共查询到20条相似文献,搜索用时 46 毫秒
1.
Randomized phase 2 trial of erlotinib in combination with high‐dose celecoxib or placebo in patients with advanced non‐small cell lung cancer 下载免费PDF全文
Karen L. Reckamp MD Marianna Koczywas MD Mihaela C. Cristea MD Jonathan E. Dowell MD He‐Jing Wang PhD Brian K. Gardner PhD Ginger L. Milne PhD Robert A. Figlin MD Michael C. Fishbein MD Robert M. Elashoff PhD Steven M. Dubinett MD 《Cancer》2015,121(18):3298-3306
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Diagnostic and prognostic value of preoperative combined GFAP,IGFBP‐2, and YKL‐40 plasma levels in patients with glioblastoma 下载免费PDF全文
Jaime Gállego Pérez‐Larraya MD PhD Sophie Paris MSc Ahmed Idbaih MD PhD Caroline Dehais MD Florence Laigle‐Donadey MD Soledad Navarro MD Laurent Capelle MD Karima Mokhtari MD Yannick Marie MSc Marc Sanson MD PhD Khê Hoang‐Xuan MD PhD Jean‐Yves Delattre MD Alain Mallet MD 《Cancer》2014,120(24):3972-3980
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Hirotaka Fukasawa Tatsuo Yamamoto Yoshihide Fujigaki Taro Misaki Naro Ohashi Tatsuya Takayama Sayuri Suzuki Soichi Mugiya Toshiaki Oda Chiharu Uchida Kyoko Kitagawa Takayuki Hattori Hidetoshi Hayashi Seiichiro Ozono Masatoshi Kitagawa Akira Hishida 《International journal of cancer. Journal international du cancer》2010,127(7):1517-1525
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Aldo‐keto reductases‐mediated cytotoxicity of 2‐deoxyglucose: A novel anticancer mechanism 下载免费PDF全文
Shi‐Qing Zhang Kin‐Lam Ken Yung Sookja Kim Chung Sum‐Man Stephen Chung 《Cancer science》2018,109(6):1970-1980
2‐Deoxyglucose (2DG) is a non‐metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. It is thought to preferentially kill cancer cells by inhibiting glycolysis because cancer cells are more dependent on glycolysis for their energy needs than normal cells. However, we found that the toxicity of 2DG in cancer cells is mediated by the enzymatic activities of AKR1B1 and/or AKR1B10 (AKR1Bs), which are often overexpressed in cancer cells. Our results show that 2DG kills cancer cells because, in the process of being reduced by AKR1Bs, depletion of their cofactor NADPH leads to the depletion of glutathione (GSH) and cell death. Furthermore, we showed that compounds that are better substrates for AKR1Bs than 2DG are more effective than 2DG in killing cancer cells that overexpressed these 2 enzymes. As cancer cells can be induced to overexpress AKR1Bs, the anticancer mechanism we identified can be applied to treat a large variety of cancers. This should greatly facilitate the development of novel anticancer drugs. 相似文献
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Impact of oncogene rearrangement patterns on outcomes in patients with double‐hit non‐Hodgkin lymphoma 下载免费PDF全文
Daniel J. Landsburg MD Adam M. Petrich MD Jeremy S. Abramson MD MMSc Aliyah R. Sohani MD Oliver Press MD PhD Ryan Cassaday MD Julio C. Chavez MD Kevin Song MD Andrew D. Zelenetz MD Mitul Gandhi MD Namrata Shah MD Timothy S. Fenske MD Jesse Jaso MD L. Jeffrey Medeiros MD David T. Yang MD Chadi Nabhan MD 《Cancer》2016,122(4):559-564
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Yasuhiro Yoshimatsu Ikumi Wakabayashi Shiori Kimuro Naoya Takahashi Kazuki Takahashi Miho Kobayashi Nako Maishi Katarzyna A. Podyma‐Inoue Kyoko Hida Kohei Miyazono Tetsuro Watabe 《Cancer science》2020,111(7):2385-2399
The tumor microenvironment (TME) consists of various components including cancer cells, tumor vessels, cancer‐associated fibroblasts (CAFs), and inflammatory cells. These components interact with each other via various cytokines, which often induce tumor progression. Thus, a greater understanding of TME networks is crucial for the development of novel cancer therapies. Many cancer types express high levels of TGF‐β, which induces endothelial‐to‐mesenchymal transition (EndMT), leading to formation of CAFs. Although we previously reported that CAFs derived from EndMT promoted tumor formation, the molecular mechanisms underlying these interactions remain to be elucidated. Furthermore, tumor‐infiltrating inflammatory cells secrete various cytokines, including TNF‐α. However, the role of TNF‐α in TGF‐β‐induced EndMT has not been fully elucidated. Therefore, this study examined the effect of TNF‐α on TGF‐β‐induced EndMT in human endothelial cells (ECs). Various types of human ECs underwent EndMT in response to TGF‐β and TNF‐α, which was accompanied by increased and decreased expression of mesenchymal cell and EC markers, respectively. In addition, treatment of ECs with TGF‐β and TNF‐α exhibited sustained activation of Smad2/3 signals, which was presumably induced by elevated expression of TGF‐β type I receptor, TGF‐β2, activin A, and integrin αv, suggesting that TNF‐α enhanced TGF‐β‐induced EndMT by augmenting TGF‐β family signals. Furthermore, oral squamous cell carcinoma‐derived cells underwent epithelial‐to‐mesenchymal transition (EMT) in response to humoral factors produced by TGF‐β and TNF‐α‐cultured ECs. This EndMT‐driven EMT was blocked by inhibiting the action of TGF‐βs. Collectively, our findings suggest that TNF‐α enhances TGF‐β‐dependent EndMT, which contributes to tumor progression. 相似文献
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Long‐term outcome of dasatinib first‐line treatment in gastrointestinal stromal tumor: A multicenter, 2‐stage phase 2 trial (Swiss Group for Clinical Cancer Research 56/07) 下载免费PDF全文
Michael Montemurro MD Angela Cioffi MD Julien Dômont MD Piotr Rutkowski MD Arnaud D. Roth MD Roger von Moos MD Roman Inauen MD Maud Toulmonde MD Roger O. Burkhard MD Claudio Knuesli MD Sebastian Bauer MD Philippe Cassier MD Heike Schwarb MD Axel Le Cesne MD Dieter Koeberle MD Daniela Bärtschi CPM Daniel Dietrich Statistician Christine Biaggi CPM John Prior MD Serge Leyvraz MD 《Cancer》2018,124(7):1449-1454
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Andrea A. Martoni MD Claudio Zamagni MD Sara Quercia MD Marta Rosati MD Nicoletta Cacciari MD Alessandra Bernardi MD Alessandra Musto MD Stefano Fanti MD Donatella Santini MD Mario Taffurelli MD 《Cancer》2010,116(4):805-813
BACKGROUND:
A pathologic complete response (pCR) and minimal residual disease (pMRD) after preoperative chemotherapy (PCT) for early stage or locally advanced breast cancer (BC) correlates with a good prognosis.METHODS:
Patients who received from 6 to 8 cycles of PCT for BC were monitored by 18F‐2‐fluoro‐2‐deoxy‐D‐glucose positron emission tomography (18F‐FDG‐PET), and the maximal standardized uptake value (SUVmax) was calculated at baseline, after 2 cycles, after 4 cycles, and at the end of PCT. SUVmax percentage changes (Δ‐SUV) were compared with the pathologic response rate. Patients who had a pCR or pMRD in the tumor and an absence of cancer cells in ipsilateral axillary lymph nodes were defined as having obtained an optimal pathologic response (pR), whereas all the other conditions were classified as a pathologic nonresponse (pNR).RESULTS:
Of 34 patients, 7 (21%) achieved a pR (3 patients had a pCR, and 4 patients had pMRD). After the second cycle, the Δ‐SUV threshold with optimal negative predictive value to predict a pR was 50%. Twenty‐six patients (76%) had a Δ‐SUV >50%, including all 7 patients who had a pR and 19 patients who had a pNR. Conversely, all 8 patients who had a Δ‐SUV ≤50% had a pNR. All 8 of those patients had estrogen recepetor‐positive tumors.CONCLUSIONS:
Early evaluation of metabolic response by 18F‐FDG‐PET during PCT was able to identify 30% of patients, all with estrogen receptor‐positive tumors, who would not obtain pR after completion of chemotherapy program. Cancer 2010. © 2010 American Cancer Society. 相似文献12.
Long‐term safety and activity of cladribine in patients with extranodal B‐cell marginal zone lymphoma of the mucosa‐associated lymphoid tissue (MALT) lymphoma 下载免费PDF全文
Barbara Kiesewetter Werner Dolak Ingrid Simonitsch‐Klupp Marius E. Mayerhoefer Markus Raderer 《Hematological oncology》2017,35(2):177-186
The purine analogue 2‐chloro‐deoxyadenosine (2‐CDA, cladribine) +/? rituximab has been successfully tested in mucosa‐associated lymphoid tissue lymphoma (MALT lymphoma) patients. However, studies using cladribine in other indications have reported the potential for prolonged hematological side effects and secondary hematologic and non‐hematologic malignancies. To date, there have been no data on long‐term effects of cladribine in MALT lymphoma patients. We have analyzed a large number of 49 patients treated with cladribine at our institution 1997–2011. All patients were treated within clinical trials and had undergone a standardized follow‐up protocol minimizing a potential bias in the detection of late sequels and relapses. After a median follow‐up time of 61 months (interquartile range: 43–72) for 49 analyzed patients, 35 (71%) are alive, while 14 (29%) have died. In the entire collective, three cases (6%) of prolonged pancytopenia including manifest myelodysplastic syndrome in one patient (2%), three cases (6%) of secondary lymphoid malignancies, and five cases (10%) of non‐hematologic cancers were documented. In terms of outcome, 42/49 (86%) patients responded to cladribine‐containing treatment, and only 10/42 (24%) responding patients needed further treatment after a median time to progression of 14 months (interquartile range, 8–34). Currently, 25/35 (71%) patients being alive are in ongoing complete remission and 2/35 (6%) in ongoing stable disease, respectively. Eight patients (23%) are free of lymphoma after second‐line therapy, with the median overall survival not having been reached. Our data suggest that cladribine might be safely applied in patients with MALT lymphoma, also in terms of long‐term toxicities. These data also confirm the potential of cladribine to induce durable remissions. Copyright © 2015 John Wiley & Sons, Ltd. 相似文献
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Yi‐Chih Kuo Cheng‐Hsi Su Chin‐Yi Liu Tien‐Hua Chen Chie‐Pein Chen Hwai‐Shi Wang 《International journal of cancer. Journal international du cancer》2009,124(11):2568-2576
CD44, a transmembrane receptor for hyaluronic acid, is implicated in various adhesion‐dependent cellular processes, including cell migration, tumor cell metastasis and invasion. Recent studies demonstrated that CD44 expressed in cancer cells can be proteolytically cleaved at the ectodomain by membrane type 1‐matrix metalloproteinase (MT1‐MMP) to form soluble CD44 and that CD44 cleavage plays a critical role in cancer cell migration. Here, we show that transforming growth factor‐β (TGF‐β), a multifunctional cytokine involved in cell proliferation, differentiation, migration and pathological processes, induces MT1‐MMP expression in MDA‐MB‐435s cells. TGF‐β‐induced MT1‐MMP expression was blocked by the specific extracellular regulated kinase‐1/2 (ERK1/2) inhibitor PD98059 and the specific phosphoinositide 3‐OH kinase (PI3K) inhibitor LY294002. In addition, treatment with SP600125, an inhibitor for c‐Jun NH2‐terminal kinase (JNK), resulted in a significant inhibition of MT1‐MMP production. These data suggest that ERK1/2, PI3K, and JNK likely play a role in TGF‐β‐induced MT1‐MMP expression. Interestingly, treatment of MDA‐MB‐435s cells with TGF‐β resulted in a colocalization of MT1‐MMP and CD44 in the cell membrane and in an increased level of soluble CD44. Using an electric cell‐substrate impedance sensing cell‐electrode system, we demonstrated that TGF‐β treatment promotes MDA‐MB‐435s cell migration, involving MT1‐MMP‐mediated CD44 cleavage. MT1‐MMP siRNA transfection‐inhibited TGF‐β‐induced cancer cell transendothelial migration. Thus, this study contributes to our understanding of molecular mechanisms that play a critical role in tumor cell invasion and metastasis. © 2009 Wiley‐Liss, Inc. 相似文献
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Methylation status of HPV16 E2‐binding sites classifies subtypes of HPV‐associated oropharyngeal cancers 下载免费PDF全文
Justo Lorenzo Bermejo PhD Martin S. Kalteis Simon F. Preuss MD Inga M.C. Seuthe Jutta Kolligs Dipl.‐Ing Ernst‐Jan M. Speel PhD Nadine Olthof PhD Bernd Kremer MD Steffen Wagner PhD Jens P. Klussmann MD Magnus von Knebel Doeberitz MD 《Cancer》2015,121(12):1966-1976
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Nicole Simonavicius Katja Honert Sandra Schäfer Ute Reuning Mathias Heikenwalder Bernard Mari Achim Krüger 《International journal of cancer. Journal international du cancer》2015,136(10):2304-2315
The tetraspanin CD63 is implicated in pro‐metastatic signaling pathways but, so far, it is unclear, how CD63 levels affect the tumor cell phenotype. Here, we investigated the effect of CD63 modulation in different metastatic tumor cell lines. In vitro, knock down of CD63 induced a more epithelial‐like phenotype concomitant with increased E‐cadherin expression, downregulation of its repressors Slug and Zeb1, and decreased N‐cadherin. In addition, β‐catenin protein was markedly reduced, negatively affecting expression of the target genes MMP‐2 and PAI‐1. β‐catenin inhibitors mimicked the epithelial phenotype induced by CD63 knock down. Inhibition of β‐catenin upstream regulators PI3K/AKT or GSK3β could rescue the mesenchymal phenotype underlining the importance of the β‐catenin pathway in CD63‐regulated cell plasticity. CD63 knock down‐induced phenotypical changes correlated with a decrease of experimental metastasis whereas CD63 overexpression enhanced the tumor cell‐intrinsic metastatic potential. Taken together, our data show that CD63 is a crucial player in the regulation of the tumor cell‐intrinsic metastatic potential by affecting cell plasticity. 相似文献
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Patient‐reported quality‐of‐life outcomes after de‐escalated chemoradiation for human papillomavirus‐positive oropharyngeal carcinoma: Findings from a phase 2 trial 下载免费PDF全文
John V. Hegde MD Narek Shaverdian MD Megan E. Daly MD Carol Felix BS Deborah L. Wong MD PhD Michael H. Rosove MD Jordan H. Garst BS Pin‐Chieh Wang PhD Darlene Veruttipong MPH Shyam Rao MD PhD Ruben C. Fragoso MD PhD Jonathan W. Riess MD Michael L. Steinberg MD Allen M. Chen MD 《Cancer》2018,124(3):521-529
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Evan M. Hersh MD Steven J. O'Day MD Antoni Ribas MD Wolfram E. Samlowski MD Michael S. Gordon MD Deganit E. Shechter MS Alicia A. Clawson MS Rene Gonzalez MD 《Cancer》2010,116(1):155-163
BACKGROUND:
nab‐Paclitaxel (ABI‐007, Abraxane), a 130‐nM, albumin‐bound (nab) particle form of Cremophor‐free paclitaxel, is approved for metastatic breast cancer. In the current study, the efficacy and safety of nab‐paclitaxel were evaluated in previously treated and chemotherapy‐naive patients with metastatic melanoma (MM).METHODS:
Patients with histologically or cytologically confirmed, measurable MM were enrolled. nab‐Paclitaxel was administered intravenously weekly for 3 of 4 weeks at a dose of 100 mg/m2 (in previously treated patients) or 150 mg/m2 (in chemotherapy‐naive patients).RESULTS:
Thirty‐seven patients were treated in each cohort. The response rate was 2.7% in the previously treated cohort and 21.6% in the chemotherapy‐naive cohort; the response plus stable disease rate was 37.8% and 48.6% in the previously treated and chemotherapy‐naive cohorts, respectively. The median progression‐free survival (PFS) was 3.5 months and 4.5 months, and the median survival was 12.1 months and 9.6 months, respectively. The probability of being alive and free of disease progression at 6 months was 27% for the previously treated cohort and 34% for the chemotherapy‐naive cohort; the probability of surviving 1 year was 49% and 41%, respectively, for the previously treated and chemotherapy‐naive cohorts. Approximately 78% of the previously treated patients and 49% of the chemotherapy‐naive patients were treated without dose reduction. Eight (22%) chemotherapy‐naive patients discontinued therapy because of toxicities. Drug‐related toxicities included grade 3 to 4 (graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events [version 3.0]) neuropathy, alopecia, neutropenia, and fatigue.CONCLUSIONS:
nab‐Paclitaxel was found to be well tolerated and demonstrated activity in both previously treated and chemotherapy‐naive patients with MM. The response rate, PFS, and survival compared favorably with current standard dacarbazine therapy and combination therapies for melanoma. nab‐Paclitaxel therapy of MM should be investigated further in controlled clinical trials. Cancer 2010. © 2010 American Cancer Society. 相似文献18.
Matrix metalloproteinase (MMP)‐9 activity is controlled by the balance between MMP‐9 and its major tissue inhibitor of metalloproteinases (TIMPs). We hypothesised whether Candida proteinases may affect local tissue inflammatory processes by modifying these molecules. The effects of sonicated cells and concentrated growth media of six Candida species on MMP‐9, TIMP‐1 and TIMP‐2 were tested. Incubated samples were analysed by Western blot and detected by enhanced chemoluminescence techniques. The residual activity of degraded TIMP‐1 was evaluated by a casein degradation assay. The proteinase activity of the microbial strains was also assessed by a fluorimetric assay, and the action of inhibitors on MMP‐14 and Candida parapsilosis Cp2 was demonstrated. Cell fractions of both strains of C. parapsilosis exerted a weak ability to convert 92‐kDa proMMP‐9 to 86‐kDa active form. Cell fractions of both strains of Candida albicans, C. parapsilosis Cp2, Candida glabrata reference strain, and both strains of Candida krusei fragmented TIMP‐1 (28 kDa) to a 24‐kDa species, which associated with reduced inhibitory activity on MMP‐9 caseinolysis. Our findings indicate that Candida can participate in tissue inflammation by modifying the host’s MMP‐9 and their inhibitors. A rapid fluorimetric assay can be adapted for Candida proteinases. 相似文献
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Combined treatment with chrysin and 1,2,3,4,6‐penta‐O‐galloyl‐β‐D‐glucose synergistically inhibits LRP6 and Skp2 activation in triple‐negative breast cancer and xenografts 下载免费PDF全文
Cheng Huang Yi Jing Chen Wei‐Jen Chen Chih‐Li Lin Yu Xuan Wei Hsiu Chen Huang 《Molecular carcinogenesis》2015,54(12):1613-1625
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Prognostic value of 18F‐fluoroazomycin arabinoside PET/CT in patients with advanced non‐small‐cell lung cancer 下载免费PDF全文
Tsuneo Saga Masayuki Inubushi Mitsuru Koizumi Kyosan Yoshikawa Ming‐Rong Zhang Katsuyuki Tanimoto Atsushi Horiike Noriko Yanagitani Fumiyoshi Ohyanagi Makoto Nishio 《Cancer science》2015,106(11):1554-1560
This study evaluated the prognostic value of positron emission tomography/computed tomography (PET/CT) using 18F‐fluoroazomycin arabinoside (FAZA) in patients with advanced non‐small‐cell lung cancer (NSCLC) compared with 18F‐fluorodeoxyglucose (FDG). Thirty‐eight patients with advanced NSCLC (stage III, 23 patients; stage IV, 15 patients) underwent FAZA and FDG PET/CT before treatment. The PET parameters (tumor‐to‐muscle ratio [T/M] at 1 and 2 h for FAZA, maximum standardized uptake value for FDG) in the primary lesion and lymph node (LN) metastasis and clinical parameters were compared concerning their effects on progression‐free survival (PFS) and overall survival (OS). In our univariate analysis of all patients, clinical stage and FAZA T/M in LNs at 1 and 2 h were predictive of PFS (P = 0.021, 0.028, and 0.002, respectively). Multivariate analysis also indicated that clinical stage and FAZA T/M in LNs at 1 and 2 h were independent predictors of PFS. Subgroup analysis of chemoradiotherapy‐treated stage III patients revealed that only FAZA T/M in LNs at 2 h was predictive of PFS (P = 0.025). The FDG PET/CT parameters were not predictive of PFS. No parameter was a significant predictor of OS. In patients with advanced NSCLC, FAZA uptake in LNs, but not in primary lesions, was predictive of treatment outcome. These results suggest the importance of characterization of LN metastases in advanced NSCLC patients. 相似文献