Growth Of Normal Breast Cells Research Articles

Self-efficacy in patients with breast cancer: A health belief model approach

Background: Breast cancer is a disturbance in the growth of normal breast cells characterized by abnormal cells arising from normal cells that can infiltrate lymphatic tissue and blood vessels. This will have a major impact on patients and their families, both physically, psychologically, economically and in other aspects of life which certainly affect the patient's self-efficacy about their own ability to carry out healthy behaviors that have an impact on their treatment. One of the support efforts that can be given is the intensification of activities through the Health Belief Model.Purpose: To determine the effect of Self-efficacy in patients with breast cancer: A health belief model approachMethod: The design used in this study was a quasi-experimental design with one group pretest-posttest. Determination of the sample by purposive sampling method as many as 60 participants. Data was collected using a self-efficacy questionnaire.Results: The Marginal homogeneity test obtained a p-value = 0.001, which means that there is an effect of giving interventions with the Health Belief Model on self-efficacy in breast cancer patients.Conclusion: Intervention with the Health Belief Model approach can increase the self-efficacy of breast cancer patients who are undergoing treatment.

COPING MECHANISM OF BREAST CANCER PATIENTS UNDERGOING CHEMOTHERAPY DURING THE COVID-19 PANDEMIC

Cancer is one of the most common non-communicable and chronic diseases in the world, one of them is breast cancer. Breast cancer is a disorder in the growth of normal breast cells which is characterized by abnormal cells arising from normal cells that can infiltrate lymph tissue and blood vessels. This will have a major impact on patients undergoing chemotherapy and their families, especially during the COVID-19 pandemic. Not only physically but also psychologically, economically and in other aspects of life, which certainly affect the coping mechanisms of patients and families. One of the support efforts that can be provided by nurses as educators is the intensification of health education activities through community service activities in the form of counseling and coaching to improve the coping mechanisms of breast cancer patients.

Fibronectin assembly regulates lumen formation in breast acini.

Fibronectin (FN) is an extracellular matrix (ECM) glycoprotein that self‐assembles into FN fibrils, forming a FN matrix contributing to the stiffness of the ECM. Stromal FN stiffness in cancer has been shown to impact epithelial functions such as migration, cancer metastasis, and epithelial‐to‐mesenchymal transition. The role of the FN matrix of epithelial cells in driving such processes remains less well understood and is the focus of this study. Hypoxia, defined by low oxygen tension (<5%) is one of the hallmarks of tumor microenvironments impacting fibril reorganization in stromal and epithelial cells. Here, using the MCF10 breast epithelial progression series of cell lines encompassing normal, preinvasive, and invasive states, we show that FN fibril formation decreases during hypoxia, coinciding with a decrease in migratory potential of these cells. Conversely, we find that FN fibril disruption during three‐dimensional acinar growth of normal breast cells resulted in acinar luminal filling. Our data also demonstrates that the luminal filling upon fibril disruption in untransformed MCF10A cells results in a loss of apicobasal polarity, characteristic of pre‐invasive and invasive breast cell lines MCF10AT and MCF10 DCIS.com. Overall this is the first study that relates fibril‐mediated changes in epithelial cells as critical players in lumen clearing of breast acini and maintenance of the untransformed growth characteristic.

AP-1 blockade inhibits the growth of normal and malignant breast cells.

We have previously demonstrated that basal AP-1 transcriptional activity is high in normal human mammary epithelial cells, intermediate in immortal breast cells, and relatively low in breast cancer cells. In this study we investigated whether differences in AP-1 transcriptional activity reflect differences in breast cells' dependence on AP-1 for proliferation. The cJun dominant negative, TAM-67, was used to determine the effect of AP-1 blockade on the growth of normal, immortal and malignant breast cells. We first showed that TAM-67 inhibits AP-1 activity in normal and malignant breast cells. We then determined whether this AP-1 inhibitor affected colony forming efficiency of the immortalized and malignant breast cells. The AP-1 inhibitor reduced colony formation of immortal breast cells by over 50% (by 58% in 184B5 cells and 62% in MCF10A cells), and reduced colony formation in the breast cancer cell line MCF7 by 43%, but did not reduce colony formation in the other breast cancer cell lines (T47D, MDA MB231 and MDA MB 435). We also determined the effect of AP-1 blockade on the growth of normal breast cells using a single cell proliferation assay. Using this assay, the growth of normal breast cells was extremely sensitive to AP-1 blockade, while immortal breast cells were moderately sensitive. We next directly tested the effect of TAM-67 expression on the growth of MCF7 breast cancer cells, using cells stably transfected with TAM-67 under the control of a doxycycline-inducible promoter. Upon induction, TAM-67 was expressed and AP-1 activity was inhibited in these cells. We then measured the growth of these cells in the presence or absence of TAM-67. The results of these studies show that the growth of MCF7 cells was suppressed by the AP-1 inhibitor, TAM-67. These results demonstrate that normal and immortalized breast cells, and some breast cancer cells (such as MCF7), require AP-1 to transduce proliferative signals, while other breast cancer cells (such as T47D, MDA MB 231 and MDA MB 435) do not. These studies suggest that the AP-1 transcription factor is a potential target for future agents for the prevention or treatment of breast cancer.

Proliferative responses of epithelial cells to 8‐bromo‐cyclic AMP and to a phorbol ester change during breast Pathogenesis

We have explored the relationship of changes in proliferative responses of human mammary epithelial cells to a phorbol ester (TPA) and to 8-Br-cAMP, which modulate the activities of protein kinases A and C (PKA and PKC), with breast tumour progression. Treatment with TPA had no effect on nontumorigenic cell lines established from human fibrocystic biopsies and apparently normal tissue around a tumour. In contrast, TPA strongly inhibited the proliferation of numerous human tumorigenic breast cell lines. Treatment with 8-Br-cAMP decreased the proliferation of all studied nontumorigenic and tumorigenic cell lines. We have also studied the effect of TPA and 8-Br-cAMP on growth of epithelial cells in short-term culture obtained from surgical human mammary biopsies with different states of breast disease. Both drugs enhanced growth of normal breast cells but had no significant effects on cells from biopsies with benign breast disease. In contrast, all examined cultures from breast cancer biopsies were strongly inhibited by 8-Br-cAMP. Otherwise, TPA had an inhibitory effect only in the case of invasive ductal carcinoma of grade III. Malignant Ha-ras-transformation of nontumorigenic TPA-insensitive breast HBL-100 cells induced an inhibitory effect of TPA. In addition, a TPA-insensitive MCF7 clone was much less tumorigenic in athymic mice than the parental strain shown to be inhibited by TPA. These data suggest that the two intracellular transduction pathways change at different stages of breast pathogenesis. Alterations in the PKA pathway are early events and are probably important to cell immortalization but do not necessarily lead to malignant development. In contrast, changes in PKC pathway are rather later events associated with advanced malignant transformation.