0000000000015369

AUTHOR

Holger Moch

showing 6 related works from this author

Somatostatin-producing neuroendocrine tumors of the duodenum and pancreas: incidence, types, biological behavior, association with inherited syndrome…

2008

Somatostatin-producing neuroendocrine tumors (SOM-NETs) of the duodenum and pancreas appear to be heterogeneous. To determine their clinicopathological profiles, respective data were analyzed on a series of 82 duodenal and 541 pancreatic NETs. In addition, the clinical records of 821 patients with duodenal or pancreatic NETs were reviewed for evidence of a somatostatinoma syndrome. Predominant or exclusive expression of somatostatin was found in 21 (26%) duodenal and 21 (4%) pancreatic NETs. They were classified as sporadic (n=31) or neurofibromatosis type 1 (NF1)-associated duodenal NETs (n=3), gangliocytic paragangliomas (GCPGs; n=6), or poorly differentiated neuroendocrine carcinomas (pd…

AdultMaleCancer Researchmedicine.medical_specialtyEndocrinology Diabetes and Metabolism610 Medicine & healthNeuroendocrine tumorsGastroenterologyParagangliomaEndocrinologyDuodenal NeoplasmsInternal medicine10049 Institute of Pathology and Molecular PathologySomatostatinomaMultiple Endocrine Neoplasia Type 1MedicineHumansMEN11306 Cancer ResearchGenetic Predisposition to DiseaseNeurofibromatosisMultiple endocrine neoplasia610 Medicine & healthAgedAged 80 and overbusiness.industryIncidenceSyndromeSomatostatinomaMiddle Agedmedicine.diseasePrognosis1310 EndocrinologyPancreatic Neoplasms2712 Endocrinology Diabetes and MetabolismNeuroendocrine Tumorsmedicine.anatomical_structureSomatostatinOncologyDuodenum570 Life sciences; biology2730 OncologyFemalebusinessPancreasSomatostatinFollow-Up Studies
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Germinal Centers Determine the Prognostic Relevance of Tertiary Lymphoid Structures and Are Impaired by Corticosteroids in Lung Squamous Cell Carcino…

2018

Abstract In solid tumors, the presence of lymph node–like structures called tertiary lymphoid structures (TLS) is associated with improved patient survival. However, little is known about how TLS develop in cancer, how their function affects survival, and whether they are affected by cancer therapy. In this study, we used multispectral microscopy, quantitative pathology, and gene expression profiling to analyze TLS formation in human lung squamous cell carcinoma (LSCC) and in an experimental model of lung TLS induction. We identified a niche of CXCL13+ perivascular and CXCL12+LTB+ and PD-L1+ epithelial cells supporting TLS formation. We also characterized sequential stages of TLS maturation…

0301 basic medicineMaleCancer ResearchLung Neoplasmsmedicine.medical_treatmentApoptosis03 medical and health sciencesMiceLymphocytes Tumor-InfiltratingAdrenal Cortex HormonesCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsCarcinomaTumor Cells CulturedTumor MicroenvironmentMedicineAnimalsHumansCXCL13Lung cancerSurvival rateAgedCell ProliferationChemotherapyTumor microenvironmentbusiness.industryGene Expression ProfilingCancerGerminal centerMiddle Agedmedicine.diseaseGerminal CenterPrognosisXenograft Model Antitumor Assays3. Good healthMice Inbred C57BLSurvival Rate030104 developmental biologyTertiary Lymphoid StructuresOncologyCancer researchCarcinoma Squamous CellFemalebusinessFollow-Up StudiesCancer research
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Endogenous Myoglobin in Breast Cancer Is Hypoxia-inducible by Alternative Transcription and Functions to Impair Mitochondrial Activity

2011

Recently, immunohistochemical analysis of myoglobin (MB) in human breast cancer specimens has revealed a surprisingly widespread expression of MB in this nonmuscle context. The positive correlation with hypoxia-inducible factor 2α (HIF-2α) and carbonic anhydrase IX suggested that oxygen regulates myoglobin expression in breast carcinomas. Here, we report that MB mRNA and protein levels are robustly induced by prolonged hypoxia in breast cancer cell lines, in part via HIF-1/2-dependent transactivation. The hypoxia-induced MB mRNA originated from a novel alternative transcription start site 6 kb upstream of the ATG codon. MB regulation in normal and tumor tissue may thus be fundamentally diff…

0303 health sciencesGene knockdownTumor suppressor geneCell growthCellCell BiologyBiologyMitochondrionBiochemistryMolecular biology03 medical and health sciencesTransactivation0302 clinical medicinemedicine.anatomical_structure030220 oncology & carcinogenesisCancer cellmedicineCancer researchGene silencingMolecular Biology030304 developmental biologyJournal of Biological Chemistry
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Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas.

1998

Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of inherited kidney cancer characterized by a predisposition to develop multiple, bilateral papillary renal tumours. The pattern of inheritance of HPRC is consistent with autosomal dominant transmission with reduced penetrance. HPRC is histologically and genetically distinct from two other causes of inherited renal carcinoma, von Hippel-Lindau disease (VHL) and the chromosome translocation (3;8). Malignant papillary renal carcinomas are characterized by trisomy of chromosomes 7, 16 and 17, and in men, by loss of the Y chromosome. Inherited and sporadic clear cell renal carcinomas are characterized by inactivation of b…

AdultMaleGenetic LinkageUrologyMolecular Sequence DataHereditary Papillary Renal Cell CarcinomaChromosomal translocationBiologyurologic and male genital diseasesY chromosomemedicine.disease_causeProto-Oncogene MasGermlineGermline mutationGeneticsmedicineMissense mutationHumansAmino Acid SequenceCarcinoma Renal CellGerm-Line MutationAgedKidneyMutationBinding SitesSequence Homology Amino Acidbusiness.industryReceptor Protein-Tyrosine KinasesMiddle AgedProtein-Tyrosine KinasesProto-Oncogene Proteins c-metmedicine.diseasePenetranceCarcinoma PapillaryKidney NeoplasmsPedigreemedicine.anatomical_structureProto-Oncogene Proteins c-metMutationCancer researchHereditary leiomyomatosis and renal cell carcinomaFemaleTrisomybusinessKidney cancerChromosomes Human Pair 7Nature genetics
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Mass Spectrometry Imaging Differentiates Chromophobe Renal Cell Carcinoma and Renal Oncocytoma with High Accuracy

2020

Background: While subtyping of the majority of malignant chromophobe renal cell carcinoma (cRCC) and benign renal oncocytoma (rO) is possible on morphology alone, additional histochemical, immunohistochemical or molecular investigations are required in a subset of cases. As currently used histochemical and immunohistological stains as well as genetic aberrations show considerable overlap in both tumors, additional techniques are required for differential diagnostics. Mass spectrometry imaging (MSI) combining the detection of multiple peptides with information about their localization in tissue may be a suitable technology to overcome this diagnostic challenge. Patients and Methods: Formalin…

0301 basic medicineChromophobe Renal Cell Carcinoma610610 Medicine & healthmass spectrometry imagingBiologyCross-validationMass spectrometry imagingOncocytic renal tumors03 medical and health sciences0302 clinical medicineproteomics10049 Institute of Pathology and Molecular PathologymedicineRenal oncocytomachromophobe renal cell carcinomabusiness.industrymedicine.diseaseLinear discriminant analysisRandom forestSupport vector machine030104 developmental biologyOncology030220 oncology & carcinogenesis2730 OncologyDifferential diagnosisNuclear medicinebusinessrenal oncocytomaResearch PaperJournal of Cancer
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