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Objective@#To analyze the clinicopathological features and prognosis of breast invasive ductal carcinoma patients receiving radical mastectomy according to the primary tumor location.@*Methods@#From January 2008 to December 2008, 993 patients with breast invasive ductal carcinoma received radical mastectomy in Tianjin Medical University Cancer Institute and Hospital. Patients were grouped according to the primary tumor location when breast cancer was diagnosed. The clinicopathological characteristics and follow-up information of them was collected and analyzed retrospectively.@*Results@#Of the 993 patients, primary tumor located in the upper-outer quadrant (UOQ) in 556 patients (56.0%), the lower-outer quadrant (LOQ) in 97 (9.8%), the central portion in 99 (10.0%), the upper-inner quadrant (UIQ) in 186 (18.7%), and the lower-inner quadrant (LIQ) in 55 (5.5%). Patients in the central portion tended to have larger tumors, and more patients in the upper-inner quadrant received endocrine therapy. The estimated 5-year disease-free survival (DFS) rates of patients with primary lesion in the UOQ, LOQ, central portion, UIQ and LIQ were 90.3%, 88.7%, 79.8%, 86.0% and 72.7%, respectively, with significant differences (P<0.001). The 5-year overall survival (OS) rates were 97.5%, 96.9%, 90.9%, 94.1% and 87.3%, respectively, with significant differences (P<0.001). Multivariate analysis showed that 5-year recurrence and metastasis risks were significantly increased in patients with primary lesion in the central portion, UIQ and LIQ compared to other groups (P<0.001), and 5-year mortality risks were increased in these three groups (P=0.002).@*Conclusion@#Primary lesion located in central portion and inner quadrant is an independent adverse prognostic factor for patients with breast invasive ductal carcinoma patients receiving radical mastectomy.
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Objective: To analyze the feasibility of axillary lymph node staging through sentinel lymph node biopsy (SLNB) after neoad-juvant chemotherapy (NAC) in patients with node-positive breast cancer and to explore the follow-up treatment of these patients. Methods: Clinical data of 82 patients with node-positive breast cancer before NAC in Tianjin Medical University Cancer Institute and Hospital from January 2016 to January 2018 were analyzed retrospectively. All these patients accepted SLNB after NAC. The detection rate, accuracy, false negative rate (FNR), and influencing factors were analyzed. Results: A nodal pathological complete response (PCR) was achieved in 43 of 82 patients. The PCR rate was 52.4%. The detection rate, accuracy, and FNR were 97.56% (80/82), 88.75% (71/80), and 23.08% (9/39), respectively. The accuracy of 1, 2, and≥3 SLNs detected were 90.9% (20/22), 66.7% (10/15), and 95.3% (41/43), respectively. The FNRs were 20.0% (2/10), 71.4% (5/7), and 9.1% (2/22), respectively (both P<0.05). Conclusions: Due to its overall high FNR, without clinically acceptable limits, post-NAC SLNB cannot completely replace axillary lymph node dissection (ALND) in node-positive patients. However, with no less than 3 SLNs detected, SLNB can accurately evaluate the status of axillary lymph nodes.
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Objective To investigate the effects of a new c-Met inhibitor SU11274 on apoptosis and motility of c-Met-positive basal-like breast cancer cells MDA-MB-231. Methods The concentrations of SUl1274 were set to 0,0.1,1,10 and 20 μmol/L.Morphological change of apoptotic cells was analyzed by Hoechst33342,MitroTrackerRed and Yo-pro-1 staining.The apoptotic rate of MDA-MB-231 cells were determined by Annexin V/PI double-staining. The expression of apoptosis related proteins (Bcl-XL,Caspase-3 and PARP) and phosphorylation levels of c-Met and Akt were analyzed by Western blot.The capability of motility were measured by wound-healing assay and chemotaxis assay. Results After treatment by SU11274( 10 μmol/L) for 48 h,shrinking apoptotic cells of MDA-MB-231 was observed by flurescent microscope and nuclear fragmentation was seen.Annexin V/PI double-staining showed SU11274induced apoptosis of MDA-MB-231 cells (P ＜ 0.05 ),and the apoptotic rates were (7.3 ± 0.9) ％,( 14.1 ±0.6) ％,(35.5 ± 4.4) ％ and (48.2 ± 5.3 ) ％,respectively.SU11274 downregulated the expression of Bcl-XL and promoted the dissection of Caspase-3 and PARP in a dose dependent relationship.SU11274 prolongs the wound-healing time,decreases the migration cell count (P ＜ 0.05 ) and effectively inhibits the phosphorylation of c-Met and its downstream key proteins Akt in a dose-dependent manner.Conclusions C-Met inhibitor SU11274 induces apoptosis and inhibits the motility of c-Met-positive basallike breast cancer cell line MDA-MB-231,probably through inhibiting phosphorylation of c-Met/PI3K/Akt.
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Autophagy is an evolutionarily conserved lysosomal pathway for the degradation of cytoplasmic proteins,macromolecules,and organelles.Now,autophagic cell death is considered as programmed cell death type Ⅱ.In multiple studies,inhibition of autophagy will result in contrasting outcomes-survival or death.Thus,whether autophagy in cancer cells causes death or protects cells is controversial.Taken together,the manipulation of autophagy may lead to development of new cancer therapies.This article focuses on recent progresses of autophagy research related to human cancers therapy.
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Small molecule inhibitors of Bcl-2 are a novel class of anticancer drugs that target anti-apoptotic proteins. In recent years,small molecule inhibitors such as ABT-737 ,ABT-263, gossypol, apogossypol,TW-37,obatoclax, HAl4-1 have attracted much reseach attention. Preclinical trials have shown that the inhibitors have cancer killing effect on some tumors when used alone and exhibit striking synergistic effect when combined with radiotherapy and/or chemotherapy.
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Apigenin is a plant flavonoid which has various biological activities and pharmacological effects including anti-tumor, antioxidant, anti-inflammatory, sedative and so on, particularly in the anti-tumor areas. It can inhibit proliferation, invasion, metastasis and angiogenesis of tumor cells. In addition, it can also induce apoptosis and enhance chemotherapy sensitivity.