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Current Opinion in Oncology, ISSN 1040-8746, 09/2019, Volume 31, Issue 5, pp. 439 - 444
PURPOSE OF REVIEWThe aim of this review is to provide an overview of the current development of immuno-oncology in the (neo)adjuvant setting. RECENT... 
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2017, Volume 18, Issue 7, pp. 904 - 916
Summary Background Phosphatidylinositol 3-kinase (PI3K) pathway activation is a hallmark of endocrine therapy-resistant, hormone receptor-positive breast... 
Hematology, Oncology and Palliative Medicine | HETEROGENEITY | WOMEN | PALBOCICLIB | THERAPY | EXEMESTANE | ONCOLOGY | MUTATION | RESISTANCE | COMBINATION | AROMATASE INHIBITORS | PI3K INHIBITOR | Estradiol - analogs & derivatives | Humans | Middle Aged | Aminopyridines - adverse effects | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Response Evaluation Criteria in Solid Tumors | Alanine Transaminase - blood | Receptors, Estrogen - analysis | Fulvestrant | Receptors, Progesterone - analysis | Breast Neoplasms - chemistry | Neoplasm Metastasis | Hyperglycemia - chemically induced | DNA, Neoplasm - blood | DNA Mutational Analysis | Exanthema - chemically induced | Postmenopause | Female | Morpholines - adverse effects | Aminopyridines - administration & dosage | Drug Eruptions - etiology | Double-Blind Method | Morpholines - administration & dosage | Estradiol - administration & dosage | Survival Rate | Signal Transduction - genetics | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Disease-Free Survival | Retreatment | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Aspartate Aminotransferases - blood | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Breast Neoplasms - pathology | Aged | Biomarkers, Tumor - genetics | Receptor, ErbB-2 - analysis | Antimitotic agents | Medical colleges | Clinical trials | Product development | Breast cancer | Postmenopausal women | Hormones | Antineoplastic agents | Analysis
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2012, Volume 13, Issue 9, pp. 897 - 905
Summary Background No effective standard treatment exists for patients with radioiodine-refractory, advanced differentiated thyroid carcinoma. We aimed to... 
Hematology, Oncology and Palliative Medicine | CRITERIA | MALIGNANT-TUMORS | SOLID TUMORS | ONCOLOGY | PAPILLARY | SORAFENIB | INHIBITOR | CARCINOMA | ZD6474 | Carcinoma | Humans | Middle Aged | Bone Neoplasms - secondary | Male | Antineoplastic Agents - therapeutic use | Diarrhea - chemically induced | Young Adult | Lung Neoplasms - secondary | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Adult | Female | ErbB Receptors - antagonists & inhibitors | Thyroid Neoplasms - mortality | Double-Blind Method | Kaplan-Meier Estimate | Electrocardiography - drug effects | Heart Conduction System - drug effects | Lymphatic Metastasis | Thyroid Cancer, Papillary | Disease-Free Survival | Adenocarcinoma, Follicular | Thyroid Neoplasms - drug therapy | Carcinoma, Papillary | Piperidines - therapeutic use | Quinazolines - therapeutic use | Piperidines - adverse effects | Adolescent | Quinazolines - adverse effects | Skin Neoplasms - secondary | Survival Analysis | Thyroid Neoplasms - secondary | Aged | Thyroid Neoplasms - pathology | Tyrosine | Care and treatment | Thyroid cancer | Clinical trials | Product development | Metastasis | Vascular endothelial growth factor | Cancer | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Cancer and Oncology | Medicin och hälsovetenskap | Cancer och onkologi
Journal Article
Cancers, ISSN 2072-6694, 12/2017, Volume 9, Issue 12, p. 172
p53 protects cells from genetic assaults by triggering cell-cycle arrest and apoptosis. Inactivation of p53 pathway is found in the vast majority of human... 
P53 reactivation | Drug combination | APR-246 | PRIMA-1 | Cancer | P53 | Proteins | Missense mutation | Developmental stages | p53 Protein | Clinical trials | Mutation | Cancer therapies | Apoptosis | Tumors | Life Sciences | p53 reactivation | drug combination | cancer | PRIMA-1Met | p53
Journal Article
Current Clinical Pharmacology, ISSN 1574-8847, 2015, Volume 10, Issue 4, p. 253
Journal Article
Cancer Chemotherapy and Pharmacology, ISSN 0344-5704, 4/2008, Volume 61, Issue 4, pp. 535 - 548
Journal Article
Breast Cancer Research and Treatment, ISSN 0167-6806, 12/2014, Volume 148, Issue 3, pp. 553 - 561
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 03/2010, Volume 28, Issue 8, pp. 1301 - 1307
Journal Article
Journal Article
CANCERS, ISSN 2072-6694, 08/2019, Volume 11, Issue 8, p. 1093
Radiotherapy (RT) in patients with melanoma historically showed suboptimal results, because the disease is often radioresistant due to various mechanisms such... 
ACTIVATION | CANCER CELLS | p53 activation | melanoma | COMBINATION | (V600E)BRAF inhibition | RADIATION-THERAPY | BRAF INHIBITOR | ONCOLOGY | IN-VIVO | radiotherapy | RESISTANCE | TARGETING P53 | SKIN | intrinsic and acquired resistance | VEMURAFENIB | V600EBRAF inhibition
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 07/2013, Volume 31, Issue 20, pp. 2586 - 2592
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 10/2007, Volume 357, Issue 17, pp. 1695 - 1704
Journal Article
European Journal of Cancer, ISSN 0959-8049, 03/2016, Volume 55, pp. 98 - 110
Intrinsic and acquired resistance of metastatic melanoma to BRAF and/or MEK inhibitors, which is often caused by activation of the PI3K/AKT survival pathway,... 
Vemurafenib | PRIMA-1Met | Drug resistance | V600E/KBRAF | Melanoma | p53 | BRAF | PRIMA-1
Journal Article
Journal Article