Biological characterization of soft tissue sarcomas

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

Research output: Contribution to journalLetter

3 Citations (Scopus)

Abstract

Soft tissue 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 diagnostic biomarker has been hampered by several critical factors. First, malignant soft tissue sarcomas are rarely observed in the clinic with fewer than 15,000 newly cases diagnosed each year in the United States. Another complicating factor is that soft tissue 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 clinical treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of soft tissue 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 soft tissue sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic and/or tumour suppressive signal cascades, i.e., interferon-γ (IFN-γ), tumour protein 53 (TP53) and/or retinoblastoma (RB) pathway directly impact sarcomagenesis. It is the goal of many in the physiological community that the use of several mouse models will serve as powerful in vivo tools for further understanding of sarcomagenesis and potentially identify new diagnostic biomarker and therapeutic strategies against human soft tissue sarcomas.

Original languageEnglish
Article number368
JournalAnnals of Translational Medicine
Volume3
Issue number22
DOIs
Publication statusPublished - 2015 Dec 1

Fingerprint

Sarcoma
Neoplasms
Biomarkers
Retinoblastoma
Gene Amplification
Gene Deletion
Cell Lineage
Interferons
Therapeutics
Genome
Mutation
Proteins

Keywords

  • Proteasome beta subunit 9/β1i (PSMB9/β1i)
  • Retinoblastoma (RB)
  • Sarcoma
  • Sarcomagenesis
  • Tumour protein 53 (TP53)

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Hayashi, T., Horiuchi, A., Sano, K., Kanai, Y., Yaegashi, N., Aburatani, H., & Konishi, I. (2015). Biological characterization of soft tissue sarcomas. Annals of Translational Medicine, 3(22), [368]. https://doi.org/10.3978/j.issn.2305-5839.2015.12.33

Biological characterization of soft tissue sarcomas. / Hayashi, Takuma; Horiuchi, Akiko; Sano, Kenji; Kanai, Yae; Yaegashi, Nobuo; Aburatani, Hiroyuki; Konishi, Ikuo.

In: Annals of Translational Medicine, Vol. 3, No. 22, 368, 01.12.2015.

Research output: Contribution to journalLetter

Hayashi, T, Horiuchi, A, Sano, K, Kanai, Y, Yaegashi, N, Aburatani, H & Konishi, I 2015, 'Biological characterization of soft tissue sarcomas', Annals of Translational Medicine, vol. 3, no. 22, 368. https://doi.org/10.3978/j.issn.2305-5839.2015.12.33
Hayashi, Takuma ; Horiuchi, Akiko ; Sano, Kenji ; Kanai, Yae ; Yaegashi, Nobuo ; Aburatani, Hiroyuki ; Konishi, Ikuo. / Biological characterization of soft tissue sarcomas. In: Annals of Translational Medicine. 2015 ; Vol. 3, No. 22.
@article{be0704ceae684bdd89607f557454c7c0,
title = "Biological characterization of soft tissue sarcomas",
abstract = "Soft tissue 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 diagnostic biomarker has been hampered by several critical factors. First, malignant soft tissue sarcomas are rarely observed in the clinic with fewer than 15,000 newly cases diagnosed each year in the United States. Another complicating factor is that soft tissue 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 clinical treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of soft tissue 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 soft tissue sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic and/or tumour suppressive signal cascades, i.e., interferon-γ (IFN-γ), tumour protein 53 (TP53) and/or retinoblastoma (RB) pathway directly impact sarcomagenesis. It is the goal of many in the physiological community that the use of several mouse models will serve as powerful in vivo tools for further understanding of sarcomagenesis and potentially identify new diagnostic biomarker and therapeutic strategies against human soft tissue sarcomas.",
keywords = "Proteasome beta subunit 9/β1i (PSMB9/β1i), Retinoblastoma (RB), Sarcoma, Sarcomagenesis, Tumour protein 53 (TP53)",
author = "Takuma Hayashi and Akiko Horiuchi and Kenji Sano and Yae Kanai and Nobuo Yaegashi and Hiroyuki Aburatani and Ikuo Konishi",
year = "2015",
month = "12",
day = "1",
doi = "10.3978/j.issn.2305-5839.2015.12.33",
language = "English",
volume = "3",
journal = "Annals of Translational Medicine",
issn = "2305-5839",
publisher = "AME Publishing Company",
number = "22",

}

TY - JOUR

T1 - Biological characterization of soft tissue sarcomas

AU - Hayashi, Takuma

AU - Horiuchi, Akiko

AU - Sano, Kenji

AU - Kanai, Yae

AU - Yaegashi, Nobuo

AU - Aburatani, Hiroyuki

AU - Konishi, Ikuo

PY - 2015/12/1

Y1 - 2015/12/1

N2 - Soft tissue 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 diagnostic biomarker has been hampered by several critical factors. First, malignant soft tissue sarcomas are rarely observed in the clinic with fewer than 15,000 newly cases diagnosed each year in the United States. Another complicating factor is that soft tissue 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 clinical treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of soft tissue 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 soft tissue sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic and/or tumour suppressive signal cascades, i.e., interferon-γ (IFN-γ), tumour protein 53 (TP53) and/or retinoblastoma (RB) pathway directly impact sarcomagenesis. It is the goal of many in the physiological community that the use of several mouse models will serve as powerful in vivo tools for further understanding of sarcomagenesis and potentially identify new diagnostic biomarker and therapeutic strategies against human soft tissue sarcomas.

AB - Soft tissue 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 diagnostic biomarker has been hampered by several critical factors. First, malignant soft tissue sarcomas are rarely observed in the clinic with fewer than 15,000 newly cases diagnosed each year in the United States. Another complicating factor is that soft tissue 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 clinical treatment options available to patients as compared to other malignant tumours. In order to glean insight into the pathobiology of soft tissue 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 soft tissue sarcomas. The use of these model organisms has been successful in increasing our knowledge and understanding of how alterations in relevant oncogenic and/or tumour suppressive signal cascades, i.e., interferon-γ (IFN-γ), tumour protein 53 (TP53) and/or retinoblastoma (RB) pathway directly impact sarcomagenesis. It is the goal of many in the physiological community that the use of several mouse models will serve as powerful in vivo tools for further understanding of sarcomagenesis and potentially identify new diagnostic biomarker and therapeutic strategies against human soft tissue sarcomas.

KW - Proteasome beta subunit 9/β1i (PSMB9/β1i)

KW - Retinoblastoma (RB)

KW - Sarcoma

KW - Sarcomagenesis

KW - Tumour protein 53 (TP53)

UR - http://www.scopus.com/inward/record.url?scp=85015472842&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85015472842&partnerID=8YFLogxK

U2 - 10.3978/j.issn.2305-5839.2015.12.33

DO - 10.3978/j.issn.2305-5839.2015.12.33

M3 - Letter

AN - SCOPUS:85015472842

VL - 3

JO - Annals of Translational Medicine

JF - Annals of Translational Medicine

SN - 2305-5839

IS - 22

M1 - 368

ER -