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Is CD146 pivotal in neoplasm invasion and blastocyst embedding?

Blastocyst embedding is very similar to neoplasm invasion. Blastocyst embedding is seeding the young plant of life, while neoplasm invasion is knocking at the door of death. Overexpression of melanoma cell adhesion molecule (CD146 or MCAM), a novel member of the immunoglobulingene superfamily, promo... Full description

Journal Title: Medical Hypotheses 2011, Vol.76(3), pp.378-380
Main Author: Chen, Wei
Other Authors: Cao, Gang , Zhang, Sen-Lin
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0306-9877 ; DOI: 10.1016/j.mehy.2010.10.045
Link: http://dx.doi.org/10.1016/j.mehy.2010.10.045
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recordid: sciversesciencedirect_elsevierS0306-9877(10)00458-5
title: Is CD146 pivotal in neoplasm invasion and blastocyst embedding?
format: Article
creator:
  • Chen, Wei
  • Cao, Gang
  • Zhang, Sen-Lin
subjects:
  • Tumors
  • Melanoma
ispartof: Medical Hypotheses, 2011, Vol.76(3), pp.378-380
description: Blastocyst embedding is very similar to neoplasm invasion. Blastocyst embedding is seeding the young plant of life, while neoplasm invasion is knocking at the door of death. Overexpression of melanoma cell adhesion molecule (CD146 or MCAM), a novel member of the immunoglobulingene superfamily, promotes invasion, metastasis, growth and survival of malignant cells, and implantation of blastocyst embedding in placenta. We hypothesize that CD146 may be a key gene both in neoplasm invasion and blastocyst embedding because of its ability in regulating cell invasion. The regulation of CD146 expression may be a control switch in the progress of the neoplasm invasion and blastocyst embedding. If the hypothesis is correct, the inhibition of CD146 can be used to prevent and/or treat tumor invasion. Current treatment modalities of tumor invasion include different therapies: surgical resection, radiotherapy, chemotherapy, etc. These treatments are all non-specific to tumor cells. If further studies proof our hypothesis, CD146 may be a candidate target gene in gene therapy of tumor invasion and in regulation of blastocyst embedding.
language: eng
source:
identifier: ISSN: 0306-9877 ; DOI: 10.1016/j.mehy.2010.10.045
fulltext: fulltext
issn:
  • 03069877
  • 0306-9877
url: Link


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descriptionBlastocyst embedding is very similar to neoplasm invasion. Blastocyst embedding is seeding the young plant of life, while neoplasm invasion is knocking at the door of death. Overexpression of melanoma cell adhesion molecule (CD146 or MCAM), a novel member of the immunoglobulingene superfamily, promotes invasion, metastasis, growth and survival of malignant cells, and implantation of blastocyst embedding in placenta. We hypothesize that CD146 may be a key gene both in neoplasm invasion and blastocyst embedding because of its ability in regulating cell invasion. The regulation of CD146 expression may be a control switch in the progress of the neoplasm invasion and blastocyst embedding. If the hypothesis is correct, the inhibition of CD146 can be used to prevent and/or treat tumor invasion. Current treatment modalities of tumor invasion include different therapies: surgical resection, radiotherapy, chemotherapy, etc. These treatments are all non-specific to tumor cells. If further studies proof our hypothesis, CD146 may be a candidate target gene in gene therapy of tumor invasion and in regulation of blastocyst embedding.
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abstractBlastocyst embedding is very similar to neoplasm invasion. Blastocyst embedding is seeding the young plant of life, while neoplasm invasion is knocking at the door of death. Overexpression of melanoma cell adhesion molecule (CD146 or MCAM), a novel member of the immunoglobulingene superfamily, promotes invasion, metastasis, growth and survival of malignant cells, and implantation of blastocyst embedding in placenta. We hypothesize that CD146 may be a key gene both in neoplasm invasion and blastocyst embedding because of its ability in regulating cell invasion. The regulation of CD146 expression may be a control switch in the progress of the neoplasm invasion and blastocyst embedding. If the hypothesis is correct, the inhibition of CD146 can be used to prevent and/or treat tumor invasion. Current treatment modalities of tumor invasion include different therapies: surgical resection, radiotherapy, chemotherapy, etc. These treatments are all non-specific to tumor cells. If further studies proof our hypothesis, CD146 may be a candidate target gene in gene therapy of tumor invasion and in regulation of blastocyst embedding.
pubElsevier Ltd
doi10.1016/j.mehy.2010.10.045
eissn15322777