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KONG LAB

The Kong Lab focuses on advancing the understanding and treatment of pancreatic ductal adenocarcinoma (PDAC) through innovative research in several key areas:

KRAS Inhibition

We use a variety of preclinical models to replicate human PDAC, aiming to predict its response to KRAS inhibition.

In Vivo Models of PDAC

A significant focus of our laboratory is the development of transgenic mouse models that reflect both the molecular and histological diversity of PDAC. By modifying the cell of origin and genetic makeup, we create multiple mouse models that emulate characteristic features of human PDAC, including desmoplastic reactions and immune-exclusion phenotypes.

Cancer Signal Simulation

Our team is dedicated to simulating alterations in cancer signaling during pancreatic organ regeneration and carcinogenesis. We concentrate particularly on the dynamics of KRAS and mTOR signaling pathways in PDAC development, with a major emphasis on the adaptive changes following KRAS and mTOR inhibition.

Patient-Derived PDAC Models and Therapeutic Testing

We are developing advanced patient-derived PDAC models that can be readily used to predict potential therapeutic responses. These individualized three-dimensional organoid models allow us to mimic the complexities of PDAC, offering a unique platform for studying therapeutic responses. 

Arbeitsgruppenleiter

PD Dr. Dr. med. Bo Kong


Team

Teamleiter
PD Dr. Dr. med. Bo Kong

Leitung wissenschaftliche Fachredaktion
Prof. Dr. rer. nat. Ingrid Herr

Senior-Wissenschaftler*innen und Adviser
PD Dr. Franco Fortunato (PhD)
Dr. rer. nat. Michael Schäfer

Post Docs 
Dr. sc. hum. Bindhu Madhavan
Yina Qiao 
Kai Hu

Technische Mitarbeiter*innen
Sonja Bauer (in Mutterschutz)
Mohamad Freigeh (Mutterschaftsvertretung, ab 1.6.24)
Elvira Mohr
Sascha Hinterkopf

Doktorand*innen 
Chao Fang
Jingxiong Hu
Xiaoyan Huang
Yiqi Niu
Lingling Zhang
Qing Zhen
Yiping Yin
Zhaiyue Xu
Enis Salihi
Franz Li (HIWI)

Dr. sc. hum. Malte Hermes

Sekretärin
Ellen Watson

Finanzierung

Drittmittel

DFG 2020 DFG 2022
Wilhelm Sander Stiftung 2023
Deutsche Krebshilfe 2023
Heidelberger Stiftung Chirurgie 2023
Else Kröner-Fresenius Stiftung 2024
Hans Beger-Stiftung 2022

2025-Cell Reports Medicine

Disrupting AGR2/IGF1 paracrine and reciprocal signaling for pancreatic cancer therapy

Li H, Zhang Z, Shi Z, Zhou S, Nie S, Yu Y, Zhang L, Sun Y, Fang C, Hu J, Niu Y, Schuck K, Wang L, Jiang K, Lu Z, Kahlert C, Roth S, Loos M, Herr I, Sunami Y, Kleeff J, Friess H, Reichert M, Dantes Z, Zou X, Michalski CW, Shen S, Kong B.

2025-International Journal of Cancer

ARP2/3 complex affects myofibroblast differentiation and migration in pancreatic ductal adenocarcinoma.

Sun Y, Qiao Y, Niu Y, Madhavan BK, Fang C, Hu J, Schuck K, Traub B, Friess H, Herr I, Michalski CW, Kong B.

2021-Gastroenterology

AGR2-dependent nuclear import of RNA polymerase II constitutes a specific target of pancreatic ductal adenocarcinoma in the context of wild-type p53.

Zhang Z, Li H, Deng Y, Schuck K, Raulefs S, Maeritz N, Yu Y, Hechler T, Pahl A, Fernández-Sáiz V, Wan Y, Wang G, Engleitner T, Öllinger R, Rad R, Reichert M, Diakopoulos KN, Weber V, Li J, Shen S, Zou X, Kleeff J, Mihaljevic A, Michalski CW, Algül H, Friess H, Kong B.

2021-Gastroenterology

mTORC1 and mTORC2 converge on the Arp2/3 complex to promote Kras G12D-induced acinar-to-ductal metaplasia and early pancreatic carcinogenesis.

Zhao Y, Schoeps B, Yao D, Zhang Z, Schuck K, Tissen V, Jäger C, Schlitter AM, van der Kammen R, Ludwig C, D'Haese JG, Raulefs S, Maeritz N, Shen S, Zou X, Krüger A, Kleeff J, Michalski CW, Friess H, Innocenti M, Kong B.

2019- International Journal of Cancer

Ductal obstruction promotes formation of preneoplastic lesions from the pancreatic ductal compartment.

Cheng T, Zhang Z, Jian Z, Raulefs S, Schlitter AM, Steiger K, Maeritz N, Zhao Y, Shen S, Zou X, Ceyhan GO, Friess H, Kleeff J, Michalski CW, Kong B.

2018- Cellular and Molecular Gastroenterology and Hepatology

Glycemic Variability Promotes Both Local Invasion and Metastatic Colonization by Pancreatic Ductal Adenocarcinoma.

Jian Z, Cheng T, Zhang Z, Raulefs S, Shi K, Steiger K, Maeritz N, Kleigrewe K, Hofmann T, Benitz S, Bruns P, Lamp D, Jastroch M, Akkan J, Jäger C, Huang P, Nie S, Shen S, Zou X, Ceyhan GO, Michalski CW, Friess H, Kleeff J, Kong B.

2018 - Gut

Dynamic landscape of pancreatic carcinogenesis reveals early molecular networks of malignancy.

Kong B, Bruns P, Behler NA, Chang L, Schlitter AM, Cao J, Gewies A, Ruland J, Fritzsche S, Valkovskaya N, Jian Z, Regel I, Raulefs S, Irmler M, Beckers J, Friess H, Erkan M, Mueller NS, Roth S, Hackert T, Esposito I, Theis FJ, Kleeff J, Michalski CW.

2016-Oncogenesis

In vivo functional dissection of a context-dependent role for Hif1α in pancreatic tumorigenesis.

Cheng T, Jian Z, Li K, Raulefs S, Regel I, Shen S, Zou X, Ruland J, Ceyhan GO, Friess H, Michalski CW, Kleeff J, Kong B.

2016- Gut

A subset of metastatic pancreatic ductal adenocarcinomas depends quantitatively on oncogenic Kras/Mek/Erk-induced hyperactive mTOR signalling.

Kong B, Wu W, Cheng T, Schlitter AM, Qian C, Bruns P, Jian Z, Jäger C, Regel I, Raulefs S, Behler N, Irmler M, Beckers J, Friess H, Erkan M, Siveke JT, Tannapfel A, Hahn SA, Theis FJ, Esposito I, Kleeff J, Michalski CW.

2015-Molecular Cancer

Pancreas-specific activation of mTOR and loss of p53 induce tumors reminiscent of acinar cell carcinoma.

Kong B, Cheng T, Qian C, Wu W, Steiger K, Cao J, Schlitter AM, Regel I, Raulefs S, Friess H, Erkan M, Esposito I, Kleeff J, Michalski CW.

2015- International Journal of Surgery 

Metabolism gene signatures and surgical site infections in abdominal surgery.

Kong B, Bruns P, Raulefs S, Rieder S, Paul L, Prazeresda Costa O, Buch T, Theis FJ, Michalski CW, Kleeff J.

2011- Nature Reviews Gastroenterology & Hepatology

From tissue turnover to the cell of origin for pancreatic cancer.

Kong B, Michalski CW, Erkan M, Friess H, Kleeff J.

2010-Oncogene

AZGP1 is a tumor suppressor in pancreatic cancer inducing mesenchymal-to-epithelial transdifferentiation by inhibiting TGF-β-mediated ERK signaling.

Kong B, Michalski CW, Hong X, Valkovskaya N, Rieder S, Abiatari I, Streit S, Erkan M, Esposito I, Friess H, Kleeff J.

 

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