Antimicrobial antioxidant and cytotoxic properties associated with Chenopodium glaucum L

th different treatment patterns in axSpA.
PARPBP (PARP1 binding protein) is an important suppressor of homologous recombination during DNA repair, but the expression and function of PARPBP in breast cancer remain unclear.
PARPBP expression was analyzed in breast cancer patient samples and public datasets for its correlation with clinical outcome. The function of PARPBP in breast cancer cell proliferation and anthracycline treatment response were studied both
and
.
PARPBP was upregulated significantly at both mRNA and protein levels in breast cancer tissues compared with normal breast tissues. PARPBP high expression group had poorer overall survival (OS) than the PARPBP low expression group. Knockdown of PARPBP suppressed breast cancer cell proliferation and colony formation while overexpression of PARPBP did the opposite. We found that transcription factor forkhead box M1 (FOXM1) could activate PARPBP expression by directly binding to the promoter of PARPBP. In addition, high expression of PARPBP related with anthracycline resistance in breast cancer. Depletion of PARPBP increased breast cancer cell apoptosis and DNA damage caused by epirubicin. Moreover, tumor xenograft experiments further demonstrated that PARPBP was involved in breast cancer anthracycline resistance.
Taken together, our results highlight that PARPBP is a prognostic marker and confers anthracycline resistance on breast cancer.
Taken together, our results highlight that PARPBP is a prognostic marker and confers anthracycline resistance on breast cancer.
Endocrine sensitivity, as determined by response of the proliferation marker Ki-67 to short-term preoperative endocrine therapy (ET), is currently not included in adjuvant treatment decisions in hormone receptor (HR)+/human epidermal growth factor receptor 2 (HER2)- breast cancer (BC).
The prospective WSG-ADAPT HR+/HER2- trial included patients with N0/N1 early BC who were candidates for adjuvant chemotherapy based on clinical-pathological criteria alone. The trial utilized a genomic assessment [the Recurrence Score (RS)] plus endocrine sensitivity testing to guide treatment. All patients received 3 (±1) weeks of preoperative induction ET. According to protocol, patients with RS 0-11 or RS 12-25 plus endocrine proliferation response (EPR, post-induction Ki-67 ⩽ 10%) were to be spared adjuvant chemotherapy.
The ADAPT HR+/HER2- trial run-in phase included 407 patients with baseline RS, of whom 386 (median age 54 years) had complete data for Ki-67 at both baseline and post-induction. RS distribution 23.1% cisions in early BC is feasible using the EPR criterion post-induction Ki-67 ⩽ 10%.
NCT01779206.
NCT01779206.
Carboxyamidotriazole (CAI), a calcium channel blocker, inhibits tumor cell proliferation, metastasis, and angiogenesis. This trial aimed to determine whether CAI combined with conventional chemotherapy could prolong progression-free survival (PFS) in non-small cell lung cancer (NSCLC) patients.
Patients were assigned into groups (31 ratio) to receive either chemotherapy + CAI or chemotherapy alone. Cisplatin (25 mg/m
) was administered by intravenous infusion on days 1, 2, and 3, and vinorelbine (25 mg/m
) on days 1 and 8 of each 3-week cycle for four cycles. CAI was administered at 100 mg daily with concomitant chemotherapy; this treatment was continued after chemotherapy was ceased until serious toxicity or disease progression had occurred. PFS was the primary endpoint, and the secondary endpoints were objective response rate (ORR), disease control rate, overall survival (OS), and quality of life.
In total, 495 patients were enrolled in the trial 378 in the chemotherapy + CAI group and 117 in the chemotherapy + placebo group. PFS was significantly greater in the chemotherapy + CAI [median, 134 days; 95% confidence interval (CI) 127-139] than in the chemotherapy + placebo (median, 98 days; 95% CI 88-125) group, with a hazard ratio of 0.690 (95% CI 0.539-0.883;
 = 0.003). There was no difference in the OS rates of both groups. The ORR was greater in the chemotherapy + CAI group than in the chemotherapy + placebo group (34.6%
25.0%,
 = 0.042). Adverse events of ⩾grade 3 occurred more frequently in the CAI group [256 (68.1%)
64 (55.2%);
 = 0.014].
CAI + platinum-based chemotherapy prolonged PFS and could be a useful therapeutic option to treat NSCLC.
chinadrugtrials.org.cn identifier CTR20160395.
chinadrugtrials.org.cn identifier CTR20160395.
Frozen shoulder is a painful glenohumeral joint condition. Pain-related beliefs are recognized drivers of function in musculoskeletal conditions. This cross-sectional study investigates associations between pain-related beliefs and arm function in frozen shoulder.
Pain intensity, arm function (Disabilities of the Arm, Shoulder and Hand Questionnaire (DASH)), pain catastrophizing (Pain Catastrophizing Scale (PCS)), pain-related fear (Tampa Scale for Kinesiophobia (TSK-11)) and pain self-efficacy (Pain Self-Efficacy Questionnaire (PSEQ)) were administered in 85 persons with frozen shoulder. Correlation analyses assessed associations between pain-related beliefs and arm function. Artenimol Regression analysis calculated the explained variance in arm function by pain-related beliefs.
Pain-related fear, pain catastrophizing and pain self-efficacy were significantly associated with arm function (r = 0.51; r = 0.45 and r = -0.69, all p < .0001, respectively). Thirty-one percent of variance in arm function was explained by control variables, with pain intensity being the only significant one. After adding TSK-11, PCS and PSEQ scores to the model, 26% extra variance in arm function was explained, with significant contributions of pain intensity, pain-related fear and pain self-efficacy (R
= 0.57).
Attention should be paid towards the negative effect of pain-related fear on outcomes in frozen shoulder and towards building one's pain self-efficacy given its protective value in pain management.
Attention should be paid towards the negative effect of pain-related fear on outcomes in frozen shoulder and towards building one's pain self-efficacy given its protective value in pain management.