Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours

Takuma Hayashi; Akiko Horiuchi; Kenji Sano; Nobuo Yaegashi; Hiroyuki Aburatani; Ikuo Konishi

doi:doi:10.11648/j.bio.20150305.14

| Peer-Reviewed

Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours

Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Nobuo Yaegashi, Hiroyuki Aburatani, Ikuo Konishi

Published in American Journal of Bioscience and Bioengineering (Volume 3, Issue 5)

Received: 9 September 2015 Accepted: 21 September 2015 Published: 9 October 2015

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

Sarcomas are neoplastic malignancies that typically arise in tissues of mesenchymal origin. The identification of novel molecular mechanisms leading to mesenchymal transformation and the establishment of new therapies and biomarker has been hampered by several critical factors. First, this type of malignant tumour is rarely observed in the clinic with fewer than 15, 000 newly cases diagnosed each year in the United States. Another complicating factor is that sarcomas are extremely heterogeneous as they arise in a multitude of tissues from many different cell lineages. The scarcity of clinical materials coupled with its inherent heterogeneity creates a challenging experimental environment for clinicians and scientists. Faced with these challenges, there has been extremely limited advancement in treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of sarcomas, scientists are now using mouse models whose genomes have been specifically tailored to carry gene deletions, gene amplifications, and somatic mutations commonly observed in human sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic, tumour suppressive, and signaling pathways directly impact sarcomagenesis. It is the goal of many in the biological community that the use of these mouse models will serve as powerful in vivo tools to further our understanding of sarcomagenesis and potentially identify new biomarker and therapeutic strategies.

Published in	American Journal of Bioscience and Bioengineering (Volume 3, Issue 5)
DOI	10.11648/j.bio.20150305.14
Page(s)	47-49
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2015. Published by Science Publishing Group

Keywords

Mesenchymal Tumour, Leimyosarcoma, PSMB9, TUMOUR PROTEIN 53 (TP53), RETINOBLASTOMA (RB)

References

[1]	Lasota J, Fanburg - Smith JC. (2007): Genetics for the diagnosis and treatment of mesenchymal tumors. Semin. Musculoskelet Radiol. 11 (3): 215 - 230.
[2]	Taylor BS, Barretina J, Maki RG, Antonescu CR, Singer S, Ladanyi M. (2011): Advances in sarcoma genomics and new therapeutic targets. Nat. Rev. Cancer 11 (8): 541 - 557.
[3]	Hayashi T, Faustman DL. (2002): Development of spontaneous uterine tumors in low molecular mass polypeptide - 2 knockout mice. Cancer Res. 62: 24 – 27.
[4]	Peters JM, Franke WW, Kleinschmidt JA. (1994): Distinct 19 S and 20 S subcomplexes of the 26 S proteasome and their distribution in the nucleus and the cytoplasm. J. Biol. Chem. 269: 7709 - 7718.
[5]	Lodish H, Berk A, Matsudaira P, Kaiser CA, Krieger M, Scott MP, Zipursky SL, Darnell J. (2004): "3". Mol Cell Biol (5th ed.). New York: W.H. Freeman and CO. 5: 66 - 72.
[6]	Konstantinova IM, Tsimokha AS, Mittenberg AG. (2008): Role of proteasomes in cellular regulation. Intl. Rev. Cell Mol. Biol. 267: 59 - 124.
[7]	Wang J, Maldonado MA. (2006): The Ubiquitin - Proteasome System and Its Role in Inflammatory and Autoimmune Diseases. Cell. Mol. Immunol. 3: 255 - 261.
[8]	Van Kaer L, Ashton - Rickardt PG, Eichelberger M, Gaczynska M, Nagashima K, Rock KL, Goldberg AL, Doherty PC, Tonegawa S. (1994): Altered peptidase and viral - specifi c T cell response in LMP2 mutant mice. Immunity 1: 533 - 541.
[9]	Hayashi T, Kodama S, Faustman D.: LMP2 expression and proteasome activity in NOD mice. (2000): Nature Medicine 6: 1064 - 1066.
[10]	Hayashi T, Horiuchi A, Sano K, Hiraoka N, Kasai M, Ichimura T, Sudo T, Tagawa Y, Nishimura R, Ishiko O, Kanai Y, Yaegashi N, Aburatani H, Shiozawa T, Konishi I. (2011): Potential role of LMP2 as tumor - suppressor defines new targets for uterine leiomyosarcoma therapy. Sci. Rep. 1: 180.
[11]	Hayashi T, Horiuchi A, Sano K, Hiraoka N, Kasai M, Ichimura T, Nagase S, Ishiko O, Kanai Y, Yaegashi N, Aburatani H, Shiozawa T, Konishi I. (2012): Potential role of LMP2 as an anti - oncogenic factor in human uterine leiomyosarcoma: morphological significance of calponin h1. FEBS Letters 586 (13): 1824 - 1831.
[12]	Vogelstein B, Lane D, Levine AJ. (2000): Surfing the p53 network. Nature 408 (6810): 307 - 310.
[13]	Raycroft L, Wu HY, Lozano G. (1990): Transcriptional activation by wild - type but not transforming mutants of the p53 anti - oncogene. Science 249 (4972): 1049 - 1051.
[14]	Wang LL. (2005): Biology of osteogenic sarcoma. Cancer J. 11 (4): 294–305.
[15]	Oliner JD, Kinzler KW, Meltzer PS, George DL, Vogelstein B. (1992): Amplification of a gene encoding a p53 - associated protein in human sarcomas. Nature 358 (6381): 80 - 83.
[16]	Oliner JD, Pietenpol JA, Thiagalingam S, Gyuris J, Kinzler KW, Vogelstein B. (1993): Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53. Nature 362 (6423): 857 - 860.
[17]	Ito M, Barys L, O'Reilly T, Young S, Gorbatcheva B, Monahan J, Zumstein - Mecker S, Choong PF, Dickinson I, Crowe P, Hemmings C, Desai J, Thomas DM, Lisztwan J. (2011): Comprehensive Mapping of p53 Pathway Alterations Reveals an Apparent Role for Both SNP309 and MDM2 Amplification in Sarcomagenesis. Clin. Cancer Res. 17 (3): 416 - 426.
[18]	Deshpande A, Hinds PW. (2006): The retinoblastoma protein in osteoblast differentiation and osteosarcoma. Curr. Mol. Med. 6 (7): 809 - 817.
[19]	Toguchida J, Ishizaki K, Sasaki MS, Nakamura Y, Ikenaga M, Kato M, Sugimot M, Kotoura Y, Yamamuro T. (1989): Preferential mutation of paternally derived RB gene as the initial event in sporadic osteosarcoma. Nature 338 (6211): 156 - 158.
[20]	Oda Y, Yamamoto H, Takahira T, Kobayashi C, Kawaguchi K, Tateishi N, Nozuka Y, Tamiya S, Tanaka K, Matsuda S, Yokoyama R, Iwamoto Y, Tsuneyoshi M. (2005): Frequent alteration of p 16 (INK4a)/p 14 (ARF) and p53 pathways in the round cell component of myxoid/round cell liposarcoma: p53 gene alterations and reduced p 14 (ARF) expression both correlate with poor prognosis. J. Pathol. 207 (4): 410 - 421.

Cite This Article

Plain Text BibTeX RIS

APA Style

Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Nobuo Yaegashi, Hiroyuki Aburatani, et al. (2015). Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. American Journal of Bioscience and Bioengineering, 3(5), 47-49. https://doi.org/10.11648/j.bio.20150305.14

Copy | Download

ACS Style

Takuma Hayashi; Akiko Horiuchi; Kenji Sano; Nobuo Yaegashi; Hiroyuki Aburatani, et al. Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. Am. J. BioSci. Bioeng. 2015, 3(5), 47-49. doi: 10.11648/j.bio.20150305.14

Copy | Download

AMA Style

Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Nobuo Yaegashi, Hiroyuki Aburatani, et al. Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. Am J BioSci Bioeng. 2015;3(5):47-49. doi: 10.11648/j.bio.20150305.14

Copy | Download

@article{10.11648/j.bio.20150305.14,
  author = {Takuma Hayashi and Akiko Horiuchi and Kenji Sano and Nobuo Yaegashi and Hiroyuki Aburatani and Ikuo Konishi},
  title = {Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours},
  journal = {American Journal of Bioscience and Bioengineering},
  volume = {3},
  number = {5},
  pages = {47-49},
  doi = {10.11648/j.bio.20150305.14},
  url = {https://doi.org/10.11648/j.bio.20150305.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.bio.20150305.14},
  abstract = {Sarcomas are neoplastic malignancies that typically arise in tissues of mesenchymal origin. The identification of novel molecular mechanisms leading to mesenchymal transformation and the establishment of new therapies and biomarker has been hampered by several critical factors. First, this type of malignant tumour is rarely observed in the clinic with fewer than 15, 000 newly cases diagnosed each year in the United States. Another complicating factor is that sarcomas are extremely heterogeneous as they arise in a multitude of tissues from many different cell lineages. The scarcity of clinical materials coupled with its inherent heterogeneity creates a challenging experimental environment for clinicians and scientists. Faced with these challenges, there has been extremely limited advancement in treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of sarcomas, scientists are now using mouse models whose genomes have been specifically tailored to carry gene deletions, gene amplifications, and somatic mutations commonly observed in human sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic, tumour suppressive, and signaling pathways directly impact sarcomagenesis. It is the goal of many in the biological community that the use of these mouse models will serve as powerful in vivo tools to further our understanding of sarcomagenesis and potentially identify new biomarker and therapeutic strategies.},
 year = {2015}
}

Copy | Download

TY  - JOUR
T1  - Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours
AU  - Takuma Hayashi
AU  - Akiko Horiuchi
AU  - Kenji Sano
AU  - Nobuo Yaegashi
AU  - Hiroyuki Aburatani
AU  - Ikuo Konishi
Y1  - 2015/10/09
PY  - 2015
N1  - https://doi.org/10.11648/j.bio.20150305.14
DO  - 10.11648/j.bio.20150305.14
T2  - American Journal of Bioscience and Bioengineering
JF  - American Journal of Bioscience and Bioengineering
JO  - American Journal of Bioscience and Bioengineering
SP  - 47
EP  - 49
PB  - Science Publishing Group
SN  - 2328-5893
UR  - https://doi.org/10.11648/j.bio.20150305.14
AB  - Sarcomas are neoplastic malignancies that typically arise in tissues of mesenchymal origin. The identification of novel molecular mechanisms leading to mesenchymal transformation and the establishment of new therapies and biomarker has been hampered by several critical factors. First, this type of malignant tumour is rarely observed in the clinic with fewer than 15, 000 newly cases diagnosed each year in the United States. Another complicating factor is that sarcomas are extremely heterogeneous as they arise in a multitude of tissues from many different cell lineages. The scarcity of clinical materials coupled with its inherent heterogeneity creates a challenging experimental environment for clinicians and scientists. Faced with these challenges, there has been extremely limited advancement in treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of sarcomas, scientists are now using mouse models whose genomes have been specifically tailored to carry gene deletions, gene amplifications, and somatic mutations commonly observed in human sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic, tumour suppressive, and signaling pathways directly impact sarcomagenesis. It is the goal of many in the biological community that the use of these mouse models will serve as powerful in vivo tools to further our understanding of sarcomagenesis and potentially identify new biomarker and therapeutic strategies.
VL  - 3
IS  - 5
ER  -

Copy | Download

Author Information

Takuma Hayashi

Department of Immunology and Infectious Disease, Shinshu University School of Medicine, Nagano, Japan
Akiko Horiuchi

Horiuchi Ladies Clinic, Nagano, Japan
Kenji Sano

Department of Laboratory Medicine, Shinshu University Hospital, Nagano, Japan
Nobuo Yaegashi

Department of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, Miyagi, Japan
Hiroyuki Aburatani

The Cancer System Laboratory, Research Center for Advanced Science and Technology, the University of Tokyo, Tokyo, Japan
Ikuo Konishi

Department of Obstetrics and Gynecology, Kyoto University Graduate School of Medicine, Kyoto, Japan

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Nobuo Yaegashi, Hiroyuki Aburatani, et al. (2015). Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. American Journal of Bioscience and Bioengineering, 3(5), 47-49. https://doi.org/10.11648/j.bio.20150305.14

Copy | Download

ACS Style

Takuma Hayashi; Akiko Horiuchi; Kenji Sano; Nobuo Yaegashi; Hiroyuki Aburatani, et al. Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. Am. J. BioSci. Bioeng. 2015, 3(5), 47-49. doi: 10.11648/j.bio.20150305.14

Copy | Download

AMA Style

Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Nobuo Yaegashi, Hiroyuki Aburatani, et al. Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours. Am J BioSci Bioeng. 2015;3(5):47-49. doi: 10.11648/j.bio.20150305.14

Copy | Download

@article{10.11648/j.bio.20150305.14,
  author = {Takuma Hayashi and Akiko Horiuchi and Kenji Sano and Nobuo Yaegashi and Hiroyuki Aburatani and Ikuo Konishi},
  title = {Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours},
  journal = {American Journal of Bioscience and Bioengineering},
  volume = {3},
  number = {5},
  pages = {47-49},
  doi = {10.11648/j.bio.20150305.14},
  url = {https://doi.org/10.11648/j.bio.20150305.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.bio.20150305.14},
  abstract = {Sarcomas are neoplastic malignancies that typically arise in tissues of mesenchymal origin. The identification of novel molecular mechanisms leading to mesenchymal transformation and the establishment of new therapies and biomarker has been hampered by several critical factors. First, this type of malignant tumour is rarely observed in the clinic with fewer than 15, 000 newly cases diagnosed each year in the United States. Another complicating factor is that sarcomas are extremely heterogeneous as they arise in a multitude of tissues from many different cell lineages. The scarcity of clinical materials coupled with its inherent heterogeneity creates a challenging experimental environment for clinicians and scientists. Faced with these challenges, there has been extremely limited advancement in treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of sarcomas, scientists are now using mouse models whose genomes have been specifically tailored to carry gene deletions, gene amplifications, and somatic mutations commonly observed in human sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic, tumour suppressive, and signaling pathways directly impact sarcomagenesis. It is the goal of many in the biological community that the use of these mouse models will serve as powerful in vivo tools to further our understanding of sarcomagenesis and potentially identify new biomarker and therapeutic strategies.},
 year = {2015}
}

Copy | Download

TY  - JOUR
T1  - Molecular Approaches for Understanding of the Uterine Malignant Mesenchymal Tumours
AU  - Takuma Hayashi
AU  - Akiko Horiuchi
AU  - Kenji Sano
AU  - Nobuo Yaegashi
AU  - Hiroyuki Aburatani
AU  - Ikuo Konishi
Y1  - 2015/10/09
PY  - 2015
N1  - https://doi.org/10.11648/j.bio.20150305.14
DO  - 10.11648/j.bio.20150305.14
T2  - American Journal of Bioscience and Bioengineering
JF  - American Journal of Bioscience and Bioengineering
JO  - American Journal of Bioscience and Bioengineering
SP  - 47
EP  - 49
PB  - Science Publishing Group
SN  - 2328-5893
UR  - https://doi.org/10.11648/j.bio.20150305.14
AB  - Sarcomas are neoplastic malignancies that typically arise in tissues of mesenchymal origin. The identification of novel molecular mechanisms leading to mesenchymal transformation and the establishment of new therapies and biomarker has been hampered by several critical factors. First, this type of malignant tumour is rarely observed in the clinic with fewer than 15, 000 newly cases diagnosed each year in the United States. Another complicating factor is that sarcomas are extremely heterogeneous as they arise in a multitude of tissues from many different cell lineages. The scarcity of clinical materials coupled with its inherent heterogeneity creates a challenging experimental environment for clinicians and scientists. Faced with these challenges, there has been extremely limited advancement in treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of sarcomas, scientists are now using mouse models whose genomes have been specifically tailored to carry gene deletions, gene amplifications, and somatic mutations commonly observed in human sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic, tumour suppressive, and signaling pathways directly impact sarcomagenesis. It is the goal of many in the biological community that the use of these mouse models will serve as powerful in vivo tools to further our understanding of sarcomagenesis and potentially identify new biomarker and therapeutic strategies.
VL  - 3
IS  - 5
ER  -

Copy | Download