THE UNIQUE TRANSCRIPTIONAL RESPONSE PRODUCED BY CONCURRENT ESTROGEN AND PROGESTERONE TREATMENT IN BREAST CANCER CELLS RESULTS IN UPREGULATION OF GROWTH FACTOR PATHWAYS AND SWITCHING FROM A
Tìm thấy 10,000 tài liệu liên quan tới tiêu đề "The unique transcriptional response produced by concurrent estrogen and progesterone treatment in br...":
The unique transcriptional response produced by concurrent estrogen and progesterone treatment in breast cancer cells results in upregulation of growth factor pathways and switching from a
Cells were plated for 72 h in 6-well plates in phenol red- free RPMI 1640 containing 10 % hormone stripped FBS at 5 x 10 5 / well, treated for 16 h with vehicle (ethanol; V.C), 10nM estrogen, 10 nM progesterone, 10 nM estro- gen + 10nM progesterone, or for 7[r]
RESPONDER – diagnosis of pathological complete response by vacuum-assisted biopsy after neoadjuvant chemotherapy in breast Cancer - a multicenter, confirmative, one-armed, intra-individually
performed according to standards in primary breast diag- nostics and according to the above mentioned guidelines. The intervention may be performed before surgery at a sep- arate visit, the day before surgery (e. g. during the wire loca- tion[r]
SURGERY TIME INTERVAL AND MOLECULAR SUBTYPE MAY INFLUENCE KI67 CHANGE AFTER CORE NEEDLE BIOPSY IN BREAST CANCER PATIENTS
To investigate the accuracy of core needle biopsy (CNB) in evaluating breast cancer estrogen receptor (ER), progesterone receptor (PR), HER2, and Ki67 status and to identify factors which might be associated with Ki67 value change after CNB.
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SHIFTING BREAST CANCER SURVEILLANCE FROM CURRENT HOSPITAL SETTING TO A COMMUNITY BASED SETTING: A COST-EFFECTIVENESS STUDY
This study explores the effectiveness and cost-effectiveness of surveillance after breast cancer treatment provided in a hospital-setting versus surveillance embedded in the community-based National Breast Cancer Screening Program (NBCSP).
PREVALENCE OF PERSISTENT PAIN AFTER BREAST CANCER TREATMENT BY DETECTION MODE AMONG PARTICIPANTS IN POPULATION-BASED SCREENING PROGRAMS
To date, the study of the risks and benefits of breast cancer screening has not included the onset of persistent pain after breast cancer treatment within the context of population-based screening programs. Our purpose was to investigate the prevalence of persistent pain and associated factors in wo[r]
LOW SERUM GASTRIN ASSOCIATED WITH ER+ BREAST CANCER DEVELOPMENT VIA INACTIVATION OF CCKBR/ERK/P65 SIGNALING
Gastrin is an important gastrointestinal hormone produced primarily by G-cells in the antrum of the stomach. It normally regulates gastric acid secretion and is implicated in a number of human disease states, but how its function affects breast cancer (BC) development is not documented.
INDUCTION OF ARTIFICIAL CANCER STEM CELLS FROM TONGUE CANCER CELLS BY DEFINED REPROGRAMMING FACTORS
The cancer stem cells (CSCs), a small subpopulation of cells in tumor are responsible for the tumor initiation, growth, recurrence and metastasis of cancer, as well as resistance of cancers to drugs or radiotherapy. CSCs are an important target for the development of novel strategies in cancer treat[r]
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ASSOCIATION OF TAMOXIFEN RESISTANCE AND LIPID REPROGRAMMING IN BREAST CANCER
Tamoxifen treatment of estrogen receptor (ER)-positive breast cancer reduces mortality by 31%. However, over half of advanced ER-positive breast cancers are intrinsically resistant to tamoxifen and about 40% will acquire the resistance during the treatment.
SYSTEMATIC DRUG SCREENING REVEALS SPECIFIC VULNERABILITIES AND CO-RESISTANCE PATTERNS IN ENDOCRINE-RESISTANT BREAST CANCER
The estrogen receptor (ER) inhibitor tamoxifen reduces breast cancer mortality by 31 % and has served as the standard treatment for ER-positive breast cancers for decades. However, 50 % of advanced ER-positive cancers display de novo resistance to tamoxifen, and acquired resistance evolves in 40 % o[r]
BÁO CÁO KHOA HỌC DIFFERENTIAL REGULATION OF FATTY ACID AMIDE HYDROLASE PROMOTER IN HUMAN IMMUNE CELLS AND NEURONAL CELLS BY LEPTIN AND PROGESTERONE PDF
, i.e. 0.3 lgÆmL)1)increased the nuclear levels of these Ikaros i soforms inU937 cells 2.5-fold over the controls (Fig. 3B,C). This isnoteworthy, because homo- and h eterodimer formationbetween Ik1, 2 and 3 is k nown t o greatly increase theiraffinity for[r]
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THE INSULIN-LIKE GROWTH FACTOR SYSTEM IS MODULATED BY EXERCISE IN BREAST CANCER SURVIVORS: A SYSTEMATIC REVIEW AND METAANALYSIS
Insulin-like growth factors (IGF´s) play a crucial role in controlling cancer cell proliferation, differentiation and apoptosis. Exercise has been postulated as an effective intervention in improving cancerrelated outcomes and survival, although its effects on IGF´s are not well understood.
METHYLENE BLUE PHOTODYNAMIC THERAPY INDUCES SELECTIVE AND MASSIVE CELL DEATH IN HUMAN BREAST CANCER CELLS
Breast cancer is the main cause of mortality among women. The disease presents high recurrence mainly due to incomplete efficacy of primary treatment in killing all cancer cells. Photodynamic therapy (PDT), an approach that causes tissue destruction by visible light in the presence of a photosensiti[r]
PROGNOSTIC VALUE OF ERBB4 EXPRESSION IN PATIENTS WITH TRIPLE NEGATIVE BREAST CANCER
Triple-negative breast cancer (TNBC) is known for aggressive biologic features and poor prognosis. Epidermal growth factor receptor (EGFR) overexpression in TNBC indicates poor prognosis. However, there is no previous study of the relationship between expression of the entire human epidermal growth[r]
TRASTUZUMAB WITHOUT CHEMOTHERAPY IN THE ADJUVANT TREATMENT OF BREAST CANCER: SUBGROUP RESULTS FROM A LARGE OBSERVATIONAL STUDY
The topic of trastuzumab therapy without chemotherapy in early breast cancer (EBC) has been repeatedly discussed at international consensus meetings, but is compromised by the lack of solid evidence from clinical studies.
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18FDG-PET-CT IDENTIFIES HISTOPATHOLOGICAL NON-RESPONDERS AFTER NEOADJUVANT CHEMOTHERAPY IN LOCALLY ADVANCED GASTRIC AND CARDIA CANCER: COHORT STUDY
Pathologic response to neoadjuvant chemotherapy (neoCTX) is a prognostic factor in many cancer types, and early prediction would help to modify treatment. In patients with gastric and esophagogastric junction (AEG) cancer, the accuracy of FDG PET-CT to predict early pathologic response after neoadju[r]
BÁO CÁO KHOA HỌC: ALPHA 1,3-FUCOSYLTRANSFERASE-VII REGULATES THE SIGNALING MOLECULES OF THE INSULIN RECEPTOR PATHWAY POTX
expression in cells. In addition, the phosphorylation intensity and differ-ence in phosphorylation intensity between cells with different levels ofa1,3-FucT-VII expression were attenuated significantly by the inhibitor ofInR tyrosine kina[r]
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CHAPTER 079. CANCER GENETICS (PART 10) PPTX
fractions of colon, breast, and hepatocellular cancers. Most recently, this approach has been applied to an unbiased set of genes including about two-thirds of all those known to encode proteins. Hundreds of genes not previously implicated in cancers[r]
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COMPARISON OF THE HER2, ESTROGEN AND PROGESTERONE RECEPTOR EXPRESSION PROFILE OF PRIMARY TUMOR, METASTASES AND CIRCULATING TUMOR CELLS IN METASTATIC BREAST CANCER PATIENTS
The expression of HER2, estrogen (ER) and progesterone (PR) receptor can change during the course of the disease in breast cancer (BC). Therefore, reassessment of these markers at the time of disease progression might help to optimize treatment decisions.
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Progesterone receptor blockade in human breast cancer cells decreases cell cycle progression through G2/M by repressing G2/M genes
EDTA: ethylenediaminetetraacetic acid; EGFR: epidermal growth factor receptor; ER: estrogen receptor; ERK1/2: extracellular signal-regulated protein kinases 1 and 2; FBS: fetal bovine serum; FDR: false discovery rate; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; GR: g[r]
Estrogen receptor α dependent regulation of estrogen related receptor β and its role in cell cycle in breast cancer
also mediates cell cycle regulation through p18, p21 cip and cyclin D1 in breast cancer cells. Our results also showed the up-regulation of ERR β promoter activity in ectopically co-expressed ER α and ERR β breast cancer[r]