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  • 1
    Abstract: Many cell lines derived from solid cancers can form spheroids, which recapitulate tumor cell clusters and are more representative of the in vivo situation than 2D cultures. During spheroid formation, a small proportion of a variety of different colon cancer cell lines did not integrate into the sphere and lost cell-cell adhesion properties. An enrichment protocol was developed to augment the proportion of these cells to 100% purity. The basis for the separation of spheroids from non-spheroid forming (NSF) cells is simple gravity-sedimentation. This protocol gives rise to sub-populations of colon cancer cells with stable loss of cell-cell adhesion. SW620 cells lacked E-cadherin, DLD-1 cells lost alpha-catenin and HCT116 cells lacked P-cadherin in the NSF state. Knockdown of these molecules in the corresponding spheroid-forming cells demonstrated that loss of the respective proteins were indeed responsible for the NSF phenotypes. Loss of the spheroid forming phenotype was associated with increased migration and invasion properties in all cell lines tested. Hence, we identified critical molecules involved in spheroid formation in different cancer cell lines. We present here a simple, powerful and broadly applicable method to generate new sublines of tumor cell lines to study loss of cell-cell adhesion in cancer progression.
    Type of Publication: Journal article published
    PubMed ID: 29348601
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  • 2
    ISSN: 1432-0711
    Keywords: Keywords Factor V Leiden ; Recurrent abortion ; Therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We report a case with one intrauterine fetal death (IUFD) at 32 weeks of gestation, one premature delivery at the same week, and one abortion of unknown etiology at 12 weeks of gestation. We discuss that the presence of homozygosity for Factor V Leiden may be associated with placental insufficiency in this woman. Application of anticoagulant therapy may have been beneficial in her current pregnancy.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0012-1606
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Reproduktionsmedizin 15 (1999), S. 55-64 
    ISSN: 1434-808X
    Keywords: Schlüsselwörter Spermiendefekte ; Transgene Tiere ; Idiopathische Infertilität ; Spermatogenese ; Spermiogenese ; Key words Sperm defects ; Male infertility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract The genetic reasons for male infertility are still poorly understood. In approximately 30 % of infertile men no reason for their defect in spermatogenesis can be found (idiopathic infertility). In a high percentage of these patients single gene defects are assumed to be responsible for the infertility. Well-known reasons for infertility are microdeletions on the long arm of the Y chromosome. In approximately 3–18 % of patients with azoospermia or severe oligospermia these deletions can be detected by using molecular techniques. In 4–6 % of infertile men chromosomal abnormalities are responsible for their andrological disorder. While numeric aberrations are widely observed in patients with azoospermia, alterations in chromosomal structure are prominent in patients with oligozoospermia. Chromosomal anomalies can be found only in rare cases of patients with structural or functional sperm defects. Up to now the genetic basis has only be described for a few functional or structural sperm defects (immotile cilia syndrome, globozoospermia). More recently, it became possible to identify genes involved in spermatogenesis and to investigate their functions in male germ cell differentiation by using new tools of molecular biology, e. g. gene replacement techniques in the mouse. For the majority of these genes homologous human genes are known. However, the role of these genes in human spermatogenesis and their relevance for male fertility have still to be elucidated.
    Notes: Zusammenfassung Die genetische Ursachen männlicher Infertilität sind auch heute noch weitgehend unverstanden. Bei ca. 30 % der infertilen Männern kann keine Ursache für ihre Fertilitätsstörung gefunden werden (sog. idiopathische Infertilität). Bei einem Großteil dieser Männer sind vermutlich Mutationen in Fertilitäts–relevanten Genen für die andrologische Störung verantwortlich. Schon länger bekannt sind Mikrodeletionen im langen Arm des Y-Chromosoms als Ursache für eine Infertilität. Bei ca. 3–18 % der Patienten mit Azoospermie oder schwerer Oligozoospermie lassen sich solche Deletionen molekularbiologisch nachweisen. Chromosomale Anomalien sind bei ca. 4–6 % der infertilen Männer die Ursache ihrer andrologischen Störung. Während numerische Aberrationen gehäuft bei Azoospermikern nachgewiesen werden, finden sich strukturelle chromosomale Veränderungen vermehrt bei Oligozoospermikern. Nur in einzelnen Fällen werden chromosomale Anomalien bei Patienten mit strukturellen oder funktionellen Spermiendefekten beobachtet. Insgesamt sind erst wenige genetisch bedingte funktionelle oder strukturelle Spermiendefekte bekannt (Immotile Cilia Syndrome, Globozoospermie). Durch neue molekularbiologische Techniken gelang es in den letzten Jahren im Tiermodell, Spermatogenese–relevante Gene zu identifizieren und ihre Funktionen in der männlichen Keimzelldifferenzierung aufzuzeigen. Für die meisten dieser Gene sind bereits homologe Gene des Menschen bekannt, die Rolle dieser Gene in der humanen Spermatogenese und die Bedeutung von Mutationen in diesen Genen muß allerdings noch überprüft werden.
    Type of Medium: Electronic Resource
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