Cyclin D1 in parathyroid disease

被引:32
作者
Mallya, SM [1 ]
Arnold, A [1 ]
机构
[1] Univ Connecticut, Ctr Hlth, Ctr Mol Med, Farmington, CT 06030 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2000年 / 5卷
关键词
parathyroid; adenoma; cyclins; neoplasms; cancer; tumor; growth; proliferation; review;
D O I
10.2741/Mallya
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Primary hyperparathyroidism (HPT), most commonly due to parathyroid adenoma, is a disorder characterized by excessive secretion of PTH. So far, abnormalities in two genes, cyclin DI and MEN1, have been implicated in the development of parathyroid adenomas. Cyclin D1, now an established Oncogene involved in numerous human cancers, was first identified and recognized as an Oncogene in the study of parathyroid tumors. A subset of parathyroid adenomas contains a clonal rearrangement that places the PTH gene's regulatory sequences in proximity to the cyclin D1 Oncogene causing its overexpression, and 20-40% of parathyroid adenomas overexpress the cyclin D1 protein. Transgenic animal models have further confirmed the role of cyclin D1 as a driver of abnormal parathyroid cell proliferation. Future studies on the mechanism of cyclin D1's oncogenicity and its interactions with other parathyroid growth regulators will further our understanding of parathyroid cell biology and may prove useful clinically.
引用
收藏
页码:D367 / D371
页数:5
相关论文
共 43 条
  • [1] Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription
    Agarwal, SK
    Guru, SC
    Heppner, C
    Erdos, MR
    Collins, RM
    Park, SY
    Saggar, S
    Chandrasekharappa, SC
    Collins, FS
    Spiegel, AM
    Marx, SJ
    Burns, AL
    [J]. CELL, 1999, 96 (01) : 143 - 152
  • [2] Comparative genomic hybridization analysis of human parathyroid tumors
    Agarwal, SK
    Schröck, E
    Kester, MB
    Burns, AL
    Heffess, CS
    Ried, T
    Marx, SJ
    [J]. CANCER GENETICS AND CYTOGENETICS, 1998, 106 (01) : 30 - 36
  • [3] CLONAL LOSS OF ONE CHROMOSOME-11 IN A PARATHYROID ADENOMA
    ARNOLD, A
    KIM, HG
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1989, 69 (03) : 496 - 499
  • [4] Arnold A, 1995, J INVEST MED, V43, P543
  • [5] MONOCLONALITY AND ABNORMAL PARATHYROID-HORMONE GENES IN PARATHYROID ADENOMAS
    ARNOLD, A
    STAUNTON, CE
    KIM, HG
    GAZ, RD
    KRONENBERG, HM
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1988, 318 (11) : 658 - 662
  • [6] MOLECULAR-CLONING AND CHROMOSOMAL MAPPING OF DNA REARRANGED WITH THE PARATHYROID-HORMONE GENE IN A PARATHYROID ADENOMA
    ARNOLD, A
    KIM, HG
    GAZ, RD
    EDDY, RL
    FUKUSHIMA, Y
    BYERS, MG
    SHOWS, TB
    KRONENBERG, HM
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (06) : 2034 - 2040
  • [7] MONOCLONALITY OF PARATHYROID TUMORS IN CHRONIC-RENAL-FAILURE AND IN PRIMARY PARATHYROID HYPERPLASIA
    ARNOLD, A
    BROWN, MF
    URENA, P
    GAZ, RD
    SARFATI, E
    DRUEKE, TB
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (05) : 2047 - 2053
  • [8] Parathyroid MEN1 gene mutations in relation to clinical characteristics of nonfamilial primary hyperparathyroidism
    Carling, T
    Correa, P
    Hessman, O
    Hedberg, J
    Skogseid, B
    Lindberg, D
    Rastad, J
    Westin, G
    Åkerström, G
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (08) : 2960 - 2963
  • [9] Positional cloning of the gene for multiple endocrine neoplasia-type 1
    Chandrasekharappa, SC
    Guru, SC
    Manickam, P
    Olufemi, SE
    Collins, FS
    EmmertBuck, MR
    Debelenko, LV
    Zhuang, ZP
    Lubensky, IA
    Liotta, LA
    Crabtree, JS
    Wang, YP
    Roe, BA
    Weisemann, J
    Boguski, MS
    Agarwal, SK
    Kester, MB
    Kim, YS
    Heppner, C
    Dong, QH
    Spiegel, AM
    Burns, AL
    Marx, SJ
    [J]. SCIENCE, 1997, 276 (5311) : 404 - 407
  • [10] LOSS OF THE RETINOBLASTOMA TUMOR-SUPPRESSOR GENE IN PARATHYROID CARCINOMA
    CRYNS, VL
    THOR, A
    XU, HJ
    HU, SX
    WIERMAN, ME
    VICKERY, AL
    BENEDICT, WF
    ARNOLD, A
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1994, 330 (11) : 757 - 761