다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

CA : A Cancer Journal for Clinicians

Biomechanical stress is a major stimulus for cardiac hypertrophy and the transition to heart failure. By generating mice that harbor a ventricular restricted knockout of the gp130 cytokine receptor via Cre-IoxP-mediated recombination, we demonstrate a critical role for a gp130-dependent myocyte survival pathway in the transition to heart failure. Such conditional mutant mice have normal cardiac structure and function, but during aortic pressure overload, these mice display rapid onset of dilated cardiomyopathy and massive induction of myocyte apoptosis versus the control mice that exhibit compensatory hypertrophy. Thus, cardiac myocyte apoptosis is a critical point in the transition between compensatory cardiac hypertrophy and heart failure. gp130-dependent cytokines may represent a novel therapeutic strategy for preventing in vivo heart failure.

IS103 Loss of a gp130 Cardiac Muscle Cell Survival Pathway Is a Critical Event in the Onset of Heart Failure During Biomechanical Stress

Background National Central Cancer Registry of China (NCCRC) updated nationwide cancer statistics using population-based cancer registry data in 2014 collected from all available cancer registries. Methods In 2017, 449 cancer registries submitted cancer registry data in 2014, among which 339 registries' data met the criteria of quality control and were included in analysis. These cancer registries covered 288,243,347 population, accounting for about 21.07% of the national population in 2014. Numbers of nationwide new cancer cases and deaths were estimated using calculated incidence and mortality rates and corresponding national population stratified by area, sex, age group and cancer type. The world Segi's population was applied for age-standardized rates. Results A total of 3,804,000 new cancer cases were diagnosed, the crude incidence rate was 278.07/100,000 (301.67/100,000 in males, 253.29/100,000 in females) and the age-standardized incidence rate by world standard population (ASIRW) was 186.53/100,000. Calculated age-standardized incidence rate was higher in urban areas than in rural areas (191.6/100,000 vs. 179.2/100,000). South China had the highest cancer incidence rate while Southwest China had the lowest incidence rate. Cancer incidence rate was higher in female for population between 20 to 54 years but was higher in male for population younger than 20 years or over 54 years. A total of 2,296,000 cancer deaths were reported, the crude mortality rate was 167.89/100,000 (207.24/100,000 in males, 126.54/100,000 in females) and the age-standardized mortality rate by world standard population (ASMRW) was 106.09/100,000. Calculated age-standardized mortality rate was higher in rural areas than in urban areas (110.3/100,000 vs. 102.5/100,000). East China had the highest cancer mortality rate while North China had the lowest mortality rate. The mortality rate in male was higher than that in female. Common cancer types and major causes of cancer death differed between age group and sex. Conclusions Heavy cancer burden and its disparities between area, sex and age group pose a major challenge to public health in China. Nationwide cancer registry plays a crucial role in cancer prevention and control.

/pdf/cancer-incidence-and-mortality-in-china-2014-4e2woagh1c.pdf

Cancer incidence and mortality in China, 2014.

// Qi Wu 1, * , Juanjuan Li 1, * , Shan Zhu 1 , Juan Wu 2 , Chuang Chen 1 , Qian Liu 1 , Wen Wei 1 , Yimin Zhang 1 , Shengrong Sun 1 1 Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, P. R. China 2 Department of Pathology, Renmin Hospital of Wuhan University, Wuhan, Hubei, P. R. China * These authors contributed equally to this work Correspondence to: Shengrong Sun, email: sun137@sina.com Yimin Zhang, email: dryiminzhang@163.com Keywords: breast cancer subtypes, distant metastases, SEER Received: November 01, 2016      Accepted: February 20, 2017      Published: March 02, 2017 ABSTRACT Background and Aims: This study aimed to access possible relationships between breast cancer subtypes and sites of distant metastasis in breast cancer. Results: A total of 243,896 patients, including 226,451 cases in control groups were identified. Bone metastasis was found in 8848 cases, compared with 1,000 brain metastasis cases, 3434 liver metastasis cases and 4167 lung metastasis cases. Patients with all subtypes were most prone to bone metastases, the incidence of bone metastasis in HR+/HER2+ subtype was up to 5.1 %. Further, HR−/HER2+ subtype patients had a higher probability of brain (OR = 1.978) metastasis compared to HR+/HER2− subtype patients. In addition, liver metastasis was more frequently observed in the HER2 positive subtypes compared with HER2 negative subtypes. Patients with TN primarily presented lung metastasis, but it made no difference in the probability of lung metastases of all subtypes. Materials and Methods: Using the 2010–2013 Surveillance, Epidemiology, and End Results Program(SEER) data, a retrospective, population-based cohort study to investigate tumor subtypes-specific differences in the sites of distant metastasis. Metastatic patterns information was provided for bone, brain, liver and lung. The breast cancer was classified into four subtypes: hormone receptor (HR) +/ human epidermal growth factor receptor 2 (HER2) −, HR+/HER2+, HR−/HER2+ and triple negative (TN). Conclusions: The pathological subtypes of breast cancer are clearly different in metastatic behavior with regard to the sites of distant metastasis, emphasizing that this knowledge may help to determine the appropriate strategy for follow-up and guide personalized medicine.

/pdf/breast-cancer-subtypes-predict-the-preferential-site-of-xvcb34vnd6.pdf

Breast cancer subtypes predict the preferential site of distant metastases: a SEER based study

Characteristics of breast cancer in Central China, literature review and comparison with USA

// Juanjuan Li 1, * , Yue Xia 2, * , Qi Wu 1 , Shan Zhu 1 , Chuang Chen 1 , Wen Yang 1 , Wen Wei 1 and Shengrong Sun 1 1 Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, P. R. China 2 Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, P. R. China * These authors have contributed equally to this work Correspondence to: Shengrong Sun, email: sun137@sina.com Keywords: outcomes, inflammatory breast cancer, molecular subtypes, SEER program Received: January 20, 2017      Accepted: March 24, 2017      Published: April 19, 2017 ABSTRACT Background: The aim of this study was to evaluate the outcomes of patients with inflammatory breast cancer (IBC), with emphasis on the role of molecular subtypes and radiotherapy. Methods: A retrospective cohort study to investigate overall survival (OS) and breast cancer-specific mortality (BCSM) in patients with IBC was conducted using data obtained by the Surveillance, Epidemiology, and End Results (SEER) program from 2010–2013. Cox multivariate regression was used to calculate the adjusted Hazard Ratios (aHR). Results: 403 patients were eligible for this study. Patients in the group with hormone receptors (HR)+/HER2- subtype had an OS of 79.6% compared with 89.0 % in the group with (HR)+/HER2+ subtype and 76.8% in the HR-/HER2+ group and 62.9% in the triple-negative (TN) group. BCSM was 16.3% for the HR+/HER2- group, 9.8% for the HR+/HER2+ group, 21.7% for the HR-/HER2+ group, and 30.5% for the TN group. For distant metastases, the results showed that there was a high probability of bone metastasis in HR-positive groups, brain and liver metastasis in HER2-positive groups, and lung metastasis in the TN group. Multivariate analysis demonstrated that estrogen receptor and HER2 positivity were associated with better survival and that the TN subtype had a poorer OS and BCSM compared with other subtypes (P<0.05). Furthermore, patients who received radiotherapy were more likely to have improved survival (P< 0.05). Conclusion: Inflammatory breast cancer appears to alter the prognosis in association with the receptor status and molecular subtypes. Radiotherapy was still considered to be a crucial treatment for patients with IBC.

/pdf/outcomes-of-patients-with-inflammatory-breast-cancer-by-1ga1e4ips4.pdf

Outcomes of patients with inflammatory breast cancer by hormone receptor- and HER2-defined molecular subtypes: A population-based study from the SEER program

The involvement of unfolded protein response (UPR) activation in tumor survival and resistance to chemotherapies suggests a new anticancer strategy targeting UPR pathway. Arctigenin, a natural product, has been recently identified for its antitumor activity with selective toxicity against cancer cells under glucose starvation with unknown mechanism. Here we found that arctigenin specifically blocks the transcriptional induction of two potential anticancer targets, namely glucose-regulated protein-78 (GRP78) and its analog GRP94, under glucose deprivation, but not by tunicamycin. The activation of other UPR pathways, e.g., XBP-1 and ATF4, by glucose deprivation was also suppressed by arctigenin. A further transgene experiment showed that ectopic expression of GRP78 at least partially rescued arctigenin/glucose starvation-mediated cell growth inhibition, suggesting the causal role of UPR suppression in arctigenin-mediated cytotoxicity under glucose starvation. These observations bring a new insight into the mechanism of action of arctigenin and may lead to the design of new anticancer therapeutics.

https://www.researchgate.net/profile/De_Hua_Yu/publication/45695876_Arctigenin_Suppresses_Unfolded_Protein_Response_and_Sensitizes_Glucose_Deprivation-Mediated_Cytotoxicity_of_Cancer_Cells/links/54218fc10cf2ce3a91b7921d.pdf?disableCoverPage=true

Arctigenin suppresses unfolded protein response and sensitizes glucose deprivation-mediated cytotoxicity of cancer cells.

The ubiquitin-proteasome system and the autophagy-lysosome pathway are the two main routes for eukaryotic intracellular protein clearance. Inhibition of proteasome activity leads to cell death. Due to the dual roles of autophagy in tumor cell survival and death, the effect of suppression of autophagy on breast cancer cells remains to be elucidated. We investigated whether inhibition of the proteasome is capable of inducing autophagy, and we assessed the effect of combined inhibition of the proteasome and autophagy on human breast cancer MCF-7 cells. The proteasome inhibitor bortezomib was used to induce autophagy in MCF-7 cells, and the effect of autophagy on the proliferation of MCF-7 cells was investigated using the autophagy inhibitor 3-MA. Cell viability was measured by MTT assay. The expression of autophagy‑related proteins was determined by Western blot analysis and the GFP-LC3 redistribution was detected using a fluorescence microscope after MCF-7 cells were infected with a GFP-LC3-expressing adenovirus. MCF-7 cell proliferation was inhibited and autophagy was activated in the same dose‑dependent manner. Bortezomib induced a dose‑dependent increase in LC3-II. However, when MCF-7 cells were co-treated with bortezomib and 3-MA, 3-MA blocked the increase in LC3-II protein expression and led to a significant inhibition of cell proliferation. Inhibition of the proteasome may induce autophagy in human breast cancer MCF-7 cells and 3-MA could inhibit autophagy induced by the proteasome inhibitor. A combination of 3-MA and bortezomib increases cell death. These findings indicate that suppression of the two intracellular degradation systems may shed new light on breast cancer control.

https://www.spandidos-publications.com/10.3892/mmr.2011.590/download

Wen Wei

Papers

Breast cancer subtypes predict the preferential site of distant metastases: a SEER based study

Characteristics of breast cancer in Central China, literature review and comparison with USA

Outcomes of patients with inflammatory breast cancer by hormone receptor- and HER2-defined molecular subtypes: A population-based study from the SEER program

Arctigenin suppresses unfolded protein response and sensitizes glucose deprivation-mediated cytotoxicity of cancer cells.

An autophagy inhibitor enhances the inhibition of cell proliferation induced by a proteasome inhibitor in MCF-7 cells.