Our purpose was to understand the effects of normoxia or hypoxia on 5-fluorouracil  (5-FU) treatment in triple negative breast cancer (TNBC) cells, and characterize the molecular changes in hypoxia inducible factors (HIFs) and cyclooxygenase-2 (COX-2) following treatment.  Cell viability and protein levels of HIFs and COX-2 were determined after wild type and HIF silenced MDA-MB-231 cells, and wild type SUM-149 cells, were treated with 5-FU under normoxia or hypoxia.  5-FU reduced cell viability to the same levels irrespective of normoxia or hypoxia.  HIF silenced MDA-MB-231 cells showed comparable changes in cell viability, supporting observations that hypoxia and the HIF pathways did not significantly influence cell viability reduction by 5-FU.  Our data suggest that HIF-2aaccumulation may predispose cancer cells to cell death under hypoxia.  SUM-149 cells that have higher COX-2 and HIF-2afollowing 24 h of hypoxia, were more sensitive to 96 h of hypoxia compared to MDA-MB-231 cells, and were more sensitive to 5-FU than MDA-MB-231 cells.  COX-2 levels changed with hypoxia and with 5-FU treatment but patterns were different between the two cell lines.  At 96 h, COX-2 increased in both untreated and 5-FU treated cells under hypoxia in MDA-MB-231 cells.  In SUM-149 cells, only treatment with 5-FU increased COX-2 at 96 h of hypoxia.  Cells that survive hypoxia and 5-FU treatment may exhibit a more aggressive phenotype.  Our results support understanding interactions between HIF and COX-2 with chemotherapeutic agents under normoxia and hypoxia, and investigating the use of COX-2 inhibitors in these settings.

Aims: there has been an increasing awareness of the potential for oncology care to result in long-term financial burdens and financial toxicity. Patients who report cancer-related financial problems or high costs are more likely to forgo or delay prescription medications and medical care.
Materials and Methods: we examined financial distress using data from a survey of 164 breast cancer survivors who had completed primary therapy for the disease.
Key Findings: among respondents, 8.6% (13 of 151) reported that “being less able to provide for the financial needs of their family” was as a severe problem; 14.4% (22 of 153) reported “difficulty in meeting medical expenses” was a severe problem; and 8.4% (13 of 154) reported that “no money for cost of or co-payment for medical visits” was a severe problem. About 8.4% (13 of 154) of the respondents reported that “no money for cost of or co-payment for medicine” was a severe problem. In logistic regression analysis, younger age and lower household income were significant predictors of financial distress. In multiple linear regression analysis, younger age and lower household income were significant predictors of financial distress.
Significance: financial toxicity remains a major issue in breast cancer care. Efforts are needed to ensure patients experiencing high levels of financial toxicity are able to access recommended care. In addition, patients should talk with their providers about the costs of oncology care and about opportunities to reduce costs while maintaining high quality of care.

Pinus massoniana bark extract (PMBE) is a traditional Chinese medicine used for the treatment of various health disorders. Previous studies have demonstrated that PMBE may induce the apoptosis of hepatoma and colon cancer cells, and one of the potential mechanisms is by activating p53 to up-regulate the expression of p21. The P53/P21 signaling pathway is also one of the main mechanisms to regulate cell senescence. Therefore, we wonder if PMBE is able to induce hepatoma cells into senescence by inhibiting their growth. In the current study, the effects of PMBE on the viability of human hepatoma HepG2 cells were detected using an MTT assay. The phenotypes of HepG2 cells with PMBE treatment were detected with β-Galactosidase staining assay. The results revealed that the growth of HepG2 cells was inhibited by PMBE at dose-dependent manner when PMBE concentration is above 50 µg/ml, furthermore, PMBE could induce HepG2 cells into senescence at concentration of 40 µg/ml. These findings indicated that PMBE significantly inhibited the growth of HepG2 cells and induced them into senescence, while the potential mechanism and its safety in normal cells require further investigation.

Proanthocyanidins (PAs) is the main constituent of Pinus massoniana bark extract (PMBE). PMBE was reported to induce cell cycle arrest and apoptosis in HeLa cells. During cell division, cells synthesize protein in G1 and G2 phases and replicate chromatin in S phase during interphase, which increases cell mass. Nesprins, a kind of protein encoded by syne gene, is a vital part of cytoskeleton and plays a role in cell cycle progress and cell division. HeLa cells were used as a model to examine effects of PMBE on cell growth and Nesprins expression with MTT assay and RT- PCR analysis, respectively. The cell size was evaluated by counting the cell number in a fixed area under microscope. The results showed that the size of survival HeLa cells in PMBE-treated group was obviously larger than that of those in control group (p = 0.00223, < 0.01), while the mRNA expression level of Nesprin-2 decreased significantly in PMBE-treated group (p = 0.0201, < 0.05). On this account, we put forward a hypothesis that PMBE inhibits the expression of syne-2, which leads to the decrease of Nesprin-2 and further results in the size increase of HeLa cells.

We present here a rare case of primary mammary angiosarcoma in 48-year-old female patient. After 3 years without treatment, the woman presented to the hospital with locally advanced tumor in right mammary gland, involving the overlying skin and bleeding. Radical mastectomy was performed with axillary lymph-node dissection. The CT scan revealed solitary liver metastasis. After an overview of different cases of primary angiosarcoma of the breast published in the literature, we discuss the importance of histological criteria and immunohistochemical methods, as well as the optimal multimodal treatment in these patients. Poorly differentiated primary mammary angiosarcoma (grade 3) is an invasive neoplasm with high risk of local recurrence and distant metastases. The multimodal treatment involves radical mastectomy with or without axillary lymph-node dissection. Adjuvant radiotherapy and adjuvant chemotherapy help the local tumor control, reduce recurrences and increase overall survival.