Commercialisation Advisory Group (ComAG)

The Gastro-Intestinal Viral Oncology Group focuses on infectious causes of gastro-intestinal cancer with a special emphasis on Barrett’s oesophagus, a precancerous condition of the oesophagus.

This was the first group in the world to hypothesise (2009 & 2010) and publish (2013, 2014, 2015) evidence to show that human papillomavirus infection is strongly incriminated in the aetiology of Barrett’s dysplasia and oesophageal adenocarcinoma.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The Gastro-Intestinal Viral Oncology Group focuses on infectious causes of gastro-intestinal cancer with a special emphasis on Barrett’s oesophagus, a precancerous condition of the oesophagus.

This was the first group in the world to hypothesise (2009 & 2010) and publish (2013, 2014, 2015) evidence to show that human papillomavirus infection is strongly incriminated in the aetiology of Barrett’s dysplasia and oesophageal adenocarcinoma.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The Gastro-Intestinal Viral Oncology Group focuses on infectious causes of gastro-intestinal cancer with a special emphasis on Barrett’s oesophagus, a precancerous condition of the oesophagus.

This was the first group in the world to hypothesise (2009 & 2010) and publish (2013, 2014, 2015) evidence to show that human papillomavirus infection is strongly incriminated in the aetiology of Barrett’s dysplasia and oesophageal adenocarcinoma.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The Gastro-Intestinal Viral Oncology Group focuses on infectious causes of gastro-intestinal cancer with a special emphasis on Barrett’s oesophagus, a precancerous condition of the oesophagus.

This was the first group in the world to hypothesise (2009 & 2010) and publish (2013, 2014, 2015) evidence to show that human papillomavirus infection is strongly incriminated in the aetiology of Barrett’s dysplasia and oesophageal adenocarcinoma.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.

The Gastro-Intestinal Viral Oncology Group focuses on infectious causes of gastro-intestinal cancer with a special emphasis on Barrett’s oesophagus, a precancerous condition of the oesophagus.

This was the first group in the world to hypothesise (2009 & 2010) and publish (2013, 2014, 2015) evidence to show that human papillomavirus infection is strongly incriminated in the aetiology of Barrett’s dysplasia and oesophageal adenocarcinoma.

The following are world first discoveries made by the Group led by Professor Shan Rajendra.

Demonstrated that both increasing hr-HPV viral load and integration status is linked with more severe disease along the Barrett’s metaplasia-dysplasia-adenocarcinoma sequence.

In a prospective study showed that persistent hr-HPV infection and p53 overexpression (mutation of a tumour suppressor gene) are associated with treatment failure after endoscopic treatment of Barrett’s dysplasia and oesophageal adenocarcinoma

Discovered that HPV associated oesophageal adenocarcinoma had a distinct distribution of molecular aberrations/genomic abnormalities compared with HPV negative oesophageal cancer indicating different biological mechanisms of tumour formation

Hybrid sequences containing HPV16 and the human genome were identified in oesophageal cancer providing evidence for a host-viral interaction

Recently discovered a molecular signature characteristic of HPV driven Barrett’s dysplasia and oesophageal adenocarcinoma.

The Group’s findings have been subject of invited lectures and oral presentations at the EUROGIN (European Genital Infections and Neoplasia) Conferences in Florence 2013, Seville 2015, Salzburg 2016, Amsterdam 2017, OESO Conf (UEGW) in Vienna, 2014 & 2016, 5th Asia-Pacific Gastroesophageal Cancer Congress, Brisbane 2015, and the British Society of Gastroenterology, Endoscopy Masterclass, Nottingham 2015.