Update 25 december 2015:

Hier enkele studies naar effecten van aanvullende complementaire middelen en behandelingen bij testiskanker - zaadbalkanker. Het zijn er niet veel omdat er weinig onderzoek naar wordt gedaan blijkbaar.

Testiskanker - kiemcelkanker, zaadbalkanker:

632) Samuels ML et al ; Cancer Treatment Rep 65 : 615-27 ; Intraveneuze hyperalimentatie bij patiënten met uitgezaaide testiskanker welke chemo krijgen vergroot de kans op levensbedreigende infecties ; dit onderzoek ondersteunt de hypothese dat extra calorieen e.d. beter voor de kanker zijn dan voor de patient.

783)Drott C et al ; Surgery 103:499-506;1988; Intermitterend extra calorieen voor patienten die chemo krijgen voor testiskanker gaat de vermagering die samenhangt met deze chemo en die behoorlijk lang aanhoudt niet aantoonbaar tegen.

848) Samuels ML ; Cancer Treatment Reports 65:615-27;1981 ; Hyperalimentatie bij testiskanker leidt tot niet significant minder regressies, wat al geen reclame is, maar ook nog eens tot significant meer infecties ; uit deze en de vorige studie blijkt maar weer dat hyperalimentatie in principe niet aan te bevelen is.

2324)Christensen JF et al; Br J Cancer  2014 Jul 8;111(1):8-16;PMID 24867693 ; Bij patienten met kiemcelkanker blijkt weerstandstraining blijkt de integriteit/kwaliteit van de spieren tijdens chemo meer in stand te houden.

28 april 2011: ik ben de website kanker-actueel aan het herzien en laat onderstaand bericht staan omdat dit nog steeds relevante informatie geeft.

1 maart 2005:: Bron: Nature Reviews Cancer 5, 210-222 (2005); doi:10.1038/nrc1568

Nederlandse artsen en wetenschappers maakten een overzicht van de behandelmogelijkheden bij teelbalkanker - germcancer en vooral waarom deze vorm van kanker zo goed te behandelen is met chemokuren. Hier het abstract uit Nature van deze week. Onderaan artikel staat korte autobiografie van de Nederlandse auteurs. Wie wil betalen kan het volledige artikel ook opvragen bij Nature.

TESTICULAR GERM-CELL TUMOURS IN A BROADER PERSPECTIVE

J. Wolter Oosterhuis & Leendert H. J. Looijenga.

Abstract
The germ-cell tumours are a fascinating group of neoplasms because of their unusual biology and the spectacular therapeutic results that have been obtained in these tumours. Traditionally, this group of neoplasms is presented in an organ-oriented approach. However, recent clinical and experimental data convincingly demonstrate that these neoplasms are one disease with separate entities that can manifest themselves in different anatomical sites. We propose five entities, in which the developmental potential is determined by the maturation stage and imprinting status of the originating germ cell. Recent progress begins to explain the apparent unpredictable development of germ-cell tumours and offers a basis for understanding their exquisite sensitivity to therapy.

Summary

 

  • Germ-cell tumours (GCTs) of all anatomical sites can be classified into five groups, characterized by their chromosomal complement and developmental potential.
  • The most significant recurrent chromosomal aberrations in type I yolk-sac tumours are loss of 1p, 4 and 6q, and gain of 1q, 12(p13) and 20q. In type II seminomas and non-seminomatous GCTs, the most significant recurrent chromosomal aberrations are gain of 7, 8, 12p, 21 and X, and loss of chromosomes 1p, 11, 13 and 18. Aberrations of 12p are the only recurrent structural abnormalities in type II GCTs. In type III spermatocytic seminomas, gain of chromosome 9 is most common.
  • The originating cell is most probably a primitive germ cell of which the developmental potential differs according to its stage of maturation and pattern of genomic imprinting.
  • Animal models are available for the different groups of GCTs, except for the type II seminomas and non-seminomatous GCTs.
  • An activating KIT mutation in codon 816 is an early pathogenetic event in bilateral testicular seminomas and non-seminomatous GCTs.
  • The transcription factor OCT3/4, a characteristic of primordial germ cells and pluripotent stem cells, is a new and robust diagnostic marker for type II seminomas and non-seminomatous GCTs, including their intratubular precursor.
  • Treatment sensitivity and resistance of GCTs probably correlates with retention and loss of embryonic characteristics (in particular, DNA-repair deficiency), respectively.

    Author biographies
    J. Wolter Oosterhuis, a professor of pathology, studied medicine and trained as a pathologist at Groningen University, Groningen, the Netherlands. He moved to Rotterdam in 1990 to become the scientific director of the Daniel den Hoed Cancer Center. Since 1998 he has been Head of the Department of Pathology — part of the Josephine Nefkens Institute — of the Erasmus University Medical Center Rotterdam, the Netherlands. Additional functions include scientific director of the postgraduate school Molecular Medicine of the Erasmus Medical Center, and of the Daniel den Hoed Cancer Foundation. His main research interests are the pathobiology and therapy resistance of gonadal and extra-gonadal germ-cell tumours.

    Leendert H. J. Looijenga, an associate professor, graduated cum laude in human biology at Groningen University. In 1990 he moved to Rotterdam, and jointly with Wolter Oosterhuis established a research group to study the pathobiology of germ-cell tumours. In 1994 he submitted his thesis on this subject. In 1998 his research group moved to the Josephine Nefkens Institute, to become part of the Department of Pathology of the Erasmus University Medical Center Rotterdam. His main research interests are the pathobiology and therapy resistance of gonadal and extra-gonadal germ-cell tumours; the pathology of dysgenetic gonads; and ploidy-regulated genes in human neoplasia.

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