play pivotal roles in human cancer. However, the underlying functions and mechanisms of m6A-lncRNA in the physiological processes of breast cancer remain unclear. Here, we found that DSCAM-AS1 is an m6A-modified lncRNA that was overexpressed in breast cancer tissues and cells, indicating poor clinical prognosis. Gain/loss functional assays suggested that DSCAM-AS1 inhibited erastin-induced ferroptosis in breast cancer cells. Mechanistically, there were remarkable m6A modification sites on both the 3'-UTR of DSCAM-AS1 and the endogenous antioxidant factor SLC7A11. M6A methyltransferase methyltransferase-like 3 (METTL3) methylated both SLC7A11 and DSCAM-AS1. Moreover, DSCAM-AS1 recognized m6A sites on the SLC7A11 mRNA, thereby enhancing its stability. Taken together, these findings indicated a potential therapeutic strategy for breast cancer ferroptosis in an m6A-dependent manner.

Background: Breast cancer has become the most frequently diagnosed cancer in the world. Detection at an early stage, frequently allows women to benefit from breast conserving surgery. However, some patients are not satisfied with the breast shape after breast-conserving surgery, and autologous tissue flaps are needed to fill the defect in the resection area. The modified lateral thoracic artery perforator (LTAP) flap isn't one of the commonly used flaps in breast surgery and has the advantages of a reliable blood supply, simple operation and few postoperative complications. In this study, we aimed to evaluate the feasibility and effectiveness of a modified LTAP flap for repairing partial breast defects after breast-conserving surgery. Methods: In this study, we retrospectively analyzed the clinical data of 126 patients treated with LTAP flaps to repair local breast defects at Affiliated Hospital of Guangdong Medical University between January 2020 and June 2021. Data were collected on the demographic characteristics of these patients, tumor size and location, type of axillary lymph node surgery, availability of adjuvant chemotherapy and radiotherapy, and postoperative complications. Results: The median weight of the tumor specimen was 185 g (range, 170-320 g), and this glandular tissue accounted for 30% to 40% of the total breast volume. The average flap size was 10.5 cm x2.5 cm (length range, 8-15 cm, width range: 2-4 cm). The minimum follow-up time was 6 months, with an average of 10 months (range, 6-22 months). The mean operative time was 130 minutes (range: 90-180 minutes), and the mean hospital stay was 3 days (range, 2-5 days). All modified LTAP flaps survived completely without donor site complications. None of the patients required revision surgery on the postoperative breast. Conclusions: The modified LTAP flap is a reliable method for repairing partial breast defects after breastconserving surgery. It has the advantages of a simple operation, a reliable blood supply, fewer postoperative complications, and a high flap survival rate. It is especially suitable for Asian women with small breast volumes and can achieve good breast contouring effects.

Background:Breast cancer is the most common gynecological malignancy and the leading cause of cancer-related deaths in women. P-element induced wimpy testis (PIWI)-interacting RNAs (piRNAs) are novel non-coding RNAs whose abnormal expressions have been closely associated with multiple cancers. This study explored the roles and possible mechanisms of piRNA-31106 in breast cancer.Methods:The expression of piRNA-31106 in breast cancer tissues and cells was detected by reverse transcription polymerase chain reaction (RT-PCR). The pcDNA vector containing piRNA-31106 (pcDNA-piRNA-31106) and a short hairpin (sh)RNA containing piRNA-31106 (shRNA-piRNA-31106) were used to interfere with piRNA-31106 expression in breast cancer cells. The effects on cell proliferation, apoptosis/cell cycle, invasion, and metastasis were detected via Cell Counting Kit-8 (CCK-8), flow cytometry, transwell assays, and scratch tests, respectively. The protein expressions of murine double minute 2 (MDM2), cyclin-dependent kinase 4 (CDK4), and cyclinD1 were detected by Western blot analysis. The N6-methyladenosine (m6A) RNA methylation level and the binding relationship between piRNA-31106 and METTL3 were analyzed. The role of METTL3 in the regulation of breast cancer by piRNA-31106 was further analyzed by using small interfering (si)RNA targeting METTL3.Results:PiRNA-31106 was highly expressed in breast cancer tissues and cell lines MDA-MB-231 and MCF-7. Overexpression of piRNA-31106 promoted the viability, invasion, and migration of breast cancer, inhibited apoptosis, and promoted the expressions of MDM2, CDK4, and cyclinD1. Inhibition of piRNA-31106 showed the opposite effect. In addition, piRNA-31106 promoted the m6A methylation levels and facilitated methyltransferase-like 3 (METTL3) expression in MDA-MB-231 and MCF-7 cells. RNA immunoprecipitation (RIP) assays confirmed the binding relationship between piRNA-31106 and METTL3. Further experiments demonstrated that si-METTL3 could inhibit the regulatory effects of piRNA-31106 on breast cancer.Conclusions:PiRNA-31106 was significantly highly expressed in breast cancer and could promote breast cancer progression by regulating METTL3-mediated m6A RNA methylation.

BACKGROUND:Chronic radiative chest wall ulcers are common in patients undergoing radiation therapy. If not treated early, then symptoms such as erosion, bleeding and infection will appear on the skin. In severe cases, ulcers invade the ribs and pleura, presenting a mortality risk. Small ulcers can be repaired with pedicle flaps. Because radioactive ulcers often invade the thorax, surgeons need to remove large areas of skin and muscle, and sometimes ribs. Repairing large chest wall defects are a challenge for surgeons.CASE SUMMARY:A 74-year-old female patient was admitted to our department with chest wall skin ulceration after radiation therapy for left breast cancer. The patient was diagnosed with chronic radioactive ulceration. After multidisciplinary discussion, the authors performed expansive resection of the chest wall ulcers and repaired large chest wall defects using a deep inferior epigastric perforator (DIEP) flap combined with a high-density polyethylene (HDPE) patch. The patient was followed-up 6 mo after the operation. No pigmentation or edema was found in the flap.CONCLUSION:DIEP flap plus HDPE patch is one of the better treatments for radiation-induced chest wall ulcers.

To discover the utility of pedicled latissimus dorsi kiss flap for the reconstruction of chest wall defect after mastectomy. This study was a systemic analysis of 12 female patients with breast tumors who were treated at Affiliated Hospital of Guangdong Medical University from January 2018 to December 2019. Among them, three patients had malignant lobular breast tumors, and nine patients had locally advanced breast cancer. After extensive resection of the primary tumor, the chest wall skin, and soft tissue, a large defect was left in the chest wall of each patient. Based on the design and structure of the kiss flap, two semicircular flaps of equal diameter were designed in the latissimus dorsi region, and their blood supply was retained from the same vascular trunk. Two flaps were transferred to the chest wall through a subcutaneous tunnel, and the incision in the donor area was sutured directly. Finally, two equal semicircle flaps were adjusted to fit the defect and then fixed on the chest wall. Referred to the design of the kiss flap, the area of the latissimus dorsi was increased to cover a larger chest wall defect. We have used this flap to reconstruct chest wall defects on twelve patients. Their age ranged from 24 to 62. The largest defect was 20 x 12 cm, and the smallest defect was 15 x 10 cm in diameter. Postoperative follow-up time was 5-9 months (mean time: 6.2 months): Follow-up observations demonstrated that all the flaps were healed well without edema or extravasation and donor area of all cases was closed well. In addition, no local recurrence or distant metastasis was observed in all patients.

目的 探讨早期乳腺癌行保乳术的安全性和有效性.方法 100例早期乳腺癌患者,根据手术方式不同分为保乳术组和改良根治术组,每组50例.改良根治术组患者行改良根治术治疗,保乳术组患者行保乳术治疗.比较两组手术相关指标、术后患侧胸部美观度、并发症发生情况及术后局部复发率、远处转移率、生存率.结果 保乳术组患者的手术时间(112.23±5.65)min、住院时间(6.68±1.74)d、 引流时长(6.67±2.16)d短于改良根治术组的(120.30±9.23)min、(8.52±2.25)d、(8.52±2.25)d,术中出血量(34.23±13.77)ml、引流量(245.25±146.69)ml少于改良根治术组的(47.79±5.23)、(305.86±28.01)ml,差异具有统计学意义(P<0.05).保乳术组患者的术后患侧胸部美观度90％(45/50)高于改良根治术组的0,差异具有统计学意义(P<0.05).两组并发症发生率比较差异无统计学意义(P>0.05).两组术后局部复发率、远处转移率和生存率比较,差异均无统计学意义(P>0.05).结论 在掌握手术指征及保乳技巧前提下,治疗早期乳腺癌采取保乳术不仅保留了乳房,且提高了患者的生活质量,减轻了患者的心理负担,值得在临床中大力推广.

BACKGROUND:In recent years, breast cancer is the most common malignancy in women. The traditional method of surgery is to remove a woman's breast completely, which has a negative impact on her work and life. Today, women have a fiery pursuit to maintain their perfect figure, which has forced breast surgeon to find a new surgical approach to maintain the shape of the breast after surgery.METHODS:This study systematically analyzed and summarized the incision design and repair of glandular defects in early-stage breast cancer patients by oncoplastic breast techniques. By summarizing the methods of oncoplastic breast surgery (OBS) in different quadrants, it could help beginners to master this technology more quickly, so as to provide better help for breast cancer patients.RESULTS:A total of 216 breast cancer patients who underwent OBS from January 2016 to June 2020 at the Affiliated Hospital of Guangdong Medical University were included in this study. In patients treated with the volume-displacement method and the volume-replacement method, 92.6% and 86.2% of patients achieved excellent breast shape, respectively.CONCLUSIONS:OBS is a safe and effective way to treat early-stage breast cancer while obtaining better breast shape, reducing postoperative psychological trauma, and improving quality of life.

Objective:To explore the expression and clinical significance of eukaryotic initiation factor 4E (eIF4E) and Krüppel-like factor 4 (KLF4) in breast carcinoma tissues.Methods:The expression levels of eIF4E protein and KLF4 protein in 73 cases of human breast carcinoma tissues and non-cancerous adjacent breast tissues (5 cm distance away from the margin of breast carcinoma) of patients pathologically confirmed from January 2016 to October 2020 on Affiliated Hospital of Guangdong Medical University were examined by envision immunohistochemistry. The statistical analysis of Chi-square test in combination with clinical data were carried out.Results:The eIF4E protein expression rate in breast cancer tissues was significantly higher than that in the corresponding paracancerous tissues [79.45% (58/73) vs. 20.55% (15/73), χ2=50.658, P<0.01]. The eIF4E expression level was significantly correlated with breast cancer tumor size, histological grade, TNM stage. The eIF4E expression level was significantly correlated with tumor size, histological grade, TNM stage (tumor node metastasis stage), and lymph node metastasis ( χ2=4.842, 9.230, 7.103, 5.560, P<0.05). KLF4 protein expression rate in breast cancer tissues was significantly higher than eIF4E protein expression rate in corresponding paraneoplastic tissues [24.66% (18/73) vs. 64.38% (47/73), χ2=23.321, P<0.01]. The KLF4 expression level was significantly correlated with histological differentiation degree, TNM stage, and lymph node metastasis of breast cancer ( χ2=8.977, 6.403, 5.256, P<0.05). Conclusion:This study suggested the high expression of eIF4E and low expression of KLF4 in breast carcinoma tissues. Detecting the expression levels of eIF4E and KLF4 might be help further understand the biological behavior of breast carcinoma and predict its prognosis.

Objective:To investigate the clinical effect of the transverse rectus abdominismuscle (TRAM) on reconstruction of the breast.Methods:The clinical data of 23 patients receiving TRAM breast reconstruction in our department from Jan. 2018 to Dec. 2019 were retrospectively analyzed.Results:The operation time of 23 patients ranged from 240 to 360 mins, andthe average time was about 300 mins. Intraoperative bleeding was about 120 to 200 ml, with an average of 170 ml. All the flaps survived successfully, but 2 cases were complicated with local fat necrosis. The postoperative period was between 6 and 12 months. No local tumor recurrence or metastasis was found inall patients during postoperative follow-up, and the breast shape was maintained in good condition.Conclusion:TRAM can make up for the regret of breast loss caused by breast cancer in female patients. It can bring confidence in life and work to female patients, and the technology is safe and reliable, which is worthy of promotion.

Objective We investigate the molecular mechanism underlying inhibitory effects of cordycepin on proliferation,apoptosis,migration and invasion of breast cancer.We focus on the role of HOXD10 in inhibitory effects of cordycepin.Methods Two individual breast cancer cell lines,MCF-7 and MDA-MB-231,were used in this study to investigate the effects of cordycepin on proliferation,apoptosis,migration and invasion of breast cancer,by cell counting kit-8 (CCK-8) assays,flow cytometry and Transwell assays.The small interfering RNAs (siRNAs) targeted HOXD10 were transfected into MCF-7 and MDA-MB-231 cells to knock down HOXD10.We investigate the role of HOXD10 by comparing the difference between group NC and group siRNAs.Results The A values of cordycepin treated MCF-7 and MDA-MB-231 cells were significantly lower than those of control group (DMSO group) (MCF-7cells:0.665 ± 0.004 vs.0.733 ± 0.005,t =10.450,and MDA-MB-231cells:0.632 ± 0.005 vs.0.722 ± 0.005,t =13.330,P ＜ 0.05),which means the proliferation of breast cancer cells was significantly inhibited,The apoptosis rateof cordycepin treated MCF-7 and MDA-MB-231 cells were significantly higher than those of control group (MCF-7cells:20.200 ± 0.322 vs.5.500 ± 0.000,t =45.730,MDA-MB-231 cells:21.800 ± 1.493 vs.5.367 ± 0.318,t =10.760,P ＜ 0.05).There were significantly fewer migrated MCF-7 and MDA-MB-231 cells in cordycepin group than in control group(MCF-7 cells:28.670 ± 1.764 vs.83.330 ± 2.186,t=19.460,MDA-MB-231cells:29.000 ± 2.646 vs.114.700 ± 3.180,t =20.710,P ＜ 0.05).There were significantly fewer invasive MCF-7 and MDA-MB-231 cells in eordycepin group than control group(MCF-7cells:24.670 ± 2.603 vs.49.000 ± 1.528,t =8.0620,MDA-MB-231cells:12.330 ± 1.453 vs.36.670 ± 2.728,t =7.872,P ＜ 0.05).After transfection of MCF-7 and MDA-MB-231 cells with siRNA and intervention with cordycepin,the proliferation of breast cancer cells was inhibited (MCF-7cells:0.627 ± 0.004 vs.0.648 ±0.006,t=2.951,MDA-MB-23 cells:0.620 ±0.006 vs.0.635 ±0.004,t=2.087,P ＜ 0.05).The apoptosis rate of the treatment group was significantly higher than the control group (MCF-7 cells:20.470 ± 0.260 vs.16.300 ± 0.153,t =13.800,MDA-MB-23 cells:19.170 ± 0.167 vs.17.030 ±0.186,t =8.5520,P ＜0.05).There were significantly fewer migrated MCF-7 andMDA-MB-231 cells in siRNA group than in control group (MCF-7cells:11.000 ± 2.082 vs.30.330 ± 2.028,t =6.653,MDA-MB-23cells:11.330 ± 1.4530 vs.23.000 ± 1.528,t =5.534,P ＜0.05).There were significantly fewer invasive MCF-7 and MDA-MB-231cells in siRNA group than control group(MCF-7 cells:16.330 ± 1.764 vs.23.670 ± 1.760,t =2.940,MDA-MB-2 cells:9.333 ± 1.453 vs.19.670 ± 2.333,t =3.759,P ＜ 0.05).Those values above are statistically significant.Conclusion Cordycepin induces apoptosis and inhibits proliferation,migration and invasion of breast cancer.2.Suppression of HOXD10 promptes the effects of cordycepin on proliferation,apoptosis,migration and invasion of breast cancer.

MicroRNA (miR)-125a-5p has shown the potential for suppressing tumorigenesis and development; however, the effects of miR-125a-5p on breast cancer cells remains unknown. The aim of this study was to evaluate the effects and underlying mechanisms of miR-125a-5p in MCF-7 breast cancer cells. MCF-7 cells were transfected with miR-125a-5p mimic or miR-125a-5p small interfering RNA to produce miR-125a-5p overexpressing/knockdown cells. Cell proliferation was assessed by an MTT assay, and cell migration ability was determined by an in vitro scratch assay. Hoechst 33258 staining and flow cytometry were performed to assess the effects of miR-125a-5p on MCF-7 apoptosis. Western blotting and reverse transcription-quantitative polymerase chain reaction were used for measuring phosphatase and tensin homolog (PTEN), phosphorylated (p)-mitogen-activated protein kinase kinase (MEK1/2)/MEK1/2, p-ERK1/2/ERK1/2, B-cell lymphoma-2 (Bcl-2), cleaved caspase-3, and miR-125a-5p expression. miR-125a-5p overexpression inhibited the proliferation and migration, but promoted the apoptosis of MCF-7 cells. These effects were associated with increases in PTEN and cleaved caspase-3 expression, and decreases in p-MEK1/2/MEK1/2, p-ERK1/2/ERK1/2, and Bcl-2. Silencing of miR-125a-5p exhibited opposing effects on MCF-7 cells. These observations suggested that miR-125a-5p participates in the regulation of multiple functions of MCF-7 cells by promoting the expression of PTEN tumor suppressor genes, activating MEK1/2/ERK1/2 signaling, and regulating caspase-3/Bcl-2 signaling. Thus, it may be a suitable target for breast cancer gene therapy.

目的 探讨Hiwi基因表达对乳腺癌细胞侵袭和转移能力的影响.方法 使用western blot法分析62例乳腺癌患者的病理组织标本和24例确诊乳腺组织功能正常无癌变现象的志愿者的组织标本的Hiwi表达水平.结果 Hiwi在乳腺癌组织中的表达水平(1.708±0.065)显著高于正常乳腺组织中的表达水平(0.706±0.044),P<0.05.正常表达组的穿膜乳腺癌细胞数为(73.55±6.43)个,显著高于下调表达组的穿膜乳腺癌细胞数(46.71±6.15)个,P<0.05.结论 Hiwi基因表达水平与乳腺癌癌细胞侵袭和转移能力正相关.Hiwi基因有可能成为良好的乳腺癌检测指标和治疗靶点.

目的:观察延龄草总皂苷对乳腺癌细胞MDA-MB-231裸鼠皮下移植瘤的影响及相关机制.方法:培养乳腺癌细胞MDA-MB-231,接种至BALB/c裸鼠背部皮下.接种后第5天通过腹腔注射的方式给裸鼠予延龄草总皂苷治疗,每隔3天测量移植瘤的体积以及裸鼠的体重;实验结束时,采用TUNEL试剂盒检测移植瘤细胞的凋亡情况;Western blot法检测凋亡相关蛋白剪切型caspase-3,8,9表达的变化.结果:延龄草总皂苷可有效地抑制裸鼠移植瘤的增殖,实验结束时,肿瘤的体积分别为:模型组(1142.24±164.32)mm3,延龄草总皂苷(5 mg/kg)(552.90±49.71)mm3,延龄草总皂苷(10 mg/kg)(269.78±48.84)mm3.延龄草总皂苷能诱导移植瘤细胞的凋亡,可浓度依赖性地促进细胞中剪切型caspase-3,9的表达.结论:延龄草总皂苷可有效地抑制MDA-MB-231裸鼠移植瘤的增殖,其方式可能通过caspase依赖的方式促使MDA-MB-231发生凋亡.

Objective To investigate the occurrence and development of FOXO1 gene process and its clinical significance in breast carcinoma. Methods The protein and mRNA expression of FOXO1 gene were detected in 50 cas-es of breast carcinoma, 20 cases of benign breast lesion and 37 cases of adjacent normal breast tissue by an immunohisto-chemical method (steptavidin peroxidase, SP) and fluorescence-based real-time reverse transcription PCR (RT-PCR). These tissue samples were taken from the patients who admitted to the Affiliated Hospital of Guangdong Medical Col-lege from June 2012 to January 2013. Results The positive rate of FOXO1 protein in the cancer group was 46.0%, while the positive rates in the benign group and the adjacent group were respectively 75.0%and 70.2%. The results of RT-PCR showed that the expression of FOXO1 mRNA in the cancer group, the adjacent cancer group and the benign group were (0.526 ± 0.011), (0.885 ± 0.017), (0.841 ± 0.026), respectively; the protein and mRNA expression of FOXO1 gene in the cancer group were significantly lower than those in the adjacent cancer group and benign group (P<0.05). The protein and mRNA expression of FOXO1 gene was associated with tumor size, lymph node metastasis (P<0.05), but it had no relationship with menopausal status, age, HER2 receptor protein (HER2), estrogen receptor (ER), progesterone receptor (PR), Ki67 (P>0.05). Conclusion The protein and mRNA expression of FOXO1 gene is associated with tu-mor size and axillary lymph node metastasis, which means that FOXO1 can be used as one of the biological parameters to determine the prognosis of breast carcinoma.

目的 分析青年期急性下肢深静脉血栓形成(LEDVT)的临床特点及诊治方法,为提高临床上对青年期急性LEDVT的认识及警惕.方法 回顾分析17例青年期急性LEDVT的临床资料.结果 17例均通过超声检查诊断为青年期急性LEDVT的患者,经抗凝、溶栓等治疗,其中效果优者5例,良好者6例,优良率为64.7％,有血栓形成后综合征者6例,占35.3％.结论 青年期急性LEDVT有较高的血栓形成后综合征的发生率,临床医师需加强对青年期急性LEDVT的认识,做到早期诊断和规范治疗,以进一步减少血栓形成后综合征的发生.