• Asian Pacific Journal of Cancer Prevention
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• 제16권6호
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• pp.2465-2472
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• 2015

Background: The Quality Audit (BQA) program of the Breast Surgeons of Australia and New Zealand (NZ) collects data on early female breast cancer and its treatment. BQA data covered approximately half all early breast cancers diagnosed in NZ during roll-out of the BQA program in 1998-2010. Coverage increased progressively to about 80% by 2008. This is the biggest NZ breast cancer database outside the NZ Cancer Registry and it includes cancer and clinical management data not collected by the Registry. We used these BQA data to compare socio-demographic and cancer characteristics and survivals by ethnicity. Materials and Methods: BQA data for 1998-2010 diagnoses were linked to NZ death records using the National Health Index (NHI) for linking. Live cases were followed up to December $31^{st}$ 2010. Socio-demographic and invasive cancer characteristics and disease-specific survivals were compared by ethnicity. Results: Five-year survivals were 87% for Maori, 84% for Pacific, 91% for other NZ cases and 90% overall. This compared with the 86% survival reported for all female breast cases covered by the NZ Cancer Registry which also included more advanced stages. Patterns of survival by clinical risk factors accorded with patterns expected from the scientific literature. Compared with Other cases, Maori and Pacific women were younger, came from more deprived areas, and had larger cancers with more ductal and fewer lobular histology types. Their cancers were also less likely to have a triple negative phenotype. More of the Pacific women had vascular invasion. Maori women were more likely to reside in areas more remote from regional cancer centres, whereas Pacific women generally lived closer to these centres than Other NZ cases. Conclusions: NZ BQA data indicate previously unreported differences in breast cancer biology by ethnicity. Maori and Pacific women had reduced breast cancer survival compared with Other NZ women, after adjusting for socio-demographic and cancer characteristics. The potential contributions to survival differences of variations in service access, timeliness and quality of care, need to be examined, along with effects of comorbidity and biological factors.

• Asian Pacific Journal of Cancer Prevention
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• 제15권16호
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• pp.6665-6668
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• 2014

Introduction: Breast cancer in young women is a relatively rare disease; however it tends to be more aggressive and is the leading cause of cancer death in this population. The aim of this study is to investigate the clinical and biological features of breast cancer arising in young Turkish breast cancer patients. Materials and Methods: Patients with breast cancer aged 35 or less (${\leq}35$ years) were selected for the study. In total 211 cases were included. Pathologic features; histologic subtypes, grade, lymphovascular invasion, axillary involvement, and stage were recorded for each. Results: The most common subtype was luminal B (36.5%), followed by luminal A (30.8%), triple negative (23.2%) and HER2+(9.5%) subtypes. Twelve percent of the patients had stage 4, 32.7% had stage 3, 46.4% had stage 2, and 6.2% had stage 1 disease at the time of diagnosis. Mean tumour diameter was 3.87 cm (range 0.3-13 cm). The axillary lymph nodes were positive in 74.4% of the patients, while lympho-vascular invasion was seen in 56.4%. Some 9.5% of patients had grade 1, 51.2% had grade 2, and 31.8% had grade 3 tumors. Conclusions: Young women with breast cancer in Turkey are more likely to present with luminal B subtype. Tumors in young women are more likely to present with advanced disease, to be high grade and and to have more lymphovascular invasion. Further research should focus on whether we need new treatment strategies for young patients with breast carcinoma.

• Journal of Plant Biotechnology
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• 제46권3호
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• pp.217-227
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• 2019

Production of therapeutic monoclonal antibodies (mAbs) using a plant platform has been considered an alternative to the mammalian cell-based production system. A plant-derived mAb CO17-1AK ($mAb^P$ COK) can specifically bind to various types of cancer cell lines. The target protein of $mAb^P$ COK is the epithelial cell adhesion molecule (EpCAM) highly expressed in human epithelial cancer cells, including breast and colorectal cancer cells. It has been hypothesized that its overexpression supports tumor growth and metastasis. A ganglioside is extended well beyond the surfaces of the various cell membranes and has roles in cell growth, inflammation, differentiation, and carcinogenesis. However, the regulation of EpCAM gene expression in breast cancers and the role of gangliosides in oncogenesis are unclear. Here, the purpose of this study was to determine the effects of $mAb^P$ COK on human breast cancer cell proliferation, apoptosis, and ganglioside expression patterns. Our results show that treatment with $mAb^P$ COK suppressed the growth of breast cancer cells and induced apoptotic cell death. It also upregulated the expression of metastasis-related gangliosides in breast cancer cells. Thus, treatment with $mAb^P$ COK may have chemo-preventive therapeutic effects against human breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제17권3호
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• pp.1003-1008
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• 2016

Breast cancer is now the leading cause of cancer death in women worldwide. Cancer progression is driven not only by cancer cell intrinsic alterations and interactions with tumor microenvironment, but also by systemic effects. Integration of multiple profiling data may provide insights into the underlying molecular mechanisms of complex systemic processes. We performed a bioinformatic analysis of two public available microarray datasets for breast tumor stroma and peripheral blood mononuclear cells, featuring integrated transcriptomics data, protein-protein interactions (PPIs) and protein subcellular localization, to identify genes and biological pathways that contribute to dialogue between tumor stroma and the peripheral circulation. Genes of the integrin family as well as CXCR4 proved to be hub nodes of the crosstalk network and may play an important role in response to stroma-derived chemoattractants. This study pointed to potential for development of therapeutic strategies that target systemic signals travelling through the circulation and interdict tumor cell recruitment.

• 통합자연과학논문집
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• 제15권4호
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• pp.153-161
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• 2022

c-Jun N-terminal kinases (JNKs) are members of MAPK family. Many genes can relay signals that promote inflammation, cell proliferation, or cell death which causes several diseases have been associated to mutations in the JNK gene family. The JNK2 gene is significantly more important in cancer development than the JNK1 and JNK3 genes. There are several different ways in which JNK2 contributes to breast cancer, and one of these is through its role in cell migration. As a result, this study's primary objective was to employ computational strategies to identify promising leads that potentially target the JNK2 protein in a strategy to alleviate breast cancer. We have derived these anticancer compounds from marine brown seaweed called Turbinaria conoides. We have identified compounds Ethane, 1, 1-diethoxy- and Butane, 2-ethoxy as promising anti-cancer drugs by molecular docking, DFT, and ADME study.

• 대한한방내과학회지
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• 제35권2호
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• pp.133-144
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• 2014

O. diffusa, C. appendiculata and F. thunbergii are reported to possess many pharmacological activities including anti-oxidant, anti-inflammatory, anti-hypertension, anti-diabetic and anti-cancer effects. However, their anti-cancer activities in human breast cancer have not been clearly elucidated yet. Objectives: In the present study, we compared the in vitro cytotoxic effects of single and complex treatment of O. diffusa, C. appendiculata and F. thunbergii in human breast cancer MDA-MB-231 cells. Methods: After we treated human breast cancer MDA-MB-231 cells with O. diffusa, C. appendiculata and F. thunbergii. we evaluated viability, growth inhibition, morphological changes, apoptotic body formation, measurement of the cell cycle and formation of DNA fragmentation of these cells. Results: We found that single treatment of O. diffusa and F. thunbergii could inhibit cell proliferation in human breast cancer MDA-MB-231 cells. However, complex treatment of O. diffusa, C. appendiculata and F. thunbergii had weak or no effect on the cell proliferation of MDA-MB-231 cells. The first, anti-proliferative effects of O. diffusa in MDA-MB-231 cells was associated with G2/M arrest of cell cycle and apoptotic cell death. The second, anti-proliferative effect of F. thunbergii in MDA-MB-231 cells was associated with apoptotic cell death. Conclusions: Taken together, these findings suggest that O. diffusa and F. thunbergii may be a potential chemotherapeutic agent for the control of human breast cancer cells, further studies will be needed to identify the molecular mechanisms.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.5811-5816
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• 2013

Background: Breast cancer is the most common cancer among women. Molecular subtypes are important in determining prognosis. This study evaluated five-year disease-free survival among four molecular subtypes in patients with early stages of breast cancer. Materials and Methods: In this retrospective descriptive-analytical study, information on patients with breast cancer between 2001-2010 was evaluated. Five hundred ninety two patients in the early stages of breast cancer (stages 1 and 2) were selected to undergo anthracycline-based chemotherapy. Relapse, death or absence (censor) were considered as the end of the study. Patients based on ER, PR and HER-2 expression were divided into four subtypes (luminal A, luminal B, HER-2 enriched and triple negative). Information based upon questionnaire was analysed. To show the patients survival rate, life table and Kaplan-Meyer methods were used, and for comparing mean survival among different groups, the Log-Rank test was utilized. Results: Mean age at diagnosis was $47.9{\pm}9.6$. Out of the 592 patients, 586 were female (99%) and 6 were male (1%). Considering breast cancer molecular subtypes, 361 patients were in the luminal A group (61%), 49 patients in the luminal B group (8.3%), 48 patients in the HER-2 enriched group (8.1%) and 134 in the triple negative group (22.6%). Mean disease-free survival was 53.7 months overall, 55.4 months for the luminal A group, 48.3 months for the luminal B group, 43 months for the HER-2enriched group and 54.6 months for the triple negatives. Disease free survival differed significantly among the molecular subtypes (p value=0.0001). Conclusions: The best disease-free survival rate was among the luminal A subgroup and the worst disease-free survival rate was among the HER-2 enriched subgroup. Disease free survival rate in the HER-2 positive groups (luminal B and HER-2 enriched) was worse than the HER-2 negative groups (luminal A and triple negative).

• Asian Pacific Journal of Cancer Prevention
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• 제13권10호
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• pp.5019-5022
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• 2012

Objective: To evaluate the predictive value of GST gene polymorphisms with regard to prognosis of breast cancer patients receiving neoadjuvant chemotherapy. Methods: A total of 159 patients were included in our study between January 2005 and January 2007. All the patients were followed up until January 2012. Genotyping was based upon the duplex polymerase-chain-reaction with the PCR-CTPP method. Results: Patients with null GSTM1 and GSTP1 Val/Val genotypes had significantly had better response rates to chemotherapy when compared with non-null GSTM1 and GSTP1 Ile/Ile genotypes (OR=1.96 and OR=2.14, respectively). Patients with the GSTM1 null genotype had a longer average survival time and significantly lower risk of death than did those with non-null genotypes (HR=0.66). Similarly, those carrying the GSTP1 Val/Val genotype had 0.54-fold the risk of death of those with GSTP1 Ile/Ile (HR=0.54). Conclusion: A significant association was found between GSTM1 and GSTP1 gene polymorphisms and clinical outcomes in breast cancer cases.

• BMB Reports
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• 제53권5호
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• pp.284-289
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• 2020

Tamoxifen, a nonsteroidal estrogen receptor (ER) antagonist, is used routinely as a chemotherapeutic agent for ER-positive breast cancer. However, it is also causes side effects, including retinotoxicity. The retinal pigment epithelium (RPE) has been recognized as the primary target of tamoxifen-induced retinotoxicity. The RPE plays an essential physiological role in the normal functioning of the retina. Nonetheless, potential therapeutic agents to prevent tamoxifen-induced retinotoxicity in breast cancer patients have not been investigated. Here, we evaluated the action mechanisms of sulfasalazine against tamoxifen-induced RPE cell death. Tamoxifen induced reactive oxygen species (ROS)-mediated autophagic cell death and caspase-1-mediated pyroptosis in RPE cells. However, sulfasalazine reduced tamoxifen-induced total ROS and ROS-mediated autophagic RPE cell death. Also, mRNA levels of tamoxifen-induced pyroptosis-related genes, IL-1β, NLRP3, and procaspase-1, also decreased in the presence of sulfasalazine in RPE cells. Additionally, the mRNA levels of tamoxifen-induced AMD-related genes, such as complement factor I (CFI), complement factor H (CFH), apolipoprotein E (APOE), apolipoprotein J (APOJ), toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4), were downregulated in RPE cells. Together, these data provide novel insight into the therapeutic effects of sulfasalazine against tamoxifen-induced RPE cell death.

• 한국임상수의학회지
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• 제21권3호
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• pp.253-258
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• 2004

DNA double-strand break (DSB) is a serious treat for the cells including mutations, chromosome rearrangements, and even cell death if not repaired or misrepaired. Ku heterodimer regulatory DNA binding subunits (Ku70/Ku80) bound to double strand DNA breaks are able to interact with 470-kDa DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and the interaction is essential for DNA-dependent protein kinase (DNA-PK) activity. The Ku80 mutants were designed to bind Ku70 but not DNA end binding activity and the peptides were treated in breast cancer cells for co-therapy strategy to see whether the targeted inhibition of DNA-dependent protein kinase (DNA-PK) activity sensitized breast cancer cells to ionizing irradiation or chemotherapy drug to develop a treatment of breast tumors by targeting proteins involved in damage-signaling pathway and/or DNA repair. We designed domains of Ku80 mutants, 26 residues of amino acids (HN-26) as a control peptide or 38 (HNI-38) residues of amino acids which contain domains of the membrane-translocation hydrophobic signal sequence and the nuclear localization sequence, but HNI-38 has additional twelve residues of peptide inhibitor region. We observed that the synthesized peptide (HNI-38) prevented DNA-PKcs from binding to Ku70/Ku80, resulting in inactivation of DNA-PK complex activity in breast cancer cells (MDA-465 and MDA-468). Consequently, the peptide treated cells exhibited poor to no DNA repair, and became highly sensitive to irradiation or chemotherapy drugs. The growth of breast cancer cells was also inhibited. These results demonstrate the possibility of synthetic peptide to apply breast cancer therapy to induce apoptosis of cancer cells.