Histological complexities of pancreatic lesions from transgenic mouse models are consistent with biological and morphological heterogeneity of human pancreatic cancer

J. D. Liao, N. V. Adsay, F. Khannani, David Grignon, A. Thakur, Faslul H. Sarkar

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Although pancreatic cancer is the fourth leading cause of cancer death, it has received much less attention compared to other malignancies. There are several transgenic animal models available for studies of pancreatic carcinogenesis, but most of them do not recapitulate, histologically, human pancratic cancer. Here we review some detailed molecular complexity of human pancreatic cancer and their reflection in histomorphological complexities of pancreatic lesions developed in various transgenic mouse models with a special concern for studying the effects of chemotherapeutic and chemopreventive agents. These studies usually require a large number of animals that are at the same age and gender and should be either homozygote or heterozygote but not a mixture of both. Only single-transgene models can meet these special requirements, but many currently available models require a mouse to simultaneously bear several transgene alleles. Thus it is imperative to identify new gene promoters or enhancers that are specific for the ductal cells of the pancreas and are highly active in vivo so as to establish new single-transgene models that yield pancreatic ductal adenocarcinomas for chemotherapeutic and chemopreventive studies.

Original languageEnglish (US)
Pages (from-to)661-676
Number of pages16
JournalHistology and Histopathology
Volume22
Issue number4-6
StatePublished - Apr 2007
Externally publishedYes

Fingerprint

Pancreatic Neoplasms
Transgenes
Transgenic Mice
Neoplasms
Genetically Modified Animals
Homozygote
Heterozygote
Pancreas
Cause of Death
Carcinogenesis
Adenocarcinoma
Animal Models
Alleles
Genes

Keywords

  • Animal model
  • Carcinogenesis
  • Molecular signaling

ASJC Scopus subject areas

  • Anatomy
  • Pathology and Forensic Medicine
  • Histology
  • Cell Biology

Cite this

Histological complexities of pancreatic lesions from transgenic mouse models are consistent with biological and morphological heterogeneity of human pancreatic cancer. / Liao, J. D.; Adsay, N. V.; Khannani, F.; Grignon, David; Thakur, A.; Sarkar, Faslul H.

In: Histology and Histopathology, Vol. 22, No. 4-6, 04.2007, p. 661-676.

Research output: Contribution to journalArticle

Liao, J. D. ; Adsay, N. V. ; Khannani, F. ; Grignon, David ; Thakur, A. ; Sarkar, Faslul H. / Histological complexities of pancreatic lesions from transgenic mouse models are consistent with biological and morphological heterogeneity of human pancreatic cancer. In: Histology and Histopathology. 2007 ; Vol. 22, No. 4-6. pp. 661-676.
@article{e78aa0be7e62446a9454dc977644c50a,
title = "Histological complexities of pancreatic lesions from transgenic mouse models are consistent with biological and morphological heterogeneity of human pancreatic cancer",
abstract = "Although pancreatic cancer is the fourth leading cause of cancer death, it has received much less attention compared to other malignancies. There are several transgenic animal models available for studies of pancreatic carcinogenesis, but most of them do not recapitulate, histologically, human pancratic cancer. Here we review some detailed molecular complexity of human pancreatic cancer and their reflection in histomorphological complexities of pancreatic lesions developed in various transgenic mouse models with a special concern for studying the effects of chemotherapeutic and chemopreventive agents. These studies usually require a large number of animals that are at the same age and gender and should be either homozygote or heterozygote but not a mixture of both. Only single-transgene models can meet these special requirements, but many currently available models require a mouse to simultaneously bear several transgene alleles. Thus it is imperative to identify new gene promoters or enhancers that are specific for the ductal cells of the pancreas and are highly active in vivo so as to establish new single-transgene models that yield pancreatic ductal adenocarcinomas for chemotherapeutic and chemopreventive studies.",
keywords = "Animal model, Carcinogenesis, Molecular signaling",
author = "Liao, {J. D.} and Adsay, {N. V.} and F. Khannani and David Grignon and A. Thakur and Sarkar, {Faslul H.}",
year = "2007",
month = "4",
language = "English (US)",
volume = "22",
pages = "661--676",
journal = "Histology and Histopathology",
issn = "0213-3911",
publisher = "Histology and Histopathology",
number = "4-6",

}

TY - JOUR

T1 - Histological complexities of pancreatic lesions from transgenic mouse models are consistent with biological and morphological heterogeneity of human pancreatic cancer

AU - Liao, J. D.

AU - Adsay, N. V.

AU - Khannani, F.

AU - Grignon, David

AU - Thakur, A.

AU - Sarkar, Faslul H.

PY - 2007/4

Y1 - 2007/4

N2 - Although pancreatic cancer is the fourth leading cause of cancer death, it has received much less attention compared to other malignancies. There are several transgenic animal models available for studies of pancreatic carcinogenesis, but most of them do not recapitulate, histologically, human pancratic cancer. Here we review some detailed molecular complexity of human pancreatic cancer and their reflection in histomorphological complexities of pancreatic lesions developed in various transgenic mouse models with a special concern for studying the effects of chemotherapeutic and chemopreventive agents. These studies usually require a large number of animals that are at the same age and gender and should be either homozygote or heterozygote but not a mixture of both. Only single-transgene models can meet these special requirements, but many currently available models require a mouse to simultaneously bear several transgene alleles. Thus it is imperative to identify new gene promoters or enhancers that are specific for the ductal cells of the pancreas and are highly active in vivo so as to establish new single-transgene models that yield pancreatic ductal adenocarcinomas for chemotherapeutic and chemopreventive studies.

AB - Although pancreatic cancer is the fourth leading cause of cancer death, it has received much less attention compared to other malignancies. There are several transgenic animal models available for studies of pancreatic carcinogenesis, but most of them do not recapitulate, histologically, human pancratic cancer. Here we review some detailed molecular complexity of human pancreatic cancer and their reflection in histomorphological complexities of pancreatic lesions developed in various transgenic mouse models with a special concern for studying the effects of chemotherapeutic and chemopreventive agents. These studies usually require a large number of animals that are at the same age and gender and should be either homozygote or heterozygote but not a mixture of both. Only single-transgene models can meet these special requirements, but many currently available models require a mouse to simultaneously bear several transgene alleles. Thus it is imperative to identify new gene promoters or enhancers that are specific for the ductal cells of the pancreas and are highly active in vivo so as to establish new single-transgene models that yield pancreatic ductal adenocarcinomas for chemotherapeutic and chemopreventive studies.

KW - Animal model

KW - Carcinogenesis

KW - Molecular signaling

UR - http://www.scopus.com/inward/record.url?scp=34247465590&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34247465590&partnerID=8YFLogxK

M3 - Article

C2 - 17357096

AN - SCOPUS:34247465590

VL - 22

SP - 661

EP - 676

JO - Histology and Histopathology

JF - Histology and Histopathology

SN - 0213-3911

IS - 4-6

ER -