Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs (PROG EXP TUMOR RES)

Publisher: Karger

Journal description

Scientists who are eager to take part in novel approaches to cancer research rely upon this series as a major information source. The individual volumes provide exceptionally detailed coverage of topics selected as either representing controversial problems or belonging to areas where the speed of developments necessitates the kind of assistance offered by integrative, critical reviews. Expertly edited as well as authored, these books have attracted broad attention as records of both the sophistication and diversity of efforts to understand, prevent or control cancerous diseases

Current impact factor: 0.25

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2011 Impact Factor
2010 Impact Factor 0.25
2009 Impact Factor 0.423
2008 Impact Factor 1.5
2007 Impact Factor 1.643
2006 Impact Factor 1.857
2005 Impact Factor 4.214
2004 Impact Factor 3.571
2003 Impact Factor

Impact factor over time

Impact factor
Year

Additional details

5-year impact 0.98
Cited half-life 0.00
Immediacy index 0.00
Eigenfactor 0.00
Article influence 0.27
Website Progress in Experimental Tumor Research website
Other titles Progress in experimental tumor research, Experimental tumor research, Fortschritte der experimentellen Tumorforschung
ISSN 0079-6263
OCLC 1695607
Material type Series
Document type Journal / Magazine / Newspaper

Publisher details

Karger

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:102-10. DOI:10.1159/000151878
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:85-91. DOI:10.1159/000151876
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:138-44. DOI:10.1159/000151882
  • Article: Leukemias
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:45-50. DOI:10.1159/000151872
  • Article: Lung Cancer
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:56-61. DOI:10.1159/000151874
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:135-7. DOI:10.1159/000151881
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:92-101. DOI:10.1159/000151877
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:1-6. DOI:10.1159/000151866
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:51-5. DOI:10.1159/000151873
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:122-34. DOI:10.1159/000151880
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:111-21. DOI:10.1159/000151879
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:25-31. DOI:10.1159/000151870
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:7-16. DOI:10.1159/000151868
  • Article: Lymphomas
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:32-44. DOI:10.1159/000151871
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:17-24. DOI:10.1159/000151869
  • Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2008; 40:62-84. DOI:10.1159/000151875
  • [Show abstract] [Hide abstract]
    ABSTRACT: Biological tools that are unleashed in malignancies are employed in a controlled manner during neuronal development. By default, early embryonic cells would become neuronal stem cells, a path that is blocked by specific signaling pathways. The future nervous system only develops where this blockade is inhibited by inductive signals from the 'organizer'. Once the future brain and spinal cord regions are determined, the mitotic potential in this region must be maintained long enough to produce all cells required, but also be controlled to avoid excessive over-production of cells. Newly generated cells must then migrate to their future destination, they must know where to settle down, and they must differentiate. To shape the developing nervous system and to adapt its functionality to the postnatal environment, cell survival must be regulated, i.e. survival of some cells is supported while death of others is induced. Thus, inductive events, proliferation, cell migration, differentiation, cell survival and cell death are highly regulated during neuronal development, while these functions are de-regulated in malignancies. The molecular pathways for neuronal development mutually modulate each other and are still present in the adult nervous system. Because many of these pathways are implicated in tumors, neurons may affect these conditions.
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2007; 39:1-29. DOI:10.1159/0000100041
  • [Show abstract] [Hide abstract]
    ABSTRACT: Other sections of this monograph, dedicated to neuronal activities in tumor tissue, have highlight the chief influence of neurotrophins, neurotransmitters, adhesion, guidance molecules and different nerve cell markers in the progression, but also for the prognostic, therapy and survey of cancers. The G-protein-coupled receptors (GPCR) are among the most successful and promising target proteins for drug discovery and therapeutic research. GPCR are frequently overexpressed in cancer cells, an interesting property for tumor imaging or for a targeted radiotherapy, using radiolabeled ligand derivatives. The tumor microenvironment contains a number of GPCR ligands (e.g., bioactive peptides, biogenic amines, purins, chemokines), known to regulate the proliferation, migration or survival of both tumoral and neural cells and that may be key actors of the neuro-neoplastic interactions. Here will be reviewed the potential utilization of substances that target a selected choice of GPCR, especially neuropeptide receptors, for a novel concept of therapy, concerning the numerous types of cancers where neurons infiltrate the tumoral mass or those where the malignant cells invade nerve branches (perineural invasion). Some molecular mechanisms linked to these GPCR (or linking GPCR to other types of membrane receptors or co-receptors), involved in these processes, will also be considered.
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2007; 39:130-53. DOI:10.1159/0000100074
  • [Show abstract] [Hide abstract]
    ABSTRACT: A tumor is not an isolated entity within an organism, but tissue that strongly interacts with its environment. This interaction is however not restricted to direct cell-to-cell interactions, but generally comprises the susceptibility of tumor cells for chemokines and cytokines, as well as neurotransmitters and hormones by the expression of the according receptors. These signal substances have influences on tumor cell functions such as proliferation and migration. The other way round, tumor cells themselves release a broad range of these signal substances, which influence the cells of the environment. One of the first and most important interactions in this respect is the angiogenesis, which was discovered about 30 years ago. Tumor cells release angiogenic factors, i.e. the vascular endothelial growth factor as well as angiogenic chemokines among others. These factors initiate the vascularization of the tumor. Recently, a similar process was found for the development of lymphatic vessels in tumors. We herein seize these observations and combine them with arguments provided in the previous chapter, which leads us to the hypothesis that tumor cells may also be able to stimulate their own innervation; a process that we have termed neoneurogenesis.
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2007; 39:91-8. DOI:10.1159/0000100049
  • [Show abstract] [Hide abstract]
    ABSTRACT: The autonomic nervous system with its two antagonistic branches, the sympathicus and the parasympathicus, regulates the activities of all body functions that are not under voluntary control. While the autonomic regulation of organ functions has been extensively studied, little attention has been given to the potential role of neurohumoral transmission at the cellular level in the development of cancer. Studies conducted by our laboratory first showed that binding of the parasympathetic neurotransmitter, acetylcholine, as well as nicotine or its nitrosated cancer-causing derivative, NNK, to nicotinic acetylcholine receptors comprised of alpha7 subunits activated a mitogenic signal transduction pathway in normal and neoplastic pulmonary neuroendocrine cells. On the other hand, beta-adrenergic receptors (Beta-ARs), which transmit signals initiated by binding of the catecholamine neurotransmitters of the sympathicus, were identified by our laboratory as important regulators of cell proliferation in cell lines derived from human adenocarcinomas of the lungs, pancreas, and breast. The tobacco-specific carcinogen NNK bound with high affinity to Beta1- and Beta2-ARs, thus activating cAMP, protein kinase A, and the transcription factor CREB. Collectively, neurotransmitter receptors of the nicotinic and Beta-adrenergic families appear to regulate cellular functions essential for the development and survival of the most common human cancers.
    Progress in experimental tumor research. Fortschritte der experimentellen Tumorforschung. Progrès de la recherche expérimentale des tumeurs 02/2007; 39:45-63. DOI:10.1159/0000100045