Relevant bibliographies by topics / 379.2/4/0941

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Academic literature on the topic '379.2/4/0941'

Author: Grafiati
Published: 29 July 2024
Last updated: 31 July 2024

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Journal articles on the topic "379.2/4/0941"

1

Sarker, D., R. Kristeleit, K. E. Mazina, J. A. Ware, Y. Yan, M. Dresser, M. K. Derynck, and J. De-Bono. "A phase I study evaluating the pharmacokinetics (PK) and pharmacodynamics (PD) of the oral pan-phosphoinositide-3 kinase (PI3K) inhibitor GDC-0941." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 3538. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.3538.

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3538 Background: The PI3K-PTEN-AKT signaling pathway is deregulated in a wide variety of cancers. GDC-0941 is a potent and selective oral inhibitor of class I PI3K and demonstrates activity in a broad range of preclinical models (breast, ovarian, lung, and prostate). Methods: Patients (pts) with histologically confirmed advanced solid tumors and ECOG PS 0–1 were treated with GDC-0941 using a 3+3 escalation design at a single institution. Treatment was a single dose with 1wk washout, followed by GDC-0941 qd on a 3wk on, 1wk off schedule. Objectives were to determine MTD and DLT, evaluate PD endpoints in surrogate (pAKT in platelet rich plasma) and tumor (pAKT and pS6 in paired tumor biopsies and FDG uptake via PET imaging) tissues, and describe anti-tumor activity. Results: Thirteen patients have been enrolled in 4 successive cohorts (15–60 mg qd). GDC-0941 was generally well-tolerated with no drug related Grade 3 or 4 AEs or DLTs to date. Grade 1 diarrhea, nausea, dysgeusia, peripheral sensory neuropathy, dry mouth, thrombocytopenia, and increased aspartate aminotransferase have been observed. Preliminary PK data suggest dose-proportional increases in fasting mean Cmax and AUC. Preliminary PD data show decreased levels of pAKT in platelet rich plasma correlated with GDC-0941 plasma concentrations. GDC-0941 effects on FDG-PET imaging is being assessed, with 1 patient with HER2+ metastatic breast cancer showing a reduction in FDG uptake and improvement of a chest wall lesion (dose level 60 mg qd). Evaluation of PI3K pathway modulation from paired tumor biopsies is underway. Conclusions: GDC-0941 is generally well tolerated when administered qd at doses associated with inhibition of pAKT in surrogate tissues. Evidence of PD activity in tumor tissue has also been observed. Dose-escalation continues and updated PK/PD data will be presented. [Table: see text]
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LoRusso, Patricia, Geoffrey Shapiro, Shuchi Sumant Pandya, Eunice Lee Kwak, Cheryl Jones, Marcia Belvin, Luna C. Musib, et al. "A first-in-human phase Ib study to evaluate the MEK inhibitor GDC-0973, combined with the pan-PI3K inhibitor GDC-0941, in patients with advanced solid tumors." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 2566. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.2566.

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2566 Background: Both RAS/RAF/MEK and PI3K/Akt signaling pathways are deregulated in many tumor types. Targeting both pathways may be more efficacious than targeting either pathway alone. In preclinical models, concurrent administration of GDC‑0973, a potent, selective, MEK1/2 inhibitor and GDC-0941, a potent class I PI3K inhibitor, shows improved efficacy compared to either agent alone dosed continuously or intermittently. Methods: A phase Ib dose-escalation study with 3+3 design was initiated in patients (pts) with advanced solid tumors to evaluate the safety and pharmacokinetics (PK) of oral dosing of GDC-0973 and GDC-0941. Pts received: concurrent GDC-0973 + GDC-0941 once daily (qd) on a 21 day on/7 day off (21/7) schedule; intermittent GDC-0973 on Days 1, 4, 8, 11, 15, 18 of a 28 day cycle + GDC-0941 qd on a 21/7 schedule (MEK int); or GDC-0973 + GDC-0941 qd on a 7 day on /7 day off schedule (7/7). Starting doses were 20 mg GDC-0973 + 80 mg GDC-0941 (21/7), 100 mg GDC-0973 + 130 mg GDC-0941 (MEK int); 40 mg GDC-0973 + 130 mg GDC-0941 (7/7). Serial plasma PK samples, FDG-PET, and CT scans were obtained. Results: 78 pts have enrolled. DLTs were G3 lipase (n=1), G4 CPK elevation (n=1). Compared to the 21/7 MTD of 40 mg GDC-0973 + 100 mg GDC-0941, higher doses of GDC-0973 + GDC-0941 were tolerated on the MEK int schedule. Overall, adverse events related to the study drug combination in ≥ 20% pts were diarrhea, rash, nausea, fatigue, vomiting, decreased appetite, dysgeusia, and elevated CPK. Preliminary analysis indicated PK of GDC-0973 and GDC-0941 are not altered when dosed in combination. Of 46 evaluable pts, 26 had an FDG-PET partial metabolic response (≥ 20% decrease in mean SUVmax from baseline) at ≥1 time points. Partial responses were observed in 3 pts (mBRAF melanoma, mBRAF pancreatic ca, mKRAS endometrioid ca); 5 pts had stable disease ≥ 5 months. Conclusions: Combination dosing of GDC‑0973 and GDC-0941 is generally well tolerated, with toxicities similar to those observed in single agent GDC-0973 and GDC-0941 phase 1 trials. There are early signs of anti-tumor activity. Dose escalation on MEK int and 7/7 schedules continues and updated data will be presented.
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De, Pradip, Yuliang Sun, Lori Friedman, Nandini Dey, and Brian Leyland-Jones. "Effect of pan-PI3K and HER2 blockade on antitumor activity in preclinical models of breast cancer resistance to trastuzumab therapy." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13570-e13570. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13570.

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e13570 Background: PI3K-AKT-mTOR pathway signaling is important for the oncogenic function of HER2. Activating alterations of this pathway are frequently observed in HER2-enriched breast cancer and generally herald a poor response and resistance to trastuzumab (T). Targeting the PI3K-AKT-mTOR pathway is an attractive strategy in HER2+ breast cancer that is refractory to trastuzumab. The hypothesis is that the suppression of this pathway by pan-PI3K inhibitor, GDC-0941 may lead to overcome trastuzumab-resistance. Methods: The antiproliferative and HER2-mediated cellular signaling (pAKT, pP70S6K, pS6RP, p4EBP1 and p-ERK) effects of GDC-0941 alone and in combination with T were evaluated in HER2 amplified T-sensitive (BT474), T-resistant (BT474HR), and HER2 amplified/PIK3CA mutated (HCC1954, UACC893) BT cell lines by MTT assay and Western blots. Athymic mice bearing BT474 and BT474HR xenograft tumors were treated with GDC-0941 and T (alone and in combination). Results: (1) GDC-0941 exhibited in vitro cell killing activity in MTT assay with IC50’s ranging from 0.35 µM to 1 µm and potency was augmented by the addition of T, (2) inhibition of phosphorylation of AKT(S473, T308), P70S6K, S6RP, and 4EBP1(T37/46, T70) was observed following GDC-0941 treatment, and the combination of GDC-0941 and T more effectively blocked the PI3K-AKT-mTOR pathway, (4) GDC-0941 dose-dependently blocked 3D-ON-TOP clonogenic growth of HER2+ cells. This effect was potentiated in the presence of T and (5) xenograft data show that the combination of GDC-0941 and T has strongly enhanced anti-tumor effect in both sensitive (82%) and resistant models (79%), something that cannot be achieved by either monotherapy. Conclusions: Our data suggest that 1) therapeutic targeting of the PI3K-AKT-mTOR signaling should be effective in abrogating resistance to T therapy in HER2+ BT, and 2) targeting both the HER2 and the PI3K signaling pathways is an attractive strategy to enhance the clinical activity of T therapy, as well as to prevent or delay the development of resistance.
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Fouda, A. S., M. A. Ismail, A. S. Abousalem, and G. Y. Elewady. "Experimental and theoretical studies on corrosion inhibition of 4-amidinophenyl-2,2′-bifuran and its analogues in acidic media." RSC Adv. 7, no. 73 (2017): 46414–30. http://dx.doi.org/10.1039/c7ra08092a.

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Corrosion inhibition studies of carbon steel (CS) in 1 M HCl by newly synthesized bichalcophene compounds namely; 4-(2,2′-bifuran-5-yl)benzamidine (MA-0947) and 6-(2,2′-bifuran-5-yl)nicotinamidine (MA-0941) and 6-[5-(thiophen-2-yl)furan-2-yl]nicotinamidine (MA-0940).
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Iyengar, Sunil, Andrew J. Clear, Andrew Owen, Lenushka Maharaj, Janet Matthews, Maria Calaminici, Rebecca Auer, et al. "PI3K Inhibition with GDC-0941 Has Greater Efficacy Compared to p110δ-Selective Inhibition with CAL-101 in Mantle Cell Lymphoma and May Be Particularly Advantageous in Multiply Relapsed Patients." Blood 118, no. 21 (November 18, 2011): 1654. http://dx.doi.org/10.1182/blood.v118.21.1654.1654.

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Abstract Abstract 1654 Background: Mantle cell lymphoma (MCL) is an incurable, aggressive subtype of non-Hodgkin lymphoma in which there is a need for novel targeted therapies. Activation of the PI3K-Akt pathway and its role in the pathogenesis of MCL has been highlighted in a number of studies. Constitutive activation of the PI3K pathway inactivates GSK-3β, a downstream target of Akt, that can phosphorylate cyclin D1 resulting in its nuclear export. There is also evidence that cyclin D1 mRNA stability and translation is enhanced by this pathway. The class Ia PI3K p110 catalytic subunit isoforms α, β and δ are primarily implicated in oncogenesis. While the PI3K p110δ isoform is known to be enriched in lymphocytes, a gain of PIK3CA (the gene encoding PI3K p110α) copy number has been shown to be a frequent alteration in MCL. The expression and relative importance of the individual Class Ia PI3K isoforms has not been documented in this disease. With the development of isoform selective inhibitors, this is an important issue that needs to be addressed. Aims: We studied the expression of class Ia PI3K isoforms in primary MCL with relation to morphological variants and disease status. We also compared the efficacy of PI3K inhibition in MCL cell lines and primary samples using two novel inhibitors, GDC-0941(predominantly p110α/δ-selective) and CAL-101 (δ-selective), both of which are in early phase clinical trials. Methods: Tissue microarrays were constructed from triplicate 1mm cores from 144 MCL biopsies and 16 tonsil controls. The levels of p110α, p110β and p110δ isoforms were then determined by immunohistochemistry using isoform-specific antibodies. The in vitro effect of PI3K inhibitors on cell viability and apoptosis was studied in 4 MCL cell lines, (Jeko-1, Granta519, REC-1 and JVM-2), and 15 primary MCL samples. Expression of the class Ia PI3K isoforms and changes in downstream targets of PI3K were determined by western blotting. Results: P110δ was expressed at a consistently higher level in MCL samples and normal tonsil controls compared to the α and β isoforms, while p110β expression was weak and significantly lower than p110α expression. On comparing expression of isoforms at diagnosis and relapse, p110α expression was significantly increased beyond 1st relapse compared to diagnostic biopsies (p=0.04) and tonsil controls (p=0.02), an observation that was even more apparent in 6 paired samples [p=0.008, median IHC score 19.6 (5.0−53.2) at diagnosis vs. 91.5 (38.6 − 129) beyond 1st relapse]. No significant change was found in the expression of p110β or p110δ between diagnostic and relapse samples. There was no significant difference in expression levels of the 3 isoforms between blastoid and non-blastoid morphological variants. Expression of both the p110α and δ isoforms was detected by western blotting in 4 MCL cell lines, but only Jeko-1 cells were sensitive to inhibition with GDC-0941. CAL-101 produced little or no apoptosis in all 4 cell lines. In primary MCL samples, GDC-0941 was consistently more potent than CAL-101, with decrease in cell viability of 32 vs. 20% at 1μM (p=0.15), 51 vs. 25% at 5μM (p=0.02) and 67 vs. 35% at 10μM (p<0.0001) GDC-0941 and CAL-101 respectively. GDC-0941 was also able to partially overcome the stimulatory effect of sCD40L and IL4 on primary MCL samples. Western blotting showed a consistent reduction in the phosphorylation of Akt and GSK-3β in sensitive MCL cells. Conclusion: Our studies demonstrate that although p110δ is the most consistently expressed isoform, the expression of the p110α subunit increases significantly in multiply relapsed MCL. This observation, in combination with significantly greater in vitro sensitivity of MCL primary samples to GDC-0941, compared to the p110δ-selective inhibitor CAL-101, provides strong evidence for further evaluation of GDC-0941 in this disease. Disclosures: Gribben: Roche: Honoraria; Celgene: Honoraria; GSK: Honoraria; Mundipharma: Honoraria; Gilead: Honoraria; Pharmacyclics: Honoraria. Joel:Astra Zeneca: Research Funding; Intellikine: Research Funding.
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Ebens, Allen J., Leanne Berry, Yung-Hsiang Chen, Gauri Deshmukh, Jake Drummond, Changchun Du, Michael Eby, et al. "A Selective PIM Kinase Inhibitor Is Highly Active In Multiple Myeloma: The Biology of Single Agent and PI3K/AKT/mTOR Combination Activity." Blood 116, no. 21 (November 19, 2010): 3001. http://dx.doi.org/10.1182/blood.v116.21.3001.3001.

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Abstract Abstract 3001 PIM kinases co-regulate several important elements of the PI3K/AKT/mTOR pathway in myeloma cells (Munugalavadla V. et al., ASH 2010 submitted abstr.). In this study we show that pan-PIM inhibition suppresses growth in myeloma cell lines, xenografts, and primary patient samples, both as a single-agent as well acting synergistically in combination with PI3K, AKT, and mTOR inhibition. The PIM kinases are a family of 3 ser/thr growth factor- & cytokine-induced proteins hypothesized to have redundant survival and growth functions. Although PIM-1,2 have been noted as highly expressed in myeloma (Claudio et al., 2002), there are few data to support potential therapeutic utility of PIM inhibition in this indication. We show myeloma cell lines express all 6 PIM protein isoforms to varying extents, and we describe the properties of a novel pan-PIM inhibitor GNE-652 with picomolar biochemical potency, an excellent selectivity profile, and favorable ADME properties. Myeloma cell lines exhibit a striking prevalence of response to GNE-652 (23 of 25 lines with IC50 < 1 micromolar, median < 0.1 micromolar) and synergy in combination with the PI3K inhibitor GDC-0941 (mean combination index values ~0.2 (n=25)). We used an unrelated compound GNE-568 which has a PIM-1,3 selective profile to test the hypothesis that PIM-2 may have a non-redundant role in myeloma cells. GNE-568 while having cellular potency against PIM-1 and PIM-3, did not have single agent activity in myeloma cell lines nor did it act synergistically with GDC-0941 (n=10 cell lines). Interestingly, PI3K and AKT inhibitors showed the greatest extent of synergy with GNE-652, whereas mTOR-selective inhibitors were synergistic to a lesser extent. Standard of care agents dexamethasone, revlimid, velcade, and melphalan also combined well with GNE-652, but to a lesser extent and not as broadly. The synergistic anti-tumor activity of GNE-652 and PI3K inhibitor GDC-0941 on cell lines or on primary myeloma bone marrow aspirates in vitro was associated with cell-cycle arrest and marked apoptosis. In addition, we found 4 of 4 myeloma xenograft mouse models tested with GNE-562 and GDC-0941 showed excellent combination efficacy that correlated with modulation of the expected pharmacodynamic markers. These results provide the rationale for further preclinical development of PIM inhibitors and provide the basis for a possible clinical development plan in multiple myeloma. Disclosures: Ebens: Genentech: Employment, Equity Ownership. Berry:Genentech: Employment, Equity Ownership. Chen:Genentech: Employment, Equity Ownership. Deshmukh:Genentech: Employment, Equity Ownership. Drummond:Genentech: Employment, Equity Ownership. Du:Genentech: Employment, Equity Ownership. Eby:Genentech: Employment, Equity Ownership. Fitzgerald:Genentech: Employment, Equity Ownership. S. Friedman:Genentech: Employment, Equity Ownership. E. Gould:Genentech: Employment, Equity Ownership. Kenny:Genentech: Employment, Equity Ownership. Maecker:Genentech: Employment, Equity Ownership. Moffat:Genentech: Employment, Equity Ownership. Moskalenko:Genentech: Employment, Equity Ownership. Pacheco:Genentech: Employment, Equity Ownership. Saadat:Genentech: Employment, Equity Ownership. Slaga:Genentech: Employment, Equity Ownership. Sun:Genentech: Employment, Equity Ownership. Wang:Genentech: Employment, Equity Ownership. Yang:Genentech: Employment, Equity Ownership. Munugalavadla:Genentech: Employment, Equity Ownership.
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Li, Haifu, Agnieszka Wozniak, Karel Van Den Bossche, Thomas Van Looy, Jasmien Wellens, Marguerite Stas, Giuseppe Floris, et al. "Efficacy of the phosphoinositol 3 kinase (PI3K) inhibitor GDC-0941 in patient- and cell-line-derived xenografts of dedifferentiated liposarcoma (DDLPS)." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e13528-e13528. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e13528.

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e13528 Background: Analysis of primary clinical specimens of DDLPS revealed evidence of AKT activation in 27% of cases (Gutierrez A, et al. Aberrant AKT activation drives well-differentiated liposarcoma. PNAS 2011; 108(39):16386-91). We evaluated the efficacy of the PI3K inhibitor GDC-0941 (GDC) alone and in combination with doxorubicin (DOX) in patient- and cell-line derived DDLPS xenografts with proven PI3K/AKT pathway activation. Methods: NMRI nu/nu mice were either injected bilaterally with 1x107SW872 cells or transplanted with human DDLPS (UZLX-STS3). Animals were randomized to 4 groups (6 mice/group) and treated for two weeks: vehicle, DOX (i.p., 1.2mg/kg/biw), GDC (p.o., 75mg/kg/qd), GDC+DOX (same dose/schedule as single agents). Efficacy was assessed by tumor volume assessment, Western blotting and histological evaluation (H&E). Mitotic and apoptotic effects were confirmed using immunostainings for phospho-histone H3 (p-H3) (for proliferation), and cleaved caspase 3 (CC3) (for apoptosis). Results: GDC and GDC+DOX significantly delayed the growth of both xenografts (74% decrease under GDC and 77% under GDC+DOX in SW872, 67% under GDC and 56% under GDC+DOX in UZLX-STS3, vs. control). GDC and GDC+DOX treatment resulted in reduced mitotic activity and increase in apoptosis, as compared to untreated tumors in both models (Table). The activation of PI3K signaling was nearly completely suppressed in the GDC and GDC+DOX treated groups in SW872, whilea weak activation of the pathway was still observed in UZLX-STS3. Conclusions: GDC-0941 has anti-tumor activity, decreases tumor proliferation and induces apoptosis in DDLPS with PI3K/AKT activation. The GDC+DOX combination did not show additive effect in vivo. [Table: see text]
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Pedraza Gracia, Manuel José, Maria Gioia Tavoni, Nicolás Bas Martín, and Antonio Carpallo Bautista. "Reseñas." Titivillus 2 (October 18, 2018): 213–28. http://dx.doi.org/10.26754/ojs_titivillus/titivillus.201603137.

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Manuel José Pedraza Gracia = Incunabula universitatis: los incunables de las bibliotecas universitarias españolas. Edición a cargo de Ramón Rodríguez Álvarez. Oviedo, Universidad de Oviedo, 2015. 313 p. ISBN: 978-84-16046-82-9. Maria Gioia Tavoni = Atti del convegno Incunabula. Printing, Trading, Collecting, Cataloguing, 10-12 settembre 2013, La Bibliofilia, 116, n. 1/3 (2014). ISSN 0006-0941. Nicolás Bas Martín = Rosa M. GREGORI ROIG, La impressora Jerònima Galés i els Mey (València, segle XVI), Valencia, Biblioteca Valenciana, 2012. 611 p. ISBN 978-84-482-5722-4. Nicolás Bas Martín = Juan GOMIS COLOMA, Menudencias de imprenta. Producción y circulación de la literatura popular (Valencia, siglo XVIII), Valencia, Institució Alfons el Magnànim, 2015. 557 p. ISBN 978-84-7822-2015. Antonio Carpallo Bautista = José Luis GONZALO SÁNCHEZ-MOLERO, Leyendo a Edo. Madrid, Consejo Superior de Investigaciones Científicas, 2013, 163 p. ISBN: 978-84-00-09660-1.
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Dey, Nandini, Yuliang Sun, Jennifer Carlson, Lori Friedman, Pradip De, and Brian Leyland-Jones. "A combination of dual PI3K-mTOR inhibitor, GDC-0980, with PARP inhibitor plus carboplatin blocked tumor growth of BRCA-competent triple-negative breast cancer cells." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 2613. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2613.

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2613 Background: PARP is a promising target in the TNBC. The PI3K pathway, in addition to its pro-proliferative effects on tumor cells, also controls the repair of DSB (Kumar, 2010; Friedman, 2009; Juvekar, 2012; Ibrahim, 2012). We hypothesize that the growth of TNBC tumor will be blocked due to the inhibition of (1) HR / NHEJ, and (2) PI3K-mTOR pathway mediated survival signals following GDC-0980 (G), when combined with PARP inhibitor (impaired DNA-SSB-repair), and carboplatin (C) (increased DNA-DSB). Methods: We tested the in vivo efficacy of a combination of G with ABT888 (A) plus C in BRCA-competent TNBC cells, and compared the triple combination arm (A+C+G) with a combination arm of A+C+ pan PI3K inhibitor GDC-0941 in mice xenograft (MDA-MB231) model. Mechanistically, we tested, (1) cell survival/ proliferation (5-7 BRCA-wt and mutant cell lines) using MTT assay, CelltiterGLO, and cell cycle analyses, (2) anchorage independent and dependent clonogenic growth (3D ON-TOP and soft-agar assay), (3) apoptosis, and (4) cell signaling marker(s). Results: (1) G alone decreased the tumor growth by 40-50%. (2) The G + A + C combination blocked the growth of established tumors by 90% as compared to control(s). (3) Interestingly, G + A + C combination had markedly higher percentage of inhibition of tumor growth than the inhibition observed in the A+C+GDC-0941 arm (36%). (4) G treatment time-dependently increased cl-caspase 3, 9, and cl-PARP and increased AnnexinV positivity both time (24 and 48 hrs) and dose dependently (50 and 200 nM) in cells. (5) G when combined with A+C was most effective in inducing apoptosis in PIK3CA-mutated BT20 cells. (6) The triple combination (50 nM G+10 μM A + 10 μM C) inhibited clonogenic growth of MDA-MB231, MDA-MB468 and BT20 cells. (7)Treatment of G decreased downstream effectors of PI3K-mTOR pathway, pAKTS473, pP70S6K and pS6RP. Conclusions: Tumor growth of BRCA-competent TNBC cells is blocked by a combination treatment of G with A+C. The profound anti-tumor effect of this triple combination can be explained by the anti-proliferative and pro-apoptotic actions of the drugs. The combination of G with A+C merits further investigation in TNBC.
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Murahashi, Satoshi, Takashi Akiyoshi, Takeshi Sano, Yosuke Fukunaga, Tetsuo Noda, Masashi Ueno, and Hitoshi Zembutsu. "Serial circulating tumour DNA analysis for locally advanced rectal cancer treated with preoperative therapy: prediction of pathological response and postoperative recurrence." British Journal of Cancer 123, no. 5 (June 22, 2020): 803–10. http://dx.doi.org/10.1038/s41416-020-0941-4.

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Books on the topic "379.2/4/0941"

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Vulpetti, Giovanni, Les Johnson, and Gregory L. Matloff. Solar Sails. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-0941-4.

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Reflecting on Literacy in Education (Master Classes in Education Series). RoutledgeFalmer, 2000.

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Reflecting on Literacy in Education (Master Classes in Education Series). RoutledgeFalmer, 2000.

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Reflecting on Literacy in Education. Routledge, 2000.

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The religion of humanity: The impact of Comtean positivism on Victorian Britain. Cambridge [Cambridgeshire]: Cambridge University Press, 1986.

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Patriotism: The Making and Unmaking of British National Identity : History and Politics (History Workshop Series). Routledge Kegan & Paul, 1989.

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Book chapters on the topic "379.2/4/0941"

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Carter, Roger. "Computers." In Students' Guide to Information Technology, 14–47. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-7506-0941-8.50006-4.

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Madkour, M. Monir. "Overview." In Brucellosis, 71–89. Elsevier, 1989. http://dx.doi.org/10.1016/b978-0-7236-0941-4.50013-4.

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Roux, J. "Brucella vaccines in humans." In Brucellosis, 244–49. Elsevier, 1989. http://dx.doi.org/10.1016/b978-0-7236-0941-4.50027-4.

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Nicoletti, P. "Control, eradication and prevention." In Brucellosis, 270–79. Elsevier, 1989. http://dx.doi.org/10.1016/b978-0-7236-0941-4.50030-4.

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Conference papers on the topic "379.2/4/0941"

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Adam, Moritz, Heather J. Andres, and Kira Rehfeld. "The role of dynamic sea ice in a simplified general circulation model used for palaeoclimate studies." In VI ECCOMAS Young Investigators Conference. València: Editorial Universitat Politècnica de València, 2021. http://dx.doi.org/10.4995/yic2021.2021.12383.

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AbstractObservational records provide a strong basis for constraining sea ice models within a narrow range of climate conditions. Given current trends away from these conditions, models need to be tested over a wider range of climate states. The past provides many such examples based on paleoclimate data, including abrupt tipping points. However, the millennial-duration of typical paleoclimatesimulations necessitates balancing the inclusion and sophistication of model processes against computational cost. We investigate the impact on climate mean states and variability of introducing sea ice dynamics into the simplified general circulation model PlaSim-LSG [1-3].Considering the technical constraints of PlaSim-LSG, we choose to integrate a modied version of the MITgcm's dynamical sea ice component [4, 5] into the model setup. We adapt the component to the structure and parallelization scheme of PlaSim-LSG, validate the physical consistency and stability of the component, and evaluate the impact of sea ice dynamics onto the simulated climate from decadal to millennial time scales. Specifically, we compare climatologies, variability and scaling of the extended model to control simulations of the preexisting setups, and quantify how additional sea ice dynamics affect well-known climatic biases of the PlaSim model family.With our extended PlaSim-LSG model we aim at capturing the key small-scale sea ice processes that are important to past climate tipping points while maintaining model efficiency for millennial simulations. Sea ice is a key component of coupled atmosphere-ocean processes that led to large-amplitude, abrupt climate variability in the past [6-8]. Therefore, the extended model can be usedto investigate the role of sea ice for such oscillations. This facilitates the understanding of processes that lead to current mismatches between palaeoclimate data and simulations, and that impact thesimulated surface climate variability [9].References[1] K. Fraedrich et al. Meteorol. Z. 14.3 (2005), 299-304. doi: 10.1127/0941-2948/2005/0043.[2] F. Lunkeit et al. Tech. rep. 2011. url: https://www.mi.uni-hamburg.de/en/arbeitsgruppen/theoretische-meteorologie/modelle/sources/psreferencemanual-1.pdf.[3] H. J. Andres et al. Clim. Past 15.4 (2019), 1621-1646. doi: 10.5194/cp-15-1621-2019.[4] J. Zhang et al. J. Geophys. Res. 102.4 (1997), 412-415.[5] M. Losch et al. Ocean Model. 33.1-2 (2010), 129-144. doi: 10.1016/j.ocemod.2009.12.008.[6] T. M. Dokken et al. Paleoceanography 28.3 (2013), 491-502. doi: 10.1002/palo.20042.[7] G. Vettoretti et al. Geophys. Res. Lett. 43.10 (2016), 5336-5344. doi: 10.1002/2016GL068891.[8] C. Li et al. Quat. Sci. Rev. 203 (2019), 1-20. doi: 10.1016/j.quascirev.2018.10.031.[9] N. Weitzel et al. presented at Fall Meeting AGU. 2020. url: https://agu.confex.com/agu/fm20/webprogram/Paper739241.html.
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Daham, Basil, Hu Li, Gordon E. Andrews, Karl Ropkins, James E. Tate, and Margaret C. Bell. "Comparison of Real World Emissions in Urban Driving for Euro 1-4 Vehicles Using a PEMS." In SAE World Congress & Exhibition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2009. http://dx.doi.org/10.4271/2009-01-0941.

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Cawthorne, Christopher, Ian A. Wilson, Antonios Danikas, Natalie Burrows, Mark Radigois, Jamil Gregory, Alison Smigova, Muhammed Babar, and Kaye J. Williams. "Abstract 362: [18F]-FLT Positron Emission Tomography can be used to image the response of sensitive tumours to PI3-Kinase inhibition with the novel agent GDC-0941." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-362.

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Wallin, JJ, J. Guan, WW Prior, LB Lee, L. Ross, LD Belmont, H. Koeppen, M. Belvin, D. Sampath, and LS Friedman. "Abstract P4-07-01: The Class I Selective PI3K Inhibitor GDC-0941 Enhances the Efficacy of Docetaxel in Human Breast Cancer Models by Increasing the Rate of Apoptosis." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p4-07-01.

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