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Oncogene addiction

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https://www.readbyqxmd.com/read/27912893/-perioperative-therapies-in-surgical-non-n2%C3%A2-non-small-cell-lung-cancer
#1
REVIEW
Anne-Marie Ruppert, Armelle Lavolé, Jalal Assouad, Jacques Cadranel, Marie Wislez
Platinum-based perioperative chemotherapy is actually the standard of care in stage II-IIIa non-small cell lung cancer (NSCLC). A benefit may also be seen in stage IB NSCLC with tumors of more than 4cm of diameter. Perioperative chemotherapy improves 5-year survival of 4 to 15%. This benefit is mainly proved by postoperative chemotherapy trials. Nevertheless, preoperative chemotherapy has advantages: a better tolerance, an estimation of tumor chemosensibility, without an increased postoperative morbimortality...
November 29, 2016: Bulletin du Cancer
https://www.readbyqxmd.com/read/27912827/new-targets-in-non-small-cell-lung-cancer
#2
REVIEW
Soo J Park, Soham More, Ayesha Murtuza, Brian D Woodward, Hatim Husain
With the implementation of genomic technologies into clinical practice, we have examples of the predictive benefit of targeted therapy for oncogene-addicted cancer and identified molecular dependencies in non-small cell lung cancer. The clinical success of tyrosine kinase inhibitors against epidermal growth factor receptor and anaplastic lymphoma kinase activation has shifted treatment emphasize the separation of subsets of lung cancer and genotype-directed therapy. Advances have validated oncogenic driver genes and led to the development of targeted agents...
February 2017: Hematology/oncology Clinics of North America
https://www.readbyqxmd.com/read/27876887/high-energy-particle-radiation-associated-oncogenic-transformation-in-normal-mice-insight-into-the-connection-between-activation-of-oncotargets-and-oncogene-addiction
#3
Natarajan Aravindan, Sheeja Aravindan, Krishnan Manickam, Mohan Natarajan
Concerns on high-energy particle radiation-induced tumorigenic transformation of normal tissue in astronauts, and in cancer patients undergoing radiotherapy, emphasizes the significance of elucidating the mechanisms involved in radiogenic transformation processes. Mostly used genetically modified or tumor-prone models are less reliable in determining human health risk in space or protracted post-treatment normal tissue toxicity. Here, in wild type C57BL/6 mice, we related the deregulation of distinctive set of tissue-specific oncotargets in major organs upon (56)Fe (600 MeV/amu; 0...
November 23, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27875549/the-synthetic-%C3%AE-nitrostyrene-derivative-cyt-rx20-inhibits-esophageal-tumor-growth-and-metastasis-via-pi3k-akt-and-stat3-pathways
#4
Wen-Chin Chiu, Yi-Chen Lee, Yu-Han Su, Yen-Yun Wang, Chun-Hao Tsai, Yi-An Hou, Chie-Hong Wang, Ying-Fong Huang, Chih-Jen Huang, Shah-Hwa Chou, Pei-Wen Hsieh, Shyng-Shiou F Yuan
The β-nitrostyrene family have been implicated for anti-cancer property. However, the pharmacological role of β-nitrostyrene in esophageal cancer remain unclear. Here, a β-nitrostyrene derivative, CYT-Rx20, was synthesized and assessed for its anti-cancer activities and underlying mechanism in esophageal cancer. CYT-Rx20 induced cytotoxicity in esophageal cancer cells by promoting apoptosis through activation of caspase cascade and poly(ADP-ribose) polymerase (PARP) cleavage. Besides, CYT-Rx20 inhibited esophageal cancer cell migration and invasion by regulating the expression of epithelial to mesenchymal transition (EMT) markers...
2016: PloS One
https://www.readbyqxmd.com/read/27872099/conflicting-signals-for-cancer-treatment
#5
Pierre Sujobert, Alain Trautmann
Next-generation sequencing technologies have provided us with a precise description of the mutational burden of cancers, making it possible to identify targetable oncogene addictions. However, the emergence of resistant clones is an inevitable limitation of therapies targeting these addictions. Alternative approaches to cancer treatment are therefore required. We propose here a novel approach, based on the notion of conflicting signals and on a phenotypic description of cancer cells. "Phenotype" is an inherently complex notion that we describe in the conceptual framework of the epigenetic landscape, with a view to bridging the gap between theory and practice at the patient's bedside...
December 1, 2016: Cancer Research
https://www.readbyqxmd.com/read/27869167/cystine-addiction-of-triple-negative-breast-cancer-associated-with-emt-augmented-death-signaling
#6
X Tang, C-K Ding, J Wu, J Sjol, S Wardell, I Spasojevic, D George, D P McDonnell, D S Hsu, J T Chang, J-T Chi
Despite the advances in the diagnosis and treatment of breast cancer, breast cancers still cause significant mortality. For some patients, especially those with triple-negative breast cancer, current treatments continue to be limited and ineffective. Therefore, there remains an unmet need for a novel therapeutic approach. One potential strategy is to target the altered metabolic state that is rewired by oncogenic transformation. Specifically, this rewiring may render certain outside nutrients indispensable...
November 21, 2016: Oncogene
https://www.readbyqxmd.com/read/27845970/role-of-the-unfolded-protein-response-in-tumor-cell-characteristics-and-cancer-outcome
#7
Antoine Galmiche, Chloé Sauzay, Eric Chevet, Olivier Pluquet
PURPOSE OF REVIEW: In the present review, we discuss the possible role of the unfolded protein response (UPR) in the acquisition of tumor cell characteristics and in the prognosis of cancer outcome, which could assist and contribute to the development of more promising therapeutic strategies. RECENT FINDINGS: Accumulating evidence supports the idea that alteration of endoplasmic reticulum proteostasis is a key player in cancer development and aggressiveness. Some UPR components were reported as independent prognostic biomarker...
January 2017: Current Opinion in Oncology
https://www.readbyqxmd.com/read/27845331/brca1-regulated-rrm2-expression-protects-glioblastoma-cells-from-endogenous-replication-stress-and-promotes-tumorigenicity
#8
Rikke D Rasmussen, Madhavsai K Gajjar, Lucie Tuckova, Kamilla E Jensen, Apolinar Maya-Mendoza, Camilla B Holst, Kjeld Møllgaard, Jane S Rasmussen, Jannick Brennum, Jiri Bartek, Martin Syrucek, Eva Sedlakova, Klaus K Andersen, Marie H Frederiksen, Jiri Bartek, Petra Hamerlik
Oncogene-evoked replication stress (RS) fuels genomic instability in diverse cancer types. Here we report that BRCA1, traditionally regarded a tumour suppressor, plays an unexpected tumour-promoting role in glioblastoma (GBM), safeguarding a protective response to supraphysiological RS levels. Higher BRCA1 positivity is associated with shorter survival of glioma patients and the abrogation of BRCA1 function in GBM enhances RS, DNA damage (DD) accumulation and impairs tumour growth. Mechanistically, we identify a novel role of BRCA1 as a transcriptional co-activator of RRM2 (catalytic subunit of ribonucleotide reductase), whereby BRCA1-mediated RRM2 expression protects GBM cells from endogenous RS, DD and apoptosis...
November 15, 2016: Nature Communications
https://www.readbyqxmd.com/read/27843631/unravelling-signal-escape-through-maintained-egfr-activation-in-advanced-non-small-cell-lung-cancer-nsclc-new-treatment-options
#9
REVIEW
Jordi Remon, Benjamin Besse
The discovery of activating epidermal growth factor receptor (EGFR) mutations has opened up a new era in the development of more effective treatments for patients with non-small cell lung cancer (NSCLC). However, patients with EGFR-activating mutated NSCLC treated with EGFR tyrosine kinase inhibitors (TKIs) ultimately develop acquired resistance (AR). Among known cases of patients with AR, 70% of the mechanisms involved in the development of AR to EGFR TKI have been identified and may be categorised as either secondary EGFR mutations such as the T790M mutation, activation of bypass track signalling pathways such as MET amplification, or histologic transformation...
2016: ESMO Open
https://www.readbyqxmd.com/read/27835915/unveiling-changes-in-the-landscape-of-patient-populations-in-cancer-early-drug-development
#10
REVIEW
Cinta Hierro, Analía Azaro, Guillem Argilés, Elena Elez, Patricia Gómez, Joan Carles, Jordi Rodon
The introduction of new Molecularly Targeted Agents (MTA) has changed the landscape in Early Drug Development (EDD) over the last two decades, leading to an improvement in clinical trial design. Previous Phase 1 (Ph1) studies with cytotoxics focused on safety objectives, only recruiting heavily pre-treated cancer patients, have been left behind. In this review, we will illustrate the slow although unstoppable change that has increasingly been observed in those populations candidate to participate in EDD trials with the advent of MTA...
November 9, 2016: Oncotarget
https://www.readbyqxmd.com/read/27822137/axitinib-has-antiangiogenic-and-antitumorigenic-activity-in-myxoid-liposarcoma
#11
Lauren T Kerr, Jacqueline F Donoghue, Alexander L Wilding, Terrance G Johns
Myxoid liposarcoma is a rare form of soft-tissue sarcoma. Although most patients initially respond well to treatment, approximately 21% relapse, highlighting the need for alternative treatments. To identify novel treatment regimens and gain a better understanding of myxoid liposarcoma tumor biology, we screened various candidate and approved targeted therapeutics and chemotherapeutics against myxoid liposarcoma cell lines. Therapeutics that target angiogenesis showed antitumor activity. The small molecule inhibitor axitinib, which targets angiogenesis by inhibiting the VEGFR and PDGFR families and c-Kit, inhibited cell cycle progression and induced apoptosis in vitro, as well as having significant antitumor activity against MLS 1765 myxoid liposarcoma xenografts in mice...
2016: Sarcoma
https://www.readbyqxmd.com/read/27807303/targeting-the-kras-pathway-in-non-small-cell-lung-cancer
#12
REVIEW
Pascale Tomasini, Preet Walia, Catherine Labbe, Kevin Jao, Natasha B Leighl
: : Lung cancer remains the leading cause of cancer-related deaths worldwide. However, significant progress has been made individualizing therapy based on molecular aberrations (e.g., EGFR, ALK) and pathologic subtype. KRAS is one of the most frequently mutated genes in non-small cell lung cancer (NSCLC), found in approximately 30% of lung adenocarcinomas, and is thus an appealing target for new therapies. Although no targeted therapy has yet been approved for the treatment of KRAS-mutant NSCLC, there are multiple potential therapeutic approaches...
November 2, 2016: Oncologist
https://www.readbyqxmd.com/read/27799360/androgen-receptor-signaling-in-castration-resistant-prostate-cancer-a-lesson-in-persistence
#13
Isabel Coutinho, Tanya Day, Wayne D Tilley, Luke A Selth
The androgen receptor (AR) signaling axis drives all stages of prostate cancer, including the lethal, drug-resistant form of the disease termed castration resistant prostate cancer (CRPC), which arises following failure of androgen deprivation therapy (ADT). Persistent AR activity in spite of ADT and the second-generation AR-targeting agents enzalutamide and abiraterone is achieved in many cases via direct alterations to the AR. Indeed, the role of AR in prostate cancer represents an archetype of therapy-mediated selection pressure and oncogene addiction...
October 31, 2016: Endocrine-related Cancer
https://www.readbyqxmd.com/read/27793177/approaches-to-modernize-the-combination-drug-development-paradigm
#14
REVIEW
Daphne Day, Lillian L Siu
Recent advances in genomic sequencing and omics-based capabilities are uncovering tremendous therapeutic opportunities and rapidly transforming the field of cancer medicine. Molecularly targeted agents aim to exploit key tumor-specific vulnerabilities such as oncogenic or non-oncogenic addiction and synthetic lethality. Additionally, immunotherapies targeting the host immune system are proving to be another promising and complementary approach. Owing to substantial tumor genomic and immunologic complexities, combination strategies are likely to be required to adequately disrupt intricate molecular interactions and provide meaningful long-term benefit to patients...
October 28, 2016: Genome Medicine
https://www.readbyqxmd.com/read/27782226/-the-evolution-of-the-treatment-of-advanced-nsclc
#15
Alessandro Morabito
The therapeutic scenario of patients with advanced non-small-cell lung cancer (NSCLC) has dramatically changed in recent years, thanks to the improvement in the knowledge of the biology of NSCLC, the discovery of targetable oncogenic drivers, and the availability of new effective drugs also for non oncogenic addicted patients, defined "wild-type" (WT). NSCLC has been the first epithelial neoplasm treated with a targeted first-line therapy in patients harbouring EGFR activating mutations or ALK rearrangements, and new targeted-based agents directed versus other molecular alterations are currently in development...
October 2016: Recenti Progressi in Medicina
https://www.readbyqxmd.com/read/27765910/suppression-of-gain-of-function-mutant-p53-with-metabolic-inhibitors-reduces-tumor-growth-in-vivo
#16
Chae Lim Jung, Hyemin Mun, Se-Young Jo, Ju-Hee Oh, ChuHee Lee, Eun-Kyung Choi, Se Jin Jang, Young-Ah Suh
Mutation of p53 occasionally results in a gain of function, which promotes tumor growth. We asked whether destabilizing the gain-of-function protein would kill tumor cells. Downregulation of the gene reduced cell proliferation in p53-mutant cells, but not in p53-null cells, indicating that the former depended on the mutant protein for survival. Moreover, phenformin and 2-deoxyglucose suppressed cell growth and simultaneously destabilized mutant p53. The AMPK pathway, MAPK pathway, chaperone proteins and ubiquitination all contributed to this process...
October 19, 2016: Oncotarget
https://www.readbyqxmd.com/read/27748760/glutamine-activates-stat3-to-control-cancer-cell-proliferation-independently-of-glutamine-metabolism
#17
A Cacace, M Sboarina, T Vazeille, P Sonveaux
Cancer cells can use a variety of metabolic substrates to fulfill the bioenergetic and biosynthetic needs of their oncogenic program. Besides bioenergetics, cancer cell metabolism also directly influences genetic, epigenetic and signaling events associated with tumor progression. Many cancer cells are addicted to glutamine, and this addiction is observed in oxidative as well as in glycolytic cells. Although both oxidative and bioreductive glutamine metabolism can contribute to cancer progression and glutamine can further serve to generate peptides (including glutathione) and proteins, we report that glutamine promotes the proliferation of cancer cells independently of its use as a metabolic fuel or as a precursor of glutathione...
October 17, 2016: Oncogene
https://www.readbyqxmd.com/read/27745897/-interest-of-crizotinib-in-a-lung-cancer-patient-with-de-novo-amplification-of-met
#18
A Rabeau, I Rouquette, J-M Vantelon, E Taranchon-Clermont, J Mazières
Targeted therapy in lung cancer changes the prognostic and treatment of patients. MET is an oncogene including exon 14 mutations and gene amplification associated with worse prognosis. We here report the case of a 47-year-old former smoker, woman, with a stage IV lung adenocarcinoma with multiple chemotherapy failure. A MET amplification was identified and the patient consequently received crizotinib. A major response was observed after eight weeks of treatment. MET amplification screening appears to be interesting with some oncogenic-addicted tumor response rate...
October 13, 2016: Revue des Maladies Respiratoires
https://www.readbyqxmd.com/read/27732857/addiction-to-coupling-of-the-warburg-effect-with-glutamine-catabolism-in-cancer-cells
#19
Bradley Smith, Xenia L Schafer, Aslihan Ambeskovic, Cody M Spencer, Hartmut Land, Joshua Munger
Metabolic reprogramming is critical to oncogenesis, but the emergence and function of this profound reorganization remain poorly understood. Here we find that cooperating oncogenic mutations drive large-scale metabolic reprogramming, which is both intrinsic to cancer cells and obligatory for the transition to malignancy. This involves synergistic regulation of several genes encoding metabolic enzymes, including the lactate dehydrogenases LDHA and LDHB and mitochondrial glutamic pyruvate transaminase 2 (GPT2)...
October 11, 2016: Cell Reports
https://www.readbyqxmd.com/read/27703839/formal-modeling-and-analysis-of-the-hexosamine-biosynthetic-pathway-role-of-o-linked-n-acetylglucosamine-transferase-in-oncogenesis-and-cancer-progression
#20
Muhammad Tariq Saeed, Jamil Ahmad, Shahzina Kanwal, Andreana N Holowatyj, Iftikhar A Sheikh, Rehan Zafar Paracha, Aamir Shafi, Amnah Siddiqa, Zurah Bibi, Mukaram Khan, Amjad Ali
The alteration of glucose metabolism, through increased uptake of glucose and glutamine addiction, is essential to cancer cell growth and invasion. Increased flux of glucose through the Hexosamine Biosynthetic Pathway (HBP) drives increased cellular O-GlcNAcylation (hyper-O-GlcNAcylation) and contributes to cancer progression by regulating key oncogenes. However, the association between hyper-O-GlcNAcylation and activation of these oncogenes remains poorly characterized. Here, we implement a qualitative modeling framework to analyze the role of the Biological Regulatory Network in HBP activation and its potential effects on key oncogenes...
2016: PeerJ
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