Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Abstract: Small cell lung cancer (SCLC) patient-derived xenografts (PDX) can be generated from biopsies or circulating tumor cells (CTC), though scarcity of tissue and low efficiency of tumor growth have previously limited these approaches. Applying an established clinical-translational pipeline for tissue collection and an automated microfluidic platform for CTC enrichment, we generated 17 biopsy-derived PDXs and 17 CTC-derived PDXs in a 2-year timeframe, at 89% and 38% efficiency, respectively. Whole-exome sequencing showed that somatic alterations are stably maintained between patient tumors and PDXs. Early-passage PDXs maintain the genomic and transcriptional profiles of the founder PDX. In vivo treatment with etoposide and platinum (EP) in 30 PDX models demonstrated greater sensitivity in PDXs from EP-naive patients, and resistance to EP corresponded to increased expression of a MYC gene signature. Finally, serial CTC-derived PDXs generated from an individual patient at multiple time points accurately recapitulated the evolving drug sensitivities of that patient's disease. Collectively, this work highlights the translational potential of this strategy.Significance: Effective translational research utilizing SCLC PDX models requires both efficient generation of models from patients and fidelity of those models in representing patient tumor characteristics. We present approaches for efficient generation of PDXs from both biopsies and CTCs, and demonstrate that these models capture the mutational landscape and functional features of the donor tumors. Cancer Discov; 8(5); 600-15. (c)2018 AACR.This article is highlighted in the In This Issue feature, p. 517.
    Type of Publication: Journal article published
    PubMed ID: 29483136
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2018-01-03
    Description: Human tumor growth depends on rapidly dividing cancer cells driving population expansion. Even advanced tumors, however, contain slowly proliferating cancer cells for reasons that remain unclear. Here, we selectively disrupt the ability of rapidly proliferating cancer cells to spawn AKT1 low daughter cells that are rare, slowly proliferating, tumor-initiating, and chemotherapy-resistant, using β1-integrin activation and the AKT1-E17K–mutant oncoprotein as experimental tools in vivo . Surprisingly, we find that selective depletion of AKT1 low slow proliferators actually reduces the growth of a molecularly diverse panel of human cancer cell xenograft models without globally altering cell proliferation or survival in vivo . Moreover, we find that unusual cancer patients with AKT1-E17K–mutant solid tumors also fail to produce AKT1 low quiescent cancer cells and that this correlates with significantly prolonged survival after adjuvant treatment compared with other patients. These findings support a model whereby human solid tumor growth depends on not only rapidly proliferating cancer cells but also on the continuous production of AKT1 low slow proliferators. Mol Cancer Ther; 17(1); 254–63. ©2017 AACR .
    Print ISSN: 1535-7163
    Electronic ISSN: 1538-8514
    Topics: Medicine
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2014-11-20
    Description: Broad and deep tumour genome sequencing has shed new light on tumour heterogeneity and provided important insights into the evolution of metastases arising from different clones. There is an additional layer of complexity, in that tumour evolution may be influenced by selective pressure provided by therapy, in a similar fashion to that occurring in infectious diseases. Here we studied tumour genomic evolution in a patient (index patient) with metastatic breast cancer bearing an activating PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha, PI(3)Kalpha) mutation. The patient was treated with the PI(3)Kalpha inhibitor BYL719, which achieved a lasting clinical response, but the patient eventually became resistant to this drug (emergence of lung metastases) and died shortly thereafter. A rapid autopsy was performed and material from a total of 14 metastatic sites was collected and sequenced. All metastatic lesions, when compared to the pre-treatment tumour, had a copy loss of PTEN (phosphatase and tensin homolog) and those lesions that became refractory to BYL719 had additional and different PTEN genetic alterations, resulting in the loss of PTEN expression. To put these results in context, we examined six other patients also treated with BYL719. Acquired bi-allelic loss of PTEN was found in one of these patients, whereas in two others PIK3CA mutations present in the primary tumour were no longer detected at the time of progression. To characterize our findings functionally, we examined the effects of PTEN knockdown in several preclinical models (both in cell lines intrinsically sensitive to BYL719 and in PTEN-null xenografts derived from our index patient), which we found resulted in resistance to BYL719, whereas simultaneous PI(3)K p110beta blockade reverted this resistance phenotype. We conclude that parallel genetic evolution of separate metastatic sites with different PTEN genomic alterations leads to a convergent PTEN-null phenotype resistant to PI(3)Kalpha inhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326538/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326538/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Juric, Dejan -- Castel, Pau -- Griffith, Malachi -- Griffith, Obi L -- Won, Helen H -- Ellis, Haley -- Ebbesen, Saya H -- Ainscough, Benjamin J -- Ramu, Avinash -- Iyer, Gopa -- Shah, Ronak H -- Huynh, Tiffany -- Mino-Kenudson, Mari -- Sgroi, Dennis -- Isakoff, Steven -- Thabet, Ashraf -- Elamine, Leila -- Solit, David B -- Lowe, Scott W -- Quadt, Cornelia -- Peters, Malte -- Derti, Adnan -- Schegel, Robert -- Huang, Alan -- Mardis, Elaine R -- Berger, Michael F -- Baselga, Jose -- Scaltriti, Maurizio -- CA105388/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- T32 CA-71345-15/CA/NCI NIH HHS/ -- T32 CA071345/CA/NCI NIH HHS/ -- T32 GM065094/GM/NIGMS NIH HHS/ -- U01 CA168409/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Feb 12;518(7538):240-4. doi: 10.1038/nature13948. Epub 2014 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, 55 Fruit Street, Boston, Massachusetts 02114, USA. ; Human Oncology and Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA. ; 1] Department of Genetics, Washington University School of Medicine, 4566 Scott Avenue, St Louis, Missouri 63110, USA [2] Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA [3] The Genome Institute, Washington University School of Medicine, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. ; 1] Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA [2] The Genome Institute, Washington University School of Medicine, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA [3] Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA. ; 1] Human Oncology and Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA [2] Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA. ; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA. ; The Genome Institute, Washington University School of Medicine, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. ; 1] Human Oncology and Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA [2] Division of Genitourinary Oncology, Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA. ; 1] Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA [2] Howard Hughes Medical Institute, Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA. ; Novartis Pharma AG, Forum 1, Novartis Campus, CH-4056 Basel, Switzerland. ; Oncology Translational Medicine, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA. ; 1] Department of Genetics, Washington University School of Medicine, 4566 Scott Avenue, St Louis, Missouri 63110, USA [2] Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA [3] The Genome Institute, Washington University School of Medicine, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA [4] Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA. ; 1] Human Oncology and Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA [2] Breast Medicine Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409150" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Breast Neoplasms/*drug therapy/*genetics/metabolism/pathology ; Drug Resistance, Neoplasm/drug effects/*genetics ; Female ; Humans ; Loss of Heterozygosity/drug effects/genetics ; Mice ; Mice, Nude ; PTEN Phosphohydrolase/*deficiency/*genetics/metabolism ; Phosphatidylinositol 3-Kinases/*antagonists & inhibitors ; Thiazoles/*pharmacology/therapeutic use ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2012-06-23
    Description: How adult tissue stem and niche cells respond to the nutritional state of an organism is not well understood. Here we find that Paneth cells, a key constituent of the mammalian intestinal stem-cell (ISC) niche, augment stem-cell function in response to calorie restriction. Calorie restriction acts by reducing mechanistic target of rapamycin complex 1 (mTORC1) signalling in Paneth cells, and the ISC-enhancing effects of calorie restriction can be mimicked by rapamycin. Calorie intake regulates mTORC1 in Paneth cells, but not ISCs, and forced activation of mTORC1 in Paneth cells during calorie restriction abolishes the ISC-augmenting effects of the niche. Finally, increased expression of bone stromal antigen 1 (Bst1) in Paneth cells-an ectoenzyme that produces the paracrine factor cyclic ADP ribose-mediates the effects of calorie restriction and rapamycin on ISC function. Our findings establish that mTORC1 non-cell-autonomously regulates stem-cell self-renewal, and highlight a significant role of the mammalian intestinal niche in coupling stem-cell function to organismal physiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387287/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387287/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yilmaz, Omer H -- Katajisto, Pekka -- Lamming, Dudley W -- Gultekin, Yetis -- Bauer-Rowe, Khristian E -- Sengupta, Shomit -- Birsoy, Kivanc -- Dursun, Abdulmetin -- Yilmaz, V Onur -- Selig, Martin -- Nielsen, G Petur -- Mino-Kenudson, Mari -- Zukerberg, Lawrence R -- Bhan, Atul K -- Deshpande, Vikram -- Sabatini, David M -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA103866/CA/NCI NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- T32CA09216/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 28;486(7404):490-5. doi: 10.1038/nature11163.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722868" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-ribosyl Cyclase/metabolism ; Animals ; Antigens, CD/metabolism ; Caloric Restriction ; Cell Count ; Cell Division/drug effects ; Cyclic ADP-Ribose/metabolism ; Energy Intake/*physiology ; Female ; GPI-Linked Proteins/agonists/metabolism ; Intestines/*cytology ; Longevity/physiology ; Male ; Mice ; Multiprotein Complexes ; Paneth Cells/*cytology/drug effects/*metabolism ; Paracrine Communication ; Proteins/antagonists & inhibitors/*metabolism ; Regeneration/drug effects ; Signal Transduction ; Sirolimus/pharmacology ; Stem Cell Niche/drug effects/*physiology ; Stem Cells/*cytology/drug effects/*metabolism ; TOR Serine-Threonine Kinases
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2011-07-16
    Description: Cancer cells adapt their metabolic processes to drive macromolecular biosynthesis for rapid cell growth and proliferation. RNA interference (RNAi)-based loss-of-function screening has proven powerful for the identification of new and interesting cancer targets, and recent studies have used this technology in vivo to identify novel tumour suppressor genes. Here we developed a method for identifying novel cancer targets via negative-selection RNAi screening using a human breast cancer xenograft model at an orthotopic site in the mouse. Using this method, we screened a set of metabolic genes associated with aggressive breast cancer and stemness to identify those required for in vivo tumorigenesis. Among the genes identified, phosphoglycerate dehydrogenase (PHGDH) is in a genomic region of recurrent copy number gain in breast cancer and PHGDH protein levels are elevated in 70% of oestrogen receptor (ER)-negative breast cancers. PHGDH catalyses the first step in the serine biosynthesis pathway, and breast cancer cells with high PHGDH expression have increased serine synthesis flux. Suppression of PHGDH in cell lines with elevated PHGDH expression, but not in those without, causes a strong decrease in cell proliferation and a reduction in serine synthesis. We find that PHGDH suppression does not affect intracellular serine levels, but causes a drop in the levels of alpha-ketoglutarate, another output of the pathway and a tricarboxylic acid (TCA) cycle intermediate. In cells with high PHGDH expression, the serine synthesis pathway contributes approximately 50% of the total anaplerotic flux of glutamine into the TCA cycle. These results reveal that certain breast cancers are dependent upon increased serine pathway flux caused by PHGDH overexpression and demonstrate the utility of in vivo negative-selection RNAi screens for finding potential anticancer targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353325/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Possemato, Richard -- Marks, Kevin M -- Shaul, Yoav D -- Pacold, Michael E -- Kim, Dohoon -- Birsoy, Kivanc -- Sethumadhavan, Shalini -- Woo, Hin-Koon -- Jang, Hyun G -- Jha, Abhishek K -- Chen, Walter W -- Barrett, Francesca G -- Stransky, Nicolas -- Tsun, Zhi-Yang -- Cowley, Glenn S -- Barretina, Jordi -- Kalaany, Nada Y -- Hsu, Peggy P -- Ottina, Kathleen -- Chan, Albert M -- Yuan, Bingbing -- Garraway, Levi A -- Root, David E -- Mino-Kenudson, Mari -- Brachtel, Elena F -- Driggers, Edward M -- Sabatini, David M -- CA103866/CA/NCI NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA103866-06A1/CA/NCI NIH HHS/ -- R01 CA103866-07/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-02/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Aug 18;476(7360):346-50. doi: 10.1038/nature10350.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21760589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/enzymology/*genetics/*metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation ; Citric Acid Cycle/physiology ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; *Genomics ; Glutamic Acid/metabolism ; Humans ; Ketoglutaric Acids/metabolism ; Melanoma/enzymology/genetics ; Mice ; Neoplasm Transplantation ; Phosphoglycerate Dehydrogenase/genetics/metabolism ; RNA Interference ; Serine/*biosynthesis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2014-11-15
    Description: Targeted cancer therapies have produced substantial clinical responses, but most tumors develop resistance to these drugs. Here, we describe a pharmacogenomic platform that facilitates rapid discovery of drug combinations that can overcome resistance. We established cell culture models derived from biopsy samples of lung cancer patients whose disease had progressed while on treatment with epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors and then subjected these cells to genetic analyses and a pharmacological screen. Multiple effective drug combinations were identified. For example, the combination of ALK and MAPK kinase (MEK) inhibitors was active in an ALK-positive resistant tumor that had developed a MAP2K1 activating mutation, and the combination of EGFR and fibroblast growth factor receptor (FGFR) inhibitors was active in an EGFR mutant resistant cancer with a mutation in FGFR3. Combined ALK and SRC (pp60c-src) inhibition was effective in several ALK-driven patient-derived models, a result not predicted by genetic analysis alone. With further refinements, this strategy could help direct therapeutic choices for individual patients.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388482/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crystal, Adam S -- Shaw, Alice T -- Sequist, Lecia V -- Friboulet, Luc -- Niederst, Matthew J -- Lockerman, Elizabeth L -- Frias, Rosa L -- Gainor, Justin F -- Amzallag, Arnaud -- Greninger, Patricia -- Lee, Dana -- Kalsy, Anuj -- Gomez-Caraballo, Maria -- Elamine, Leila -- Howe, Emily -- Hur, Wooyoung -- Lifshits, Eugene -- Robinson, Hayley E -- Katayama, Ryohei -- Faber, Anthony C -- Awad, Mark M -- Ramaswamy, Sridhar -- Mino-Kenudson, Mari -- Iafrate, A John -- Benes, Cyril H -- Engelman, Jeffrey A -- 086357/Wellcome Trust/United Kingdom -- 102696/Wellcome Trust/United Kingdom -- 1U54HG006097-01/HG/NHGRI NIH HHS/ -- P50 CA090578/CA/NCI NIH HHS/ -- P50CA090578/CA/NCI NIH HHS/ -- R01 CA137008/CA/NCI NIH HHS/ -- R01 CA164273/CA/NCI NIH HHS/ -- R01CA137008/CA/NCI NIH HHS/ -- R01CA164273/CA/NCI NIH HHS/ -- U54 HG006097/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1480-6. doi: 10.1126/science.1254721. Epub 2014 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Department of Medicine and Harvard Medical School, Boston, MA 02114, USA. ; Dana-Farber Cancer Institute, Department of Biological Chemistry and Molecular Pharmacology and Harvard Medical School, Boston, MA 02115, USA. Chemical Kinomics Research Center, Korea Institute of Science and Technology, Seoul, 136-791, South Korea. ; Massachusetts General Hospital Cancer Center, Department of Pathology and Harvard Medical School, Boston, MA 02114, USA. ; Massachusetts General Hospital Cancer Center, Department of Medicine and Harvard Medical School, Boston, MA 02114, USA. jengelman@partners.org cbenes@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25394791" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Combined Chemotherapy Protocols/*therapeutic use ; Carcinoma, Non-Small-Cell Lung/*drug therapy/enzymology/genetics ; DNA Mutational Analysis ; Drug Resistance, Neoplasm/*genetics ; Drug Screening Assays, Antitumor ; Enzyme Activation/genetics ; Humans ; Lung Neoplasms/*drug therapy/enzymology/genetics ; MAP Kinase Kinase 1/genetics/metabolism ; Molecular Targeted Therapy/*methods ; Mutation ; *Patient-Specific Modeling ; Protein Kinase Inhibitors/*therapeutic use ; Proto-Oncogene Proteins pp60(c-src)/antagonists & inhibitors ; Pyrimidines/therapeutic use ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 3/antagonists & inhibitors/genetics ; Sulfones/therapeutic use ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...