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Targeting the EGF receptor family in non-small cell lung cancerincreased complexity and future perspectives

cancer Biology & Medicine 2022年第11期19卷 1543-1564页

作者： Tobias Boch Jens Kohler Melanie Janning Sonja Loges dkfz-hector cancer institute at the university medical center Mannheim Mannheim 68135Germany Division of Personalized medical Oncology(A420) German Cancer Research Center(DKFZ)Heidelberg 69120Germany Department of Personalized Oncology University Medical Center MannheimMedical Faculty MannheimHeidelberg UniversityMannheim 68135Germany

Lung cancer remains the leading cause of cancer-associated mortality worldwide,but with the emergence of oncogene targeted therapies,treatment options have tremendously *** to their biological relevance,members of the ERBB receptor family,including the EGF receptor(EGFR),HER2,HER3 and HER4,are among the best studied oncogenic *** EGFR mutations are frequently observed in non-small cell lung cancer(NSCLC),and small molecule tyrosine kinase inhibitors(TKIs)are the established first line treatment option for patients whose tumors bear"typical/classical"EGFR mutations(exon 19 deletions,L858R point mutations).Additionally,new TKIs are rapidly evolving with better efficacy to overcome primary and secondary treatment resistance(e.g.,that due to T790M or C797S resistance mutations).Some atypical EGFR mutations,such as the most frequent exon 20 insertions,exhibit relative resistance to earlier generation TKIs through steric *** this subgroup,newer TKIs,such as mobocertinib and the bi-specific antibody amivantamab have recently been approved,whereas less frequent atypical EGFR mutations remain *** contrast to EGFR,HER2 has long remained a challenging target,but better structural understanding has led to the development of newer generations of *** recent FDA approval of the antibody-drug conjugate trastuzumab-deruxtecan for pretreated patients with HER2 mutant NSCLC has been an important therapeutic ***3 and HER4 also exert oncogenic potential,and targeted treatment approaches are being developed,particularly for ***,strategies to inhibit the oncogenic function of ERBB receptors in NSCLC are currently evolving at an unprecedented pace;therefore,this review summarizes current treatment standards and discusses the outlook for future developments.

关键词： Oncology NSCLC EGFR HER2 HER3 HER4

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Unveiling the culprit:the fusobacterium lineage that populates colorectal cancer

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Signal Transduction and Targeted Therapy 2024年第6期9卷 2349-2350页

作者： Johannes Betge Matthias P.Ebert Department of Medicine Ⅱ Medical Faculty MannheimHeidelberg UniversityMannheimGermany Junior Clinical Cooperation Unit Translational Gastrointestinal Oncology and Preclinical Models German Cancer Research Center(DKFZ)HeidelbergGermany dkfz hector cancer institute at university medical center MannheimGermany MMPU Microbiota Drug Metabolism and cancer Therapy European Molecular Biology LaboratoryHeidelbergGermany

In a recent study published in Nature,Zepeda-Rivera et al.1 discovered that one distinct clade of Fusobacterium nucleatum animalis(Fna)dominates the colorectal cancer(CRC)tumor *** work unravels a more precise understanding of a major bacterial species associated with CRC progression,thereby establishing a new focus for future studies,which may aid to develop improved microbiome-based diagnostics and treatments(Fig.1).

关键词： colorectal al. cancer

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Roles of eIF5A in the immunosurveillance of cellular senescence

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cancer Biology & Medicine 2022年第11期19卷 1523-1527页

作者： Xiangli Jiang Fabricio Loayza-Puch Department of Thoracic Oncology Tianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin's Clinical Research Center for CancerTianjin 300060China Translational Control and Metabolism German Cancer Research Center(DKFZ)Heidelberg 69120Germany

Senescence is a cellular stress response program that prevents the proliferation of oncogenically activated, genetically unstable, and/or damaged cells. Senescence was first described in 1961, when normal cultured human fibroblasts were found to enter irreversible growth arrest after multiple cell divisions, in a process known as replicative senescence1. Several types of senescence have since been identified, such as stress-induced senescence, oncogene-induced senescence, and virus-induced senescence. Despite having distinct features due to their different triggers, senescent cells share several key features.

关键词： unstable SASP senescence

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Optimizing the cancer research landscape for the benefit of patients and society: A strategic perspective of the German cancer Research center (dkfz) and its partnerships with university medical centers

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cancer Biology & Medicine 2022年第11期19卷 1517-1522页

作者： Michael Baumann German cancer Research center(dkfz) Heidelberg 69120Germany

This issue of cancer Biology & Medicine, a premium Chinese international scientific journal in this field, focuses on cooperation between Chinese and German cancer research, particularly between the Tianjin medical university cancer institute & Hospital and the German cancer Research center(dkfz) with its networking partners. This editorial provides a brief overview on dkfz’s research strategy with a focus on how a national integrated cancer research and care ecosystem is evolving that benefits patients and society.

关键词： cancer landscape centers

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Specifc inflammatory osteoclast precursors induced during chronic inflammation give rise to highly active osteoclasts associated with inflammatory bone loss

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Bone Research 2022年第3期10卷 548-564页

作者： Yaron Meirow Milena Jovanovic Yuval Zur Juliana Habib Daniele Filippo Colombo Nira Twaik Hadas Ashkenazi-Preiser Kerem Ben-Meir Ivan Mikula Jr. Or Reuven Guy Kariv Leonor Daniel Saja Baraghithy Yehuda Klein Jeroen Krijgsveld Noam Levaot Michal Baniyash The Concern Foundation Laboratories at The Lautenberg center for Immunology and cancer Research Israel-Canada Medical Research InstituteFaculty of MedicineThe Hebrew UniversityJerusalemIsrael Department of Physiology and Cell Biology Ben-Gurion University of the NegevBeer-ShevaIsrael Division of Proteomics of Stem Cells and cancer German Cancer Research Center(DKFZ)HeidelbergGermany institute for Drug Research Faculty of MedicineThe Hebrew UniversityJerusalemIsrael Hebrew university-Hadassah School of Dental Medicine JerusalemIsrael Heidelberg university Medical FacultyHeidelbergGermany

Elevated osteoclast(OC)activity is a major contributor to inflammatory bone loss(IBL)during chronic inflammatory ***,the specific OC precursors(OCPs)responding to inflammatory cues and the underlying mechanisms leading to IBL are poorly *** identified two distinct OCP subsets:Ly6C^(hi)CD11b^(hi) inflammatory OCPs(iOCPs)induced during chronic inflammation,and homeostatic Ly6C^(hi)CD11b^(lo)OCPs(hOCPs)which remained *** and proteomic characterization revealed that while iOCPs were rare and displayed low osteoclastogenic potential under normal conditions,they expanded during chronic inflammation and generated OCs with enhanced *** contrast,hOCPs were abundant and manifested high osteoclastogenic potential under normal conditions but generated OCs with low activity and were unresponsive to the inflammatory *** derived from iOCPs expressed higher levels of resorptive and metabolic proteins than those generated from hOCPs,highlighting that different osteoclast populations are formed by distinct *** further identified the TNF-αand S100A8/A9 proteins as key regulators that control the iOCP response during chronic ***,we demonstrated that the response of iOCPs but not that of hOCPs was abrogated in tnf-α^(-/-)mice,in correlation with attenuated *** findings suggest a central role for iOCPs in IBL *** can serve as potential biomarkers for IBL detection and possibly as new therapeutic targets to combat IBL in a wide range of inflammatory conditions.

关键词： inflammation inflammatory osteoclast

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Nucleoporin 88 expression in hepatitis B and C virus-related liver diseases

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World Journal of Gastroenterology 2006年第36期12卷 5870-5874页

作者： Martina Knoess Anna Kordelia Kurz Olga Goreva Nuran Bektas Kai Breuhahn Magarethe Odenthal Peter Schirmacher Hans Peter Dienes C Thomas Bock Hanswalter Zentgraf Axel zur Hausen institute of Pathology University Hospital Cologne Cologne Germany Department of Hematology/Oncology Freiburg University Medical Center Freiburg Germany institute of Pathology University of Heidelberg Heidelberg Germany Department of Molecular Pathology University Hospital Tübingen Germany German cancer Research center DKFZ Applied Tumor Virology Heidelberg Germany institute of Pathology University Hospital Freiburg Freiburg Germany

AIM: To investigate the expression of nucleoporin 88 (Nup88) in hepatitis B virus (HBV) and C virus (HCV)-related liver diseases. METHODS: We generated a new monoclonal Nup88 antibody to investigate the Nup88 protein expression by immunohistochemistry (IHC) in 294 paraffin-embedded liver specimens comprising all stages of hepatocellular carcinogenesis. In addition, in cell culture experiments HBV-positive (HepG2.2.15 and HB611) and HBV-negative (HepG2) hepatoma cell lines were tested for the Nup88 expression by Western-immunoblotting to test data obtained by ***: Specific Nup88 expression was found in chronic HCV hepatitis and unspecific chronic hepatitis, whereas no or very weak Nup88 expression was detected in normal liver. The Nup88 expression was markedly reduced or missing in mild chronic HBV infection and inversely correlated with HBcAg expression. Irrespective of the HBV- or HCV-status, increasing Nup88 expression was observed in cirrhosis and dysplastic nodules, and Nup88 was highly expressed in hepatocellular carcinomas. The intensity of Nup88 expression significantly increased during carcinogenesis (P < 0.0001) and correlated with dedifferentiation (P < 0.0001). Interestingly, Nup88 protein expression was significantly downregulated in HBV-positive HepG2.2.15 (P < 0.002) and HB611 (P < 0.001) cell lines as compared to HBV-negative HepG2 cells. CONCLUSION: Based on our immunohistochemical data, HBV and HCV are unlikely to influence the expression of Nup88 in cirrhotic and neoplastic liver tissue, but point to an interaction of HBV with the nuclear pore in chronic hepatitis. The expression of Nup88 in nonneoplastic liver tissue might reflect enhanced metabolic activity of the liver tissue. Our data strongly indicate a dichotomous role for Nup88 in non-neoplastic and neoplastic conditions of the liver.

关键词： Nucleoporin 88 Hepatitis B and C virus Hepatocellular carcinogenesis

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Rescue of p53 functions by in vitro-transcribed mRNA impedes the growth of high-grade serous ovarian cancer

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cancer Communications 2024年第1期44卷 101-126页

作者： Monika Raab Izabela Kostova Samuel Peña-Llopis Daniela Fietz Monika Kressin Seyed Mohsen Aberoumandi Evelyn Ullrich Sven Becker Mourad Sanhaji Klaus Strebhardt Department of Gynecology Medical SchoolGoethe-UniversityFrankfurt am MainGermany Translational Genomics in Solid Tumors West German Cancer CenterUniversity HospitalEssenGermany German cancer Consortium(DKTK) EssenGermany German cancer Research center(dkfz) HeidelbergGermany Histology and Embryology Institute for Veterinary AnatomyGiessenGermany Franfurt cancer institute(FCI) Goethe UniversityFrankfurt am MainGermany German cancer Consortium(DKTK) Partner site Frankfurt/Mainza partnership between DKFZ and University Hospital FrankfurtFrankfurt am MainGermany Experimental Immunology Department for Children and Adolescents MedicineUniversity Hospital FrankfurtGoethe UniversityFrankfurt am MainGermany

Background:The cellular tumor protein p53(TP53)is a tumor suppressor gene that is frequently mutated in human *** various cancer types,the very aggressive high-grade serous ovarian carcinoma(HGSOC)exhibits the high-est prevalence of TP53 mutations,present in>96%of *** intensive efforts to reactivate p53,no clinical drug has been approved to rescue p53 *** this study,our primary objective was to administer in vitro-transcribed(IVT)wild-type(WT)p53-mRNA to HGSOC cell lines,primary cells,and ortho-topic mouse models,with the aim of exploring its impact on inhibiting tumor growth and dissemination,both in vitro and in ***:To restore the activity of p53,WT p53 was exogenously expressed in HGSOC cell lines using a mammalian vector ***,IVT WT p53 mRNA was delivered into different HGSOC model systems(primary cells and patient-derived organoids)using liposomes and studied for proliferation,cell cycle progression,apoptosis,colony formation,and chromosomal *** alterations induced by p53 mRNA were analyzed using RNA sequencing in OVCAR-8 and primary HGSOC cells,followed by ingenuity path-way *** vivo effects on tumor growth and metastasis were studied using orthotopic xenografts and metastatic intraperitoneal mouse ***:Reactivation of the TP53 tumor suppressor gene was explored in differ-ent HGSOC model systems using newly designed IVT mRNA-based *** introduction of WT p53 mRNA triggered dose-dependent apoptosis,cell cycle arrest,and potent long-lasting inhibition of HGSOC cell *** analysis of OVCAR-8 cells upon mRNA-based p53 reactivation revealed significant alterations in gene expression related to p53 signaling,such as apoptosis,cell cycle regulation,and DNA *** p53 function concurrently reduces chromosomal instability within the HGSOC cells,under-scoring its crucial contribution in safeguarding genomic integrity by moderating the baselin

关键词： apoptosis cell cycle chromosomal instability HGSOC metastatic intraperitoneal mouse model HGSOC orthotopic Xenograft model high-grade serous ovarian cancer in vitro-transcribed p53-mRNA liposomal IVT mRNA delivery system patient-derived organoid patient-derived primary cancer cell

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Liver-directed treatment is associated with improved survival and increased response to immune checkpoint blockade in metastatic uveal melanoma:results from a retrospective multicenter trial

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Frontiers of Medicine 2023年第5期17卷 878-888页

作者： Elias A.T.Koch Anne Petzold Anja Wessely Edgar Dippel Markus Eckstein Anja Gesierich Ralf Gutzmer Jessica C.Hassel Harald Knorr Nicole Kreuzberg Ulrike Leiter Carmen Loquai Friedegund Meier Markus Meissner Peter Mohr Claudia Pföhler Farnaz Rahimi Dirk Schadendorf Max Schlaak Kai-Martin Thoms Selma Ugurel Jochen Utikal Michael Weichenthal Beatrice Schuler-Thurner Carola Berking Markus V.Heppt Department of Dermatology Uniklinikum ErlangenFriedrich-Alexander-University Erlangen-Nürnberg(FAU)91054ErlangenGermany Comprehensive cancer center Erlangen—European Metropolitan Area of Nürnberg(CCC ER-EMN) 91054ErlangenGermany Deutsches Zentrum Immuntherapie(DZI) Uniklinikum ErlangenFriedrich-Alexander-University Erlangen-Nürnberg(FAU)91054ErlangenGermany Bavarian cancer Research center(BZKF) Uniklinikum ErlangenÖstliche Stadtmauerstraße 3091054ErlangenGermany Department of Dermatology Ludwigshafen Medical Center67059LudwigshafenGermany institute of Pathology Uniklinikum ErlangenFriedrich-Alexander-University Erlangen-Nürnberg91054ErlangenGermany Department of Dermatology University Hospital Würzburg97080WürzburgGermany Skin cancer center Minden Department of DermatologyMühlenkreiskliniken AöRRuhr UniversityBochum Campus Minden32423MindenGermany Skin cancer center Department of Dermatology and National Center for Tumor Diseases(NCT)University Hospital Heidelberg69120HeidelbergGermany Department of Ophthalmology Uniklinikum ErlangenFriedrich-Alexander-University Erlangen-Nürnberg(FAU)91054ErlangenGermany Department of Dermatology and Venereology Skin Cancer Center at the Center of Integrated Oncology(CIO)Köln BonnUniversity Hospital of Cologne50937CologneGermany Department of Dermatology Center for DermatooncologyUniversity Hospital Tübingen72056TübingenGermany Department of Dermatology University Medical Center Mainz55131MainzGermany Skin cancer center at the university cancer center Dresden and National center for Tumor Diseases&Department of Dermatology University Hospital Carl Gustav Carus01307DresdenGermany Department of Dermatology Venereology and AllergologyGoethe University60590Frankfurt am MainGermany Department of Dermatology Elbeklinikum21614BuxtehudeGermany Department of Dermatology Saarland University Medical School66421Homburg/SaarGermany Department of Dermatology and Allergy Munich University Hospital(LMU)81377MunichGermany Departmen

Metastases of uveal melanoma(UM)spread predominantly to the *** to low response rates to systemic therapies,liver-directed therapies(LDT)are commonly used for tumor *** impact of LDT on the response to systemic treatment is unknown.A total of 182 patients with metastatic UM treated with immune checkpoint blockade(ICB)were included in this *** were recruited from prospective skin cancer centers and the German national skin cancer registry(ADOReg)of the German Dermatologic Cooperative Oncology Group(DeCOG).Two cohorts were compared:patients with LDT(cohort A,n=78)versus those without LDT(cohort B,n=104).Data were analyzed for response to treatment,progression-free survival(PFS),and overall survival(OS).The median OS was significantly longer in cohort A than in cohort B(20.1 vs.13.8 months;P=0.0016)and a trend towards improved PFS was observed for cohort A(3.0 vs.2.5 months;P=0.054).The objective response rate to any ICB(16.7%vs.3.8%,P=0.0073)and combined ICB(14.1%vs.4.5%,P=0.017)was more favorable in cohort *** data suggest that the combination of LDT with ICB may be associated with a survival benefit and higher treatment response to ICB in patients with metastatic UM.

关键词： uveal melanoma liver-directed therapy immune checkpoint blockade SIRT anti-PD-1 anti-CTLA-4

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Metabolic regulation of immune responses to cancer

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cancer Biology & Medicine 2022年第11期19卷 1528-1542页

作者： Jannis WiBfeld Anke Werner Xin Yan Nora ten Bosch Guoliang Cui Helmholtz institute for Translational Oncology(HI-TRON) Mainz 55131Germany T Cell Metabolism Group(D192) German Cancer Research Center(DKFZ)Heidelberg 69120Germany Faculty of Biosciences Heidelberg UniversityHeidelberg 69120Germany

The tumor microenvironment is an ecosystem composed of multiple types of cells, such as tumor cells, immune cells, and cancerassociated fibroblasts. cancer cells grow faster than non-cancerous cells and consume larger amounts of nutrients. The rapid growth characteristic of cancer cells fundamentally alters nutrient availability in the tumor microenvironment and results in reprogramming of immune cell metabolic pathways. Accumulating evidence suggests that cellular metabolism of nutrients, such as lipids and amino acids, beyond being essential to meet the bioenergetic and biosynthetic demands of immune cells, also regulates a broad spectrum of cellular signal transduction, and influences immune cell survival, differentiation, and anti-tumor effector function. The cancer immunometabolism research field is rapidly evolving, and exciting new discoveries are reported in high-profile journals nearly weekly. Therefore, all new findings in this field cannot be summarized within this short review. Instead, this review is intended to provide a brief introduction to this rapidly developing research field, with a focus on the metabolism of two classes of important nutrients-lipids and amino acids-in immune cells. We highlight recent research on the roles of lipids and amino acids in regulating the metabolic fitness and immunological functions of T cells, macrophages, and natural killer cells in the tumor microenvironment. Furthermore, we discuss the possibility of “editing” metabolic pathways in immune cells to act synergistically with currently available immunotherapies in enhancing anti-tumor immune responses.

关键词： Lipids amino acids cancer anti-tumor immunity T cells NK cells metabolism immunometabolism

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Survival trends of patients with non-metastatic gastric adenocarcinoma in the US and European countries:the impact of decreasing resection rates

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cancer Communications 2022年第7期42卷 648-662页

作者： Lei Huang Lina Jansen Rob H.A.Verhoeven Jelle P.Ruurda Liesbet Van Eycken Harlinde De Schutter Jan Johansson Mats Lindblad Tom B.Johannesen Vesna Zadnik Tina Zagar Sjoerd M.Lagarde Cornelis J.Hvan de Velde Petra Schrotz-King Hermann Brenner Division of Clinical Epidemiology and Aging Research German Cancer Research Center(DKFZ)Heidelberg 69120Germany medical Faculty Heidelberg of Heidelberg university Heidelberg 69120Germany German cancer Consortium German Cancer Research CenterHeidelberg 69120Germany Department of Research&Development Netherlands Comprehensive Cancer OrganizationUtrecht 3501 DBThe Netherlands Department of medical Oncology Amsterdam University Medical CentersAmsterdam 1105 AZThe Netherlands Department of Surgery University Medical Center UtrechtUtrecht 3508 GAThe Netherlands Belgian cancer Registry Brussels B-1210Belgium Department of Esophageal and Gastric Surgery Lund University HospitalLund 22185Sweden Department of Clinical Science Interventionand TechnologyDivision of SurgeryKarolinska University HospitalStockholm 17176Sweden Registry Department The Cancer Registry of NorwayOslo 0379Norway Epidemiology and cancer Registry Institute of Oncology LjubljanaLjubljana 1000Slovenia Department of Surgery Erasmus Medical Centre-University Medical Centre RotterdamRotterdam 3015 CEThe Netherlands Department of Surgical Oncology Leiden University Medical CenterLeiden 2300 RCThe Netherlands Division of Preventive Oncology German Cancer Research Center and National Center for Tumor DiseasesHeidelberg 69120Germany

Background:We previously observed decreasing resection rates of nonmetastatic gastric adenocarcinoma(GaC)in the US and some European *** and to what extent these trends affect the trends in overall survival(OS)of patients with non-metastatic GaC at the population level remain *** large international population-based cohort study aimed to assess the impact of the previously observed decreasing resection rates on multivariable-adjusted trends in the long-term OS of patients with non-metastatic ***:Individual-level data of patients with non-metastatic GaC were obtained from the national cancer registries of the Netherlands,Belgium,Sweden,Norway,and Slovenia,and the US Surveillance,Epidemiology,and End Results *** analyzed data for each country *** between year of diagnosis and OS were assessed using Cox proportional hazards regression model with adjustment for multiple prognostic variables,with and without including resection and chemotherapy as potential explanatory ***:A total of 66,398 non-metastatic GaC patients diagnosed in 2003-2016 were analyzed,with an accumulated follow-up of 172,357 *** adjustment for resection,OS was improved only slightly in the US[hazard ratio(HR)_(per year)=0.99;HR_(≥vs.<2010)=0.96],and no improvement was observed in the investigated European countries,with OS even worsening in Sweden(HR_(per year)=1.03;HR_(≥vs.<2010)=1.17).After adjusting for resection,the increasing OS trend became stronger in the US(HR_(per year)=0.98;HR_(≥vs.<2010)=0.88),and the temporal trend became insignificant in *** Slovenia(HR_(per year)=0.99;HR_(≥vs.<2010)=0.92)and Norway(HR_(per year)=0.97;HR_(≥vs.<2010)=0.86),improved OS over time emerged after resection *** OS in patients undergoing resection was observed in the US,the Netherlands,and *** for chemotherapy did not alter the observed *** analyses by tumor location showedm

关键词： gastric adenocarcinoma resection rate adjusted overall survival temporal trend prognostic factors international population-based cohort study

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