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Comparative genome hybridization reveals specific genomic imbalances during the genesis from benign through borderline to malignant ovarian tumors.

Helou, Khalil, 1966 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
Padilla-Nash, Hesed (author)
Wangsa, Danny (author)
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Karlsson, Elin, 1979 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
Österberg, Lovisa, 1978 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
Karlsson, Per, 1963 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
Ried, Thomas (author)
Knutsen, Turid (author)
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 (creator_code:org_t)
Elsevier BV, 2006
2006
English.
In: Cancer genetics and cytogenetics. - : Elsevier BV. - 0165-4608. ; 170:1, s. 1-8
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Ovarian cancer is one of the most common types of malignancy in women throughout the developed world. Despite recent therapeutic advances, long-term survival is poor because ovarian cancer is largely asymptomatic in its early stages. Comparative genomic hybridization (CGH) was applied to a series of 8 benign, 8 borderline, and 17 malignant ovarian to establish genomic imbalances associated with tumor progression. Benign and borderline tumors were characterized by losses at 1p32 approximately p11, 2q14 approximately q34, 4q13 approximately q34, 5q11 approximately q23, and 6q12 approximately q24, as well as gains of 6p and chromosome 12. Similar chromosomal changes were also detected in malignant tumors but included additional chromosomal changes: gains at 1q21 approximately q31, 2p, 3q, 5p, 7, 10p, 12p, 16p, 17, 19q, 20q, and 22q, as well as losses at X, 3p, 8p, 9, 11p, 13, 14, and 18. Some individual cases of benign and borderline tumors revealed no genetic alterations detectable by CGH, suggesting that these tumors may represent a subset of tumors that originate by an alternative mechanism of tumorigenesis. Furthermore, our findings reveal that borderline tumors are more similar to benign tumors than to malignant tumors with respect to their genetic profiles.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cancer and Oncology (hsv//eng)

Keyword

Chromosome Aberrations
Female
Genome
Human
Humans
Nucleic Acid Hybridization
Ovarian Neoplasms
genetics
pathology

Publication and Content Type

ref (subject category)
art (subject category)

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