The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma

Victoria Hodges; Christie Fumbah; Junaith Mohamed; Sheila Criswell

doi:doi:10.11648/j.crj.20221003.12

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The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma

Victoria Hodges, Christie Fumbah, Junaith Mohamed, Sheila Criswell

Published in Cancer Research Journal (Volume 10, Issue 3)

Received: 15 June 2022 Accepted: 29 June 2022 Published: 12 July 2022

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Abstract

Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of cancer with a 5-year survival of only 7% for both men and women. Despite substantial progress made in successfully personalizing treatment for other tumors such as breast, prostate, and lung, treatment for PDA remains elusive due, in part, to its unique growth pattern and lack of surveillance tools to detect early lesions. Because most PDA lesions have metastasized at the time of diagnosis and exhibit a heterogeneously infiltrative growth pattern by interdigitating malignant cells among various normal tissue components, decisive, targeted therapies are needed to remove tumor cells while leaving the surrounding benign tissues undamaged. In an effort to identify biomarkers, immunohistochemistry assays were employed to determine the expression of Ki-67, KLK7, YAP1, CK 5, CK 20, CEA, GATA3, XAF1, STAG2, CK 18, ERBB2, and P53 in 42 formalin-fixed, paraffin-embedded PDA samples. Although no statistically significant correlation was associated with tumor aggressiveness as determined by Ki-67 positivity, several pairs of markers demonstrated positive correlations with each other and included ERBB2/STAG2, ERBB/YAP1, ERBB/GATA3, ERBB/P53, GATA3/STAG2, and GATA3/YAP1. Characterization of individual tumors with respect to over- or under-expression of specific proteins may offer dual therapy targets in PDA to potentially improve patient outcomes.

Published in	Cancer Research Journal (Volume 10, Issue 3)
DOI	10.11648/j.crj.20221003.12
Page(s)	61-69
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), 2024. Published by Science Publishing Group

Keywords

Cancer, Pancreas, Therapy

References

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APA Style

Victoria Hodges, Christie Fumbah, Junaith Mohamed, Sheila Criswell. (2022). The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Research Journal, 10(3), 61-69. https://doi.org/10.11648/j.crj.20221003.12

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ACS Style

Victoria Hodges; Christie Fumbah; Junaith Mohamed; Sheila Criswell. The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Res. J. 2022, 10(3), 61-69. doi: 10.11648/j.crj.20221003.12

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AMA Style

Victoria Hodges, Christie Fumbah, Junaith Mohamed, Sheila Criswell. The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Res J. 2022;10(3):61-69. doi: 10.11648/j.crj.20221003.12

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@article{10.11648/j.crj.20221003.12,
  author = {Victoria Hodges and Christie Fumbah and Junaith Mohamed and Sheila Criswell},
  title = {The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma},
  journal = {Cancer Research Journal},
  volume = {10},
  number = {3},
  pages = {61-69},
  doi = {10.11648/j.crj.20221003.12},
  url = {https://doi.org/10.11648/j.crj.20221003.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20221003.12},
  abstract = {Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of cancer with a 5-year survival of only 7% for both men and women. Despite substantial progress made in successfully personalizing treatment for other tumors such as breast, prostate, and lung, treatment for PDA remains elusive due, in part, to its unique growth pattern and lack of surveillance tools to detect early lesions. Because most PDA lesions have metastasized at the time of diagnosis and exhibit a heterogeneously infiltrative growth pattern by interdigitating malignant cells among various normal tissue components, decisive, targeted therapies are needed to remove tumor cells while leaving the surrounding benign tissues undamaged. In an effort to identify biomarkers, immunohistochemistry assays were employed to determine the expression of Ki-67, KLK7, YAP1, CK 5, CK 20, CEA, GATA3, XAF1, STAG2, CK 18, ERBB2, and P53 in 42 formalin-fixed, paraffin-embedded PDA samples. Although no statistically significant correlation was associated with tumor aggressiveness as determined by Ki-67 positivity, several pairs of markers demonstrated positive correlations with each other and included ERBB2/STAG2, ERBB/YAP1, ERBB/GATA3, ERBB/P53, GATA3/STAG2, and GATA3/YAP1. Characterization of individual tumors with respect to over- or under-expression of specific proteins may offer dual therapy targets in PDA to potentially improve patient outcomes.},
 year = {2022}
}

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TY  - JOUR
T1  - The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma
AU  - Victoria Hodges
AU  - Christie Fumbah
AU  - Junaith Mohamed
AU  - Sheila Criswell
Y1  - 2022/07/12
PY  - 2022
N1  - https://doi.org/10.11648/j.crj.20221003.12
DO  - 10.11648/j.crj.20221003.12
T2  - Cancer Research Journal
JF  - Cancer Research Journal
JO  - Cancer Research Journal
SP  - 61
EP  - 69
PB  - Science Publishing Group
SN  - 2330-8214
UR  - https://doi.org/10.11648/j.crj.20221003.12
AB  - Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of cancer with a 5-year survival of only 7% for both men and women. Despite substantial progress made in successfully personalizing treatment for other tumors such as breast, prostate, and lung, treatment for PDA remains elusive due, in part, to its unique growth pattern and lack of surveillance tools to detect early lesions. Because most PDA lesions have metastasized at the time of diagnosis and exhibit a heterogeneously infiltrative growth pattern by interdigitating malignant cells among various normal tissue components, decisive, targeted therapies are needed to remove tumor cells while leaving the surrounding benign tissues undamaged. In an effort to identify biomarkers, immunohistochemistry assays were employed to determine the expression of Ki-67, KLK7, YAP1, CK 5, CK 20, CEA, GATA3, XAF1, STAG2, CK 18, ERBB2, and P53 in 42 formalin-fixed, paraffin-embedded PDA samples. Although no statistically significant correlation was associated with tumor aggressiveness as determined by Ki-67 positivity, several pairs of markers demonstrated positive correlations with each other and included ERBB2/STAG2, ERBB/YAP1, ERBB/GATA3, ERBB/P53, GATA3/STAG2, and GATA3/YAP1. Characterization of individual tumors with respect to over- or under-expression of specific proteins may offer dual therapy targets in PDA to potentially improve patient outcomes.
VL  - 10
IS  - 3
ER  -

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Author Information

Victoria Hodges

Department of Pathology, Methodist University Hospital, Memphis, USA
Christie Fumbah

Department of Diagnostic and Health Sciences, University of Tennessee Health Science Center, Memphis, USA
Junaith Mohamed

Department of Diagnostic and Health Sciences, University of Tennessee Health Science Center, Memphis, USA
Sheila Criswell

Department of Diagnostic and Health Sciences, University of Tennessee Health Science Center, Memphis, USA

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Victoria Hodges, Christie Fumbah, Junaith Mohamed, Sheila Criswell. (2022). The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Research Journal, 10(3), 61-69. https://doi.org/10.11648/j.crj.20221003.12

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ACS Style

Victoria Hodges; Christie Fumbah; Junaith Mohamed; Sheila Criswell. The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Res. J. 2022, 10(3), 61-69. doi: 10.11648/j.crj.20221003.12

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AMA Style

Victoria Hodges, Christie Fumbah, Junaith Mohamed, Sheila Criswell. The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma. Cancer Res J. 2022;10(3):61-69. doi: 10.11648/j.crj.20221003.12

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@article{10.11648/j.crj.20221003.12,
  author = {Victoria Hodges and Christie Fumbah and Junaith Mohamed and Sheila Criswell},
  title = {The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma},
  journal = {Cancer Research Journal},
  volume = {10},
  number = {3},
  pages = {61-69},
  doi = {10.11648/j.crj.20221003.12},
  url = {https://doi.org/10.11648/j.crj.20221003.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20221003.12},
  abstract = {Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of cancer with a 5-year survival of only 7% for both men and women. Despite substantial progress made in successfully personalizing treatment for other tumors such as breast, prostate, and lung, treatment for PDA remains elusive due, in part, to its unique growth pattern and lack of surveillance tools to detect early lesions. Because most PDA lesions have metastasized at the time of diagnosis and exhibit a heterogeneously infiltrative growth pattern by interdigitating malignant cells among various normal tissue components, decisive, targeted therapies are needed to remove tumor cells while leaving the surrounding benign tissues undamaged. In an effort to identify biomarkers, immunohistochemistry assays were employed to determine the expression of Ki-67, KLK7, YAP1, CK 5, CK 20, CEA, GATA3, XAF1, STAG2, CK 18, ERBB2, and P53 in 42 formalin-fixed, paraffin-embedded PDA samples. Although no statistically significant correlation was associated with tumor aggressiveness as determined by Ki-67 positivity, several pairs of markers demonstrated positive correlations with each other and included ERBB2/STAG2, ERBB/YAP1, ERBB/GATA3, ERBB/P53, GATA3/STAG2, and GATA3/YAP1. Characterization of individual tumors with respect to over- or under-expression of specific proteins may offer dual therapy targets in PDA to potentially improve patient outcomes.},
 year = {2022}
}

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TY  - JOUR
T1  - The Relationship Among Ki-67, ERBB2, GATA3, STAG2, P53, and YAP1 in Pancreatic Ductal Adenocarcinoma
AU  - Victoria Hodges
AU  - Christie Fumbah
AU  - Junaith Mohamed
AU  - Sheila Criswell
Y1  - 2022/07/12
PY  - 2022
N1  - https://doi.org/10.11648/j.crj.20221003.12
DO  - 10.11648/j.crj.20221003.12
T2  - Cancer Research Journal
JF  - Cancer Research Journal
JO  - Cancer Research Journal
SP  - 61
EP  - 69
PB  - Science Publishing Group
SN  - 2330-8214
UR  - https://doi.org/10.11648/j.crj.20221003.12
AB  - Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal forms of cancer with a 5-year survival of only 7% for both men and women. Despite substantial progress made in successfully personalizing treatment for other tumors such as breast, prostate, and lung, treatment for PDA remains elusive due, in part, to its unique growth pattern and lack of surveillance tools to detect early lesions. Because most PDA lesions have metastasized at the time of diagnosis and exhibit a heterogeneously infiltrative growth pattern by interdigitating malignant cells among various normal tissue components, decisive, targeted therapies are needed to remove tumor cells while leaving the surrounding benign tissues undamaged. In an effort to identify biomarkers, immunohistochemistry assays were employed to determine the expression of Ki-67, KLK7, YAP1, CK 5, CK 20, CEA, GATA3, XAF1, STAG2, CK 18, ERBB2, and P53 in 42 formalin-fixed, paraffin-embedded PDA samples. Although no statistically significant correlation was associated with tumor aggressiveness as determined by Ki-67 positivity, several pairs of markers demonstrated positive correlations with each other and included ERBB2/STAG2, ERBB/YAP1, ERBB/GATA3, ERBB/P53, GATA3/STAG2, and GATA3/YAP1. Characterization of individual tumors with respect to over- or under-expression of specific proteins may offer dual therapy targets in PDA to potentially improve patient outcomes.
VL  - 10
IS  - 3
ER  -

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