Prof. Adam E. Frampton
Imperial College London
+1
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Academic Career Length
17Years (2010-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications10 May 2018 in Nature Communications
Journal Article
Silvia OttavianiJSJustin Stebbing
Justin StebbingAdam E. FramptonSZSladana Zagorac
Sladana ZagoracJKJonathan Krell
Jonathan Krell
Leandro Castellano +12
TGF-β/Activin induces epithelial-to-mesenchymal transition and stemness in pancreatic ductal adenocarcinoma (PDAC). However, the microRNAs (miRNAs) regulated during this response have remained yet undetermined. Here, we show that TGF-β transcriptionally induces MIR100HG lncRNA, containing miR-100, miR-125b and let-7a in its intron, via SMAD2/3. Interestingly, we find that although the pro-tumourigenic miR-100 and miR-125b accordingly increase, the amount of anti-tumourigenic let-7a is unchanged, as TGF-β also induces LIN28B inhibiting its maturation. Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β effectors. We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells. Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell–cell junctions’ pathways. Together, we uncover that TGF-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis.
1 July 2015 in European Journal of Cancer
Journal Article
Adam E. FramptonJKJonathan Krell
Jonathan Krell
NJNigel B. Jamieson
Nigel B. JamiesonTGTamara M.H. Gall
Tamara M.H. Gall
Elisa GiovannettiJSJustin Stebbing
Justin Stebbing +6
1 May 2014 in JAMA Surgery
Journal Article
TGTamara M. H. Gall
Tamara M. H. GallJJJimmy Jacob
Jimmy Jacob
Adam E. FramptonJKJonathan Krell
Jonathan KrellCKCharis Kyriakides
Charis Kyriakides
LJLong R. Jiao
Long R. Jiao +2
Circulating tumor cells (CTCs) disseminate from the primary tumor and travel through the bloodstream and lymphatic system. The detection of and/or increase in the number of CTCs during a patient’s clinical course may be a harbinger of forthcoming overt metastasis. We aimed to examine the impact of 2 different surgical techniques, standard (ST) pancreaticoduodenectomy (PD) and no-touch isolation (NT) PD, on tumor behavior and outcome in patients with pancreatic cancer by using CTCs as biomarkers. In this pilot study, patients were randomized to either ST-PD (n = 6) or NT-PD (n = 6). Intraoperatively, blood samples were taken from the portal vein for measurement of CTCs before and immediately after removal of the tumor. An increase in CTCs was seen in 5 of 6 patients (83%) with ST-PD but no patients with NT-PD (P = .003). In the ST-PD and NT-PD groups, median overall survival was 13.0 and 16.7 months, respectively (P = .33); there was no difference in disease-free survival (P = .42). The use of NT-PD significantly reduced the number of CTCs in the portal vein with no benefit in survival outcomes compared with ST-PD, although more extensive studies are required.
6 February 2025 in Nature Communications
Journal Article
SSShivan Sivakumar
Shivan SivakumarAJAshwin Jainarayanan
Ashwin Jainarayanan
EAEdward Arbe-Barnes
Edward Arbe-Barnes
PSPiyush Kumar Sharma
Piyush Kumar Sharma
MLMaire Ni Leathlobhair
Maire Ni Leathlobhair
RBRachael Bashford‐Rogers
Rachael Bashford‐Rogers +31
Pancreatic ductal adenocarcinoma has a dismal prognosis. A comprehensive analysis of single-cell multi-omic data from matched tumour-infiltrated CD45+ cells and peripheral blood in 12 patients, and two published datasets, reveals a complex immune infiltrate. Patients have either a myeloid-enriched or adaptive-enriched tumour microenvironment. Adaptive immune cell-enriched is intrinsically linked with highly distinct B and T cell clonal selection, diversification, and differentiation. Using TCR data, we see the largest clonal expansions in CD8 effector memory, senescent cells, and highly activated regulatory T cells which are induced within the tumour from naïve cells. We identify pathways that potentially lead to a suppressive microenvironment, including investigational targets TIGIT/PVR and SIRPA/CD47. Analysis of patients from the APACT clinical trial shows that myeloid enrichment had a shorter overall survival compared to those with adaptive cell enrichment. Strategies for rationale therapeutic development in this disease include boosting of B cell responses, targeting immunosuppressive macrophages, and specific Treg cell depletion approaches.
1 January 2019 in The American Journal of Pathology
Journal Article
TGTamara M. H. Gall
Tamara M. H. GallSBSamuel Belete
Samuel Belete
EKEsha Khanderia
Esha Khanderia
Adam E. FramptonLJLong R. Jiao
Long R. Jiao
Journal Article
BWBing Wang
Bing WangJDJuan Deng
Juan DengVDValentina Donati
Valentina DonatiNMNabeel Merali
Nabeel MeraliAdam E. FramptonDDDong Mei Deng
Dong Mei Deng +1
Epidemiological studies have spotlighted the intricate relationship between individual oral bacteria and tumor occurrence. Porphyromonas gingivalis and Fusobacteria nucleatum, which are known periodontal pathogens, have emerged as extensively studied participants with potential pathogenic abilities in carcinogenesis. However, the complex dynamics arising from interactions between these two pathogens were less addressed. This narrative review aims to summarize the current knowledge on the prevalence and mechanism implications of P. gingivalis and F. nucleatum in the carcinogenesis of oral squamous cell carcinoma (OSCC), colorectal cancer (CRC), and pancreatic ductal adenocarcinoma (PDAC). In particular, it explores the clinical and experimental evidence on the interplay between P. gingivalis and F. nucleatum in affecting oral and gastrointestinal carcinogenesis. P. gingivalis and F. nucleatum, which are recognized as keystone or bridging bacteria, were identified in multiple clinical studies simultaneously. The prevalence of both bacteria species correlated with cancer development progression, emphasizing the potential impact of the collaboration. Regrettably, there was insufficient experimental evidence to demonstrate the synergistic function. We further propose a hypothesis to elucidate the underlying mechanisms, offering a promising avenue for future research in this dynamic and evolving field.
About Me
Adam E. Frampton is currently an honorary clinical lecturer working in the Department of Surgery and Cancer at Hammersmith Hospital, Imperial College London. He completed his general and HPB surgical training on the London Deanery (South-West Thames) rotation and is a consultant general and HPB surgeon at the Royal Surrey County Hospital, Guildford, Surrey. He undertook his undergraduate medical training at Charing Cross Hospital (ICSM) from 1997–2003 and achieved a first class intercalated BSc(Hons) in pharmacology and toxicology at Imperial College. He completed his basic surgical training in Surrey and then spent a year doing renal transplant and vascular access surgery at St. Georges Hospital, Tooting (2007–2008). At the same time, he completed an MSc with merit in surgical practice. He joined the HPB Surgical Unit at the Hammersmith Hospital in 2009 as a clinical research fellow. He was awarded his PhD in molecular oncology in 2014. He won the Moynihan Prize in May 2017 for his research, which is the most prestigious scientific award given by the Association of Surgeons of Great Britain and Ireland (ASGBI). Adam was then elected as a Fellow of the Royal Society of Biology (FRSB) in July 2017 for his contributions to small RNA and cancer biology. He was awarded the distinguished Hunterian Professorship by the Royal College of Surgeons of England in May 2018 and was elected as a Fellow of the European Society of Surgical Research (FESSR) in June 2018.