Hypertension is one of the main adverse effects of antiangiogenic tumor drugs and thus limits their application. The mechanism of hypertension caused by tyrosine kinase inhibitors (TKIs) targeting vascular endothelial growth factors is mainly related to inhibition of the nitric oxide (NO) pathway and activation of the endothelin pathway, as well as vascular rarefaction and increased salt sensitivity; consequently, prevention and treatment differ for this type of hypertension compared with primary hypertension. Apatinib is a highly selective TKI approved in China for the treatment of advanced or metastatic gastric cancer. The RhoA/ROCK pathway is involved in the pathogenesis of hypertension and mediates smooth muscle contraction, eNOS inhibition, endothelial dysfunction and vascular remodeling. In this study, in vivo experiments were performed to explore whether the RhoA/ROCK signaling pathway is part of a possible mechanism of apatinib in the treatment of gastric cancer-induced hypertension and the impairment of vascular remodeling and left ventricular function. Y27632, a selective small inhibitor of both ROCK1 and ROCK2, was combined with apatinib, and its efficacy was evaluated, wherein it can reduce hypertension induced by apatinib treatment in gastric cancer mice and weaken the activation of the RhoA/ROCK pathway by apatinib and a high-salt diet (HSD). Furthermore, Y-27632 improved aortic remodeling, fibrosis, endothelial dysfunction, superior mesenteric artery endothelial injury, left ventricular dysfunction and cardiac fibrosis in mice by weakening the activation of the RhoA/ROCK pathway. The expression of RhoA/ROCK pathway-related proteins and relative mRNA levels in mice after apatinib intervention were analyzed by various methods, and blood pressure and cardiac function indexes were compared. Endothelial and cardiac function and collagen levels in the aorta were also measured to assess vascular and cardiac fibrosis and to provide a basis for the prevention and treatment of this type of hypertension.

The aim to discuss the close relationship between the common biological mechanisms of breast cancer and hypertension, inflammation and oxidative stress, breast cancer gene mutations breast cancer susceptibility gene (BRCA), G protein-coupled receptor kinase (GRK4), etc. and breast cancer treatment includes chemotherapy, Endocrine therapy, Targeted therapy and anti-angiogenesis drugs. In antiangiogenesis drugs focusing on the mechanism of tyrosine kinase inhibitors (TKI) that may activate the rhoa/ rock pathway to cause hypertension, as well as the relationship between breast cancer and antihypertensive drugs includes angiotensin-converting enzyme inhibitors (ACEIs), Calcium channel blockers (CCBs) and β-blockers (BBs)will be explored.Background: Cardiovascular diseases (CVD) and tumors are the two major types of diseases with the highest mortality rates, while hypertension accounts for the largest proportion of CVDs. A large number of the same or similar risk factors are shared between hypertension and tumors, and they influence each other.Many patients, particularly elderly patients, often present with the coexistence of the two diseases. As medical advances have enabled clinicians to cure tumors, many patients with cancer live longer, leading to a gradual increase in the incidence of CVDs, including hypertension. With the second highest incidence among tumors, breast cancer has gradually attracted widespread attention and has been the topic of numerous studies. Studies have confirmed that CVD is one of the causes of death in elderly patients with breast cancer.Methods: Publications from 1985 to 2020 were retrieved from the Web Of Science, Cochrane Library, PubMed, EMBASE and MEDLINE database. We used a mix of MeSH and keywords.Conclusions: Hypertension and cancer may share a common mechanism. The screening and risk assessment of breast cancer in patients with hypertension must be strengthened. Breast cancer cardiology is the interdisciplinary study of oncology and cardiology, and in-depth research in this field may result in long-term improvements in the survival and prognosis of patients with both clinical hypertension and breast cancer.

This study aimed to assess the relationship between dietary sodium/potassium intake and cognition in elderly individuals with hypertension. We designed a cross-sectional study based on the 2011-2014 National Health and Nutrition Examination Survey (NHANES) 2011-2014. A multivariable-logistic regression analysis was performed to analyze the relationship between sodium/potassium intake and cognitive impairment.Restricted cubic spline (RCS) based on regression analysis to assess the nonlinear doseresponse relationship between dietary sodium intake and cognitive performance. Out of the 2276 participants included in this study, 1670 patients had hypertension. Compared with the lowest quartile of dietary sodium intake, the lowest weighted odds ratio of cognitive impairment in DSST was observed in Q4 (OR = 0.45, 0.29-0.70), and a similar trend was observed in AFT (OR = 0.34, 0.18-0.65). After adjusting the covariates, the lowest weighted multivariable-adjusted OR of cognitive impairment in DSST were also observed in Q4 (OR = 0.47, 0.26-0.84) compared with the lowest quartile of dietary sodium intake. The RCS results showed that dietary sodium intake was U-shaped and associated with the risk of cognitive impairment in the DSST (P non-linearity = 0.0067). In addition, no significant association was observed between dietary potassium intake and different dimensions of cognitive performance. In conclusion, excessively high and low low dietary sodium were associated with impairment of specific processing speed, sustained attention, and working memory for elderly patients with hypertension in the United States. However, no association was observed between dietary potassium intake and cognition.

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Background: Breast Cancers (BCs) in Caucasian (CA) and African American (AA) women have different characteristics. Recently, there have been reports, mostly focusing on Caucasians that Benign Breast Diseases (BBDs) may be risk factors for BCs. There are also a few reports of different co-occurring patterns of BBDs with BCs between the two populations. In the Clinical Breast Care Project (CBCP) more than 4,000 subjects have been enrolled following HIPAA-compliant, IRB-approved protocols, with more than 35,000 biospecimens collected. For patients requiring biopsies, an expanded pathology report for research is completed. The occurrences of any of the 131 pathologic conditions, including 66 BBDs, are recorded. All the results are reviewed by the same pathologist. The CBCP provides a uniformed pathology dataset for a comprehensive characterization of the association of BBDs with BCs.Method: The diagnoses were made from potentially multiple biopsies obtained over a short period of time, mostly within 60 days. CBCP subjects with BBD diagnosis and ethnicity information from their most recent visit were selected, giving a dataset totaling 1479 CA and 484 AA women. We studied the association between BBDs and BCs (including in situ, invasive, and malignant NOS) in these two groups using the chi-square test.Results: In both populations 6 BBDs are positively associated with BCs, including atypical ductal hyperplasia (ADH) (4% vs 15% for AA p<3.8E-05, meaning 4% cancer-free cases with ADH compared to 15% cancer cases co-occurring with it; 7% vs 16% for CA p<1.9E-08), microcalcifications (27% vs 56% for AA p<1.2E-09, 35% vs 53% for CA p<8.0E-12), multiple (peripheral) papillomas (6% vs 16% for AA p<0.0005, 4% vs 8% for CA p<0.0002), columnar cell hyperplasia (9% vs 21% for AA p<0.0003, 6% vs 18% for CA p<3.5E-12), and moderate intraductal hyperplasia (IDH) (14% vs 28% for AA p<0.0002, 14% vs 18% for CA p<0.03). On the contrary, 3 BBDs are negatively associated with BCs including fibroadenoma (30% vs 10% for AA p<4.9E-07; 21% vs 7% for CA p<1.0E-13), and mild IDH (10% vs 2% for AA p<0.003; 13% vs 7% for CA p<0.0002). Eight BBDs differentially co-occur with BCs between AA and CA. BCs in AA are associated with sclerosing adenosis (13% vs 31%, p<4.5E-06), fibrocystic changes (45% vs 61%, p<0.001), fibroadenomatoid nodule (6% vs 12%, p<0.042), and cysts (42% vs 57%, p<0.004). BCs in CA are positively associated with columnar cell hyperplasia with atypia (3% vs 8% p<3.6E-05), atypical lobular hyperplasia (1% vs 5%, p<6.0E-05), and radiation changes (0% vs 1.4% p<0.004), but negatively associated with duct ectasia (10% vs 2%, p<7.9E-10).Discussion Our findings are in accordance with established BC risk factors such as ADH and moderate IDH for both ethnic groups. We further found that 8 BBDs differentially co-occur with BCs between AA and CA groups, and interestingly the 4 significant BBDs detected in the AA group typically show >10% increased co-occurrence rate in cancer cases compared to cancer-free cases, whereas the 4 BBDs detected in the CA group almost always show a <10% co-occurrence rate overall. More research is undergoing to understand the implications of this distinct co-occurrence pattern. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 3066.