Objective: To investigate the effects of docetaxel and ADM (doxorubicin) on migration, invasion and filopodia formation of breast cancer cells. Methods: Triple-negative breast cancer MDA-MB-231 cells were divided into three groups: blank control group, docetaxel group and ADM group. CCK-8 (cell counting kit-8) assay was used to determine the IC10 (inhibitory concentration of 10%) values of docetaxel and ADM. Abilities of invasion and migration were detected by Transwell assay under IC10 of docetaxel and ADM. The effect of these concentrations on cellular proliferation was assayed by flow cytometry to detect the cell cycle. The rhodamine-phalloidin was used to stain cell cytoskeleton to observe filopodia formation after treatment with these two drugs. Results: The IC10 values of docetaxel and ADM in MDA-MB-231 cells were 1.0 ng/mL and 0.5 μg/mL, respectively. These two concentrations had no effects on cellular proliferation and cell cycle (P > 0.05). Docetaxel (1.0 ng/mL) could inhibit migration and invasion of tumor cells more effectively than ADM (0.5 μg/mL). Docetaxel inhibited filopodia formation of triple-negative breast cancer cells more effectively with a statistical significance. Conclusion: Docetaxel can obviously inhibit the migration and invasion of breast cancer cells as compared with ADM, which may be associated with suppression of filopodia formation by these agents. Copyright © 2013 by TUMOR.

Objective: To investigate the effect of cell division cycle 42 (Cdc 42) gene on the formation of filopodia suppressed by non-steroidal anti-inflammatory drugs (NSAIDs), and to explore the probable signal transduction pathway involving Cdc 42 in the inhibition effects on migration and invasion abilities of breast cancer cells induced by NSAIDs. Methods: MCF-7 cells were divided into four groups: blank control group, NS-398 (100 μmol/L)-treated group, cyclooxygenase-2 (Cox-2) small interfering RNA (siRNA)-transfected group and the negative siRNA-transfected group. The expressions of Cox-2 and Cdc42 mRNAs were detected by real-time fluorogentic quantitative PCR(RFQ-PCR), and the expressions of Cox-2 and Cdc42 proteins were measured by Western blotting. Actin-tracker Green fluorescent probe was used to examined the morphology of filopodias in MCF-7 cells. The invasion ability of MCF-7 cells was detected by using the Martrigel-coated Transwell. Results: The filopodias in MCF-7 cells disappeared in the NS-398-treated group, and the invasion ability of MCF-7 cells was also significantly decreased in this group compared with that in the blank control group (P<0.05). There was no difference in the expression level of Cox-2 mRNA or protein between the blank control group and the NS-398-treated group (P>0.05), and the difference was also not seen in the expression of Cdc42 mRNA or protein between these two groups (P>0.05). The active-Cdc42 level was significantly decreased in the NS-398-treated group compared with that in the blank control group (P<0.05). The filopodias in the Cox-2 siRNA-transfected group disappeared, and the invasion ability of MCF-7 cells transfected with Cox-2 siRNA was significantly decreased compared with that in the negative siRNA-transfected group (P<0.05). The active-Cdc42 level was also significantly decreased in MCF-7 cells transfected with Cox-2 siRNA compared with those transfected with negative siRNA (P<0.05). Conclusion: NSAIDs can suppress the invasion ability of breast cancer cells. This effect may be achieved by inhibiting the activity of Cox-2, decreasing the expression level of active-Cdc42, and suppressing the formation of filopodias.

Objective: To detect the expression of multi-drug resistance genes MDR 1 and BCRP in breast cancer stem cells and differentiated cells as well as discuss their clinical significance. Methods: The breast cancer stem cells were separated from human primary breast cancer tissue and MCF-7 cells by flow cytometry-based selection on freshly isolated cells. The expressions of MDR 1 and BCRP in different subsets of cells was measured by real-time PCR. Results: Compared with breast cancer differentiated cells, the expressions of MDR 1 and BCRP in breast cancer stem cells were significantly higher (P < 0.01), and the proportion of stem cells markedly increased after chemotherapy (P < 0.01). Conclusion: Compared with breast cancer differentiated cells, breast cancer stem cells have stronger drug-resistance against chemotherapy via over-expression of multidrug resistance genes, which is one of the key factors for failure of chemotherapy and recurrence of breast cancer.

Objective To explore the association of loss of heterozygosity (LOH) at chromosome 3p and vascular endothelial growth factor (VEGF) expression with clinicopatho logical features of breast cancer. Methods A total of 40 specimens of breast invasive ductal carcinomawere analyzed in the present study. The ductal carcinoma cells and normal breast cells were microdissected from the paraffin sections. Capillary electrophoresis method was used to detect LOH of four microsatellite loH located in the 3p site. Immunohistochemical staining was used to investigate the expression of CD34, VEGF and Her2 proteins in the 40 specimens. The association of LOH with the clinicopathological characteristics of breast carcinoma was evaluated. Results We found that in the 40 specimens LOH of D3S1038 was 20%(8/40), LOH of D3S1295 was 37. 5% (15/40), LOH ofD3S1581 was 17. 5% (7/40), and LOH ofD3S3118 was 5% (2/40). LOH was positively correlated with expression of VEGF (r=0. 658 0, P<0. 01) and MVD (r=0. 804 9, P<0. 01). We also found that LOH was significantly related to Her2 (r=0. 539 4), differentiationr = 0. 497 2), lymph node metastasis(r = 0. 506 4), and TNM stage(r = 0. 596 0, all P<0. 01). Conclusion LOH at chromosome 3p microsatellite loci is correlated with angiogenesis. Inactivation of tumor suppressor may influence angiogenesis and subsequently promote tumor growth and metastasis. Detection of LOH at chromosome 3p microsatellite lod together with angiogenesis can help to fully understand the biological characteristics of breast cancer.

Objective To explore the association of loss of heterozygosity (LOH) at chromosome 3p and vascular endothelial growth factor (VEGF) expression with clinicopathological features of breast cancer. Methods A total of 40 specimens of breast invasive ductal carcinoma were analyzed in the present study. The ductal carcinoma cells and normal breast cells were microdissected from the paraffin sections. Capillary electrophoresis method was used to detect LOH of four microsatellite loci located in the 3p site. Immunohistochemical staining was used to investigate the expression of CD34, VEGF and Her2 proteins in the 40 specimens. The association of LOH with the clinicopathological characteristics of breast carcinoma was evaluated. Results We found that in the 40 specimens LOH of D3S1038 was 20%(8/40), LOH of D3S1295 was 37.5% (15/40), LOH of D3S1581 was 17.5% (7/40), and LOH of D3S3118 was 5% (2/40). LOH was positively correlated with expression of VEGF (r=0.658 0, P<0.01) and MVD (r=0.804 9, P<0. 01). We also found that LOH was significantly related to Her2 (r=0.539 4), differentiation (r=0.497 2), lymph node metastasis(r = 0. 506 4), and TNM stage(r = 0.596 0, all P<0.01). Conclusion LOH at chromosome 3p microsatellite loci is correlated with angiogenesis. Inactivation of tumor suppressor may influence angiogenesis and subsequently promote tumor growth and metastasis. Detection of LOH at chromosome 3p microsatellite loci together with angiogenesis can help to fully understand the biological characteristics of breast cancer.

Objective: To investigate the expression of osteopontin (OPN) in normal breast epithelium, intraductal carcinoma and infiltrating ductal carcinoma and its clinical significance. Methods: The expression of OPN was examined by S-P immunohistochemistry in all specimens, and the results were statistically analyzed. Results: The positive rates of OPN in normal breast epithelium, intraductal carcinoma and infiltrating ductal carcinoma specimens were 0%(0/20), 20.0%(5/25) and 43.1%(25/58), respectively, with significant differences found between the latter two groups (P<0.05). OPN expression in breast infiltrating ductal carcinoma was not correlated with the family history, the sizes of primary tumor or patient ages, and it was correlated with histological types, clinical TNM stages and axillary lymphatic metastasis(P<0.05). Conclusion: OPN may participate in the development, progression, metastasis of breast cancer, and it may be used for predicting the prognosis of breast cancer.

Objective: To observe the clinical effect and adverse reaction of capecitabine as first-line monotherapy in elderly patients with stage II a breast cancer. Methods: From June 2002 to June 2005, 71 elderly patients with stage II a breast cancer received chemotherapy (different scheme: capecitabine group and CEF group) after operation. The efficacies and adverse reactions were evaluated and compared between the two groups. Results: The 3-year and 5-year survival rates of patients in capecitabine group were 97.06% and 94.12%, respectively; the relapse rate was 5.88%; all were comparable to those of CEF group. One of the advantages of capecitabine was its oral administration. The adverse effect of capecitabine was mainly handfoot syndrome, with an incidence of 82.35%, but was tolerable. The gastrointestinal reaction and bone marrow repression in capecitabine group were significantly lower than those in the CEF group(P<0.01). There was no giving up of treatment due to adverse reactions or fear of chemotherapy in our group. Conclusion: Capecitabine is effective and safe in the treatment of elderly patients with stage II a breast cancer; it is easy to take, with less adverse effects and better patient compliance.

Objective: To investigate the expression of targeting protein for Xenopus kinesin-like protein 2 (TPX2) in breast cancer tissue and to explore its role in proliferation, migration and invasion of breast cancer cells. Methods: The mRNA and protein expressions of TPX2 in breast cancer tissue and cell lines were assessed by quantitative RT-PCR and Western blot. The effect of TPX2 with RNA interference on proliferation, invasion and migration of breast cancer cells was observed by MTT and Transwell assays. Results: Both mRNA and protein expressions of TPX2 were upregulated in breast cancer tissues compared to tumor-adjacent tissue. TPX2 expression was also upregulated in breast cancer cell lines, and the TPX2 interfered by small interfering RNA could inhibit the proliferation, invasion and migration of breast cancer cells by inhibiting matrix metalloproteinase-2 and matrix metalloproteinase-9. Conclusions: Significantly upregulated TPX2 expression is observed in breast cancer tissue and cells, and contributes to promote the proliferation, migration and invasion of breast cancer cells.

Objective To explore the value of p53, Ki67, nm23 and epidermal growth factor receptor (EGFR) in the evaluation of the efficacy of neoadjuvant chemotherapy for locally advanced breast cancer. Methods From January 1, 2013 to March 31, 2018, 98 cases of locally advanced breast cancer in our hospital were selected as the research subjects. The changes of p53, Ki67, nm23 and EGFR before and after neoadjuvant chemotherapy and their relationship with clinical efficacy were detected. Results The positive expression of p53, Ki67 and EGFR after chemotherapy were all lower than those before chemotherapy, and the positive expression of nm23 was higher than that before chemotherapy, the difference was statistically significant (P<0. 05). The effective rate of p53 positive was lower than that of the negative ones, and the difference was statistically significant (P< 0. 05). The effective rates of Ki67 and nm23 positive were higher than that of negative ones, and the difference was statistically significant (P<0. 05). There was no statistical difference in effective rate between the positive EGFR and negative ones (P > 0. 05). Conclusion Neoadjuvant chemotherapy can significantly improve the expression of biological factors p53, Ki67, EGFR and nm23 in locally advanced breast cancer patients, and p53, Ki67 and nm23 have certain value in evaluating the curative effect of chemotherapy.

Thyroid cancer has become more prevalent in recent years. Patients urgently need efficient, personalized services based on an accurate assessment. The combination of artificial intelligence (AI) and traditional medical approaches can potentially improve the accuracy of medical decision-making. This review focuses on the use of AI to evaluate and predict the prognosis of thyroid cancer and aims to provide a foundation for the extraction of key information with AI to guide individualized treatment. First, we briefly introduce the concept and development of AI and the significance of precision medicine in the thyroid cancer. Second, the potential applications of AI in diagnosing thyroid cancer and predicting its prognosis are discussed. Furthermore, we analyze the opportunities and challenges of ultrasonic and pathological diagnostic and prognostic evaluation methods based on traditional pathological parameters and the gene mutation pathway model. Finally, we discuss the future research direction of AI in relation to thyroid cancer. Keywords: thyroid cancer, artificial intelligence, precision medicine, diagnosis, prognosis