G Adler

Publications (338)1167.82 Total impact

• Article: Chemotherapie des Kolonkarzinoms

  M. P. Lutz, G. Adler
  [show abstract] [hide abstract]
  ABSTRACT: Die Therapie des Kolonkarzinoms ist primär eine chirurgische. Eine Chemotherapie wird in fortgeschritteneren Tumorstadien eingesetzt. Dabei dient sie einerseits als adjuvante Therapie nach der Tumorresektion zur Verhinderung von Metastasen und Rezidiven und kann dort die Heilungsraten verbessern. In der palliativen Situation dient die Chemotherapie vor allem der Verlängerung der Überlebenszeit unter besonderer Berücksichtigung des Erhalts von Lebensqualität. Der vorliegende Beitrag fasst die neuesten Studienergebnisse zur chemotherapeutischen Behandlung des Kolonkarzinoms zusammen und stellt heraus, welche therapeutischen Konsequenzen daraus gezogen werden können.
  Der Internist 04/2012; 42(12):1567-1582. · 0.30 Impact Factor
• Article: Prevalence of Helicobacter pylori in the adolescent oral cavity

  A. Wichelhaus, L. Brauchli, Q. Song, G. Adler, G. Bode
  [show abstract] [hide abstract]
  ABSTRACT: BackgroundHelicobacter pylori (HP) infection usually occurs in childhood. While there are various studies on the prevalence of HP in dental plaque, ours is the first to analyze its prevalence during orthodontic therapy and its interaction with competitive bacteria in adolescents. Subjects and methodsThe prevalence of HP was examined before and during the first 12weeks of orthodontic therapy with fixed appliances in 11patients with a mean age of 12.7years. A total of 93plaque samples were analyzed using PCR. The data acquired at every consultation were the following: PCR analysis of dental plaque and 13C urea breath tests for HP, quantitative analyses of saliva for Lactobacilli and Streptococcus mutans, the interproximal plaque index (API), and sulcus bleeding index (SBI). ResultsThe prevalence of HP in plaque was 82% before orthodontic therapy, dropping to 54% during therapy (t test, p≤0.05). In contrast to HP’s prevalence, the Lactobacilli count rose (p≤0.05). The number of Streptococcus mutans bacteria in saliva decreased during orthodontic therapy (p≤0.05). ConclusionThe prevalence of HP in dental plaque amounted to 82%. Orthodontic treatment did not reduce its prevalence. The prevalence of Lactobacilli was inversely proportional to that of HP. HintergrundDie Infektion mit Helicobacter pylori (HP) findet meistens in der Kindheit statt. Zur Prävalenz von HP in dentaler Plaque liegen verschiedene Untersuchungen vor. Ziel dieser Studie war die erstmalige Analyse der Prävalenz des Bakteriums während kieferorthopädischer Therapie und deren Interaktion mit kompetitiven Bakterien bei Jugendlichen. Probanden und MethodikBei 11 Patienten eines mittleren Alters von 12,7 Jahren wurde die Prävalenz von HP vor und während der ersten 12Wochen kieferorthopädischer Therapie mit festsitzenden Apparaturen untersucht. Insgesamt wurden 93 Plaqueproben mittels Polymerasekettenreaktion (PCR) analysiert. Bei jeder Konsultation wurden folgende Daten erhoben: PCR-Analyse von dentaler Plaque und 13C-Harnstoff-Atemtest auf HP, quantitative Speichelanalysen für Lactobazillen und Streptococcus mutans, approximaler Plaqueindex (API) und Sulcus-Blutungs-Index (SBI). ErgebnisseVor kieferorthopädischer Therapie lag die Prävalenz von HP in der Plaque bei 82% und verringerte sich während der Therapie auf 54% (t-Test, p≤0,05). Im Gegensatz zur Prävalenz von HP stieg die Anzahl der Lactobazillen (p≤0,05). Die Anzahl der Streptococcus-mutans-Bakterien im Speichel verringerte sich während der orthodontischen Therapie (p≤0,05). SchlussfolgerungDie Prävalenz von HP in dentaler Plaque betrug 82%. Die orthodontische Behandlung hatte keinen negativen Einfluss auf die HP-Prävalenz. Die Prävalenz von Lactobazillen war umgekehrt proportional zu der von HP. KeywordsHelicobacter pylori–Dental plaque– 13C urea breath test–Lactobacilli–Streptococcus mutans SchlüsselwörterHelicobacter pylori –Dentale Plaque– 13C-Harnstoff-Atemtest–Lactobazillen–Streptococcus mutans
  Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie 04/2012; 72(3):187-195. · 0.86 Impact Factor
• Article: Cholezystolithiasis bei Kindern und Jugendlichen Einfluss von Adipositas und anderen Risikofaktoren

  V. Kächele, M. Wabitsch, B. Hay, M.M. Pfeiffer, G. Adler, W. Kratzer
  [show abstract] [hide abstract]
  ABSTRACT: Fragestellung. Ziel der Studie war es, Häufigkeit und Risikofaktoren der Cholezystolithiasis, insbesondere Adipositas und familiäre Belastung, Fragestellung. Ziel der Studie war es, Häufigkeit und Risikofaktoren der Cholezystolithiasis, insbesondere Adipositas und familiäre Belastung, an einem unselektierten Kollektiv von Kindern und Jugendlichen zu untersuchen. an einem unselektierten Kollektiv von Kindern und Jugendlichen zu untersuchen. Methode und Studienkollektiv. Ein Studienkollektiv von 482 Kindern einer Gemeinde in Süddeutschland zwischen 6 und 18 Jahren wurde in einer Vollerhebung (Responserate: 78%) im Rahmen einer Screeninguntersuchung zu Echinococcus multilocularis sonographisch Methode und Studienkollektiv. Ein Studienkollektiv von 482 Kindern einer Gemeinde in Süddeutschland zwischen 6 und 18 Jahren wurde in einer Vollerhebung (Responserate: 78%) im Rahmen einer Screeninguntersuchung zu Echinococcus multilocularis sonographisch untersucht. untersucht. Ergebnisse. Bei 3 von 482 Kindern, entsprechend einer Prävalenz von 0,6%, wurden Gallenblasensteine festgestellt. Keines der 3 Kinder Ergebnisse. Bei 3 von 482 Kindern, entsprechend einer Prävalenz von 0,6%, wurden Gallenblasensteine festgestellt. Keines der 3 Kinder war zum Zeitpunkt der Untersuchung übergewichtig. Als weitere Risikofaktoren fanden sich bei einem Studienteilnehmer eine war zum Zeitpunkt der Untersuchung übergewichtig. Als weitere Risikofaktoren fanden sich bei einem Studienteilnehmer eine starke Gewichtsreduktion sowie ein M. Wilson. starke Gewichtsreduktion sowie ein M. Wilson. Schlussfolgerungen. Adipositas konnte bei Kindern und Jugendlichen in der vorliegenden Studie nicht als Risikofaktor für die Cholezystolithiasis Schlussfolgerungen. Adipositas konnte bei Kindern und Jugendlichen in der vorliegenden Studie nicht als Risikofaktor für die Cholezystolithiasis bestätigt werden. bestätigt werden. Objective. To assess the prevalence of and risk factors (e. g., obesity and positive family history) for the development of cholecystolithiasis Objective. To assess the prevalence of and risk factors (e. g., obesity and positive family history) for the development of cholecystolithiasis in a non-selected collective of children and adolescents. in a non-selected collective of children and adolescents. Design and participants. A series of 482 children and adolescents aged 6–18 years underwent upper abdominal diagnostic ultrasound examinations asescents aged 6–18 years underwent upper abdominal diagnostic ultrasound examinations as part of a whole-community investigation (response rate: 78%) for Echinococcus multilocularis in a town in southern Germany. part of a whole-community investigation (response rate: 78%) for Echinococcus multilocularis in a town in southern Germany. Results. Gallbladder stones were identified in three of 482 children, corresponding to a prevalence of 0.6%. None of the three children Results. Gallbladder stones were identified in three of 482 children, corresponding to a prevalence of 0.6%. None of the three children was overweight at the time of the examination. Additional risk factors (pronounced weight reduction and Wilson's disease) was overweight at the time of the examination. Additional risk factors (pronounced weight reduction and Wilson's disease) were present in one study subject. were present in one study subject. Conclusions. Findings of the present study do not confirm the significance of obesity as a risk factor for cholecystolithiasis in children Conclusions. Findings of the present study do not confirm the significance of obesity as a risk factor for cholecystolithiasis in children and adolescents. and adolescents.
  Monatsschrift Kinderheilkunde 04/2012; 148(6):600-604. · 0.27 Impact Factor
• Article: Prevalence of Helicobacter pylori in the adolescent oral cavity: dependence on orthodontic therapy, oral flora and hygiene.

  Andrea Wichelhaus, Lorenz Brauchli, Qunsheng Song, Guido Adler, Günter Bode
  [show abstract] [hide abstract]
  ABSTRACT: Helicobacter pylori (HP) infection usually occurs in childhood. While there are various studies on the prevalence of HP in dental plaque, ours is the first to analyze its prevalence during orthodontic therapy and its interaction with competitive bacteria in adolescents. The prevalence of HP was examined before and during the first 12 weeks of orthodontic therapy with fixed appliances in 11 patients with a mean age of 12.7 years. A total of 93 plaque samples were analyzed using PCR. The data acquired at every consultation were the following: PCR analysis of dental plaque and (13)C urea breath tests for HP, quantitative analyses of saliva for Lactobacilli and Streptococcus mutans, the interproximal plaque index (API), and sulcus bleeding index (SBI). The prevalence of HP in plaque was 82% before orthodontic therapy, dropping to 54% during therapy (t test, p≤0.05). In contrast to HP's prevalence, the Lactobacilli count rose (p≤0.05). The number of Streptococcus mutans bacteria in saliva decreased during orthodontic therapy (p≤0.05). The prevalence of HP in dental plaque amounted to 82%. Orthodontic treatment did not reduce its prevalence. The prevalence of Lactobacilli was inversely proportional to that of HP.
  Fortschritte der Kieferorthopädie 07/2011; 72(3):187-95. · 0.89 Impact Factor
• Article: A single dose of intravenous zoledronate prevents glucocorticoid therapy-associated bone loss in acute flare of Crohn's disease, a randomized controlled trial.

  Jochen Klaus, M M Haenle, C Schröter, G Adler, G von Boyen, M Reinshagen, C von Tirpitz
  [show abstract] [hide abstract]
  ABSTRACT: To assess the effectiveness and safety of zoledronate (ZOL) in preventing glucocorticoid therapy-associated bone loss in patients with acute flare of Crohn's disease (CD) in a randomized, double-blind, placebo-controlled trial. Forty CD patients starting a glucocorticoid therapy (60 mg prednisolone per day) for acute flare (CD activity index (CDAI) >220) were randomized to compare the effect of ZOL (4 mg intravenous, n=20) or placebo (n=20) on change in lumbar bone mineral density (BMD). All patients received calcium citrate (800 mg) and colecalciferol (1,000 IU) daily. Dual energy X-ray absorptiometry (DXA) of the lumbar spine (L1-L4) was performed at baseline and day 90. Follow-up examinations at day 1/7/14/30 and 90 included laboratory tests and adverse event/serious adverse events reports. Thirty-six patients were available for per-protocol analysis. With placebo (n=18), a decrease in BMD was seen (T-score: -0.98 ± 0.8, day 0 and -1.25 ± 0.77, day 90, P=0.06), with ZOL (n=18) BMD increased (-1.15 ± 1.02, day 0 and -0.74 ± 1.09, day 90, P=0.03). The change in BMD under placebo (-0.26 ± 0.21) vs. ZOL (+0.41 ± 0.19) was highly significant (P=0.006). In all, 14 out of 18 patients with ZOL had an increase in BMD (+0.64 ± 0.48), 12 of 18 with placebo a decrease (-0.50 ± 0.39). Changes of clinical findings and laboratory results of inflammation (leukocytes, platelets, and C-reactive protein) were the same in- and between-groups throughout the study. With ZOL, serum bone degradation marker β-Cross-Laps decreased. Study medication was safe and well tolerated. ZOL is effective in preventing glucocorticoid therapy-induced bone loss in patients with acute flare of CD and should be considered whenever a glucocorticoid therapy is started in CD patients.
  The American Journal of Gastroenterology 03/2011; 106(4):786-93. · 7.28 Impact Factor
• Article: [Personalized therapy of gastrointestinal cancers--possibilities and limitations].

  G von Wichert, G Adler, T Seufferlein
  [show abstract] [hide abstract]
  ABSTRACT: The aim of palliative chemotherapy is to increase survival whilst maintaining optimal quality of life for the individual patient. While the best use of traditional chemotherapeutical agents continues to be explored, the introduction of targeted therapies has significantly broadened the therapeutic options. Yet it is interesting to note that the results of current trials did not always confirm the underlying molecular concepts. Recent data have suggested that altered pathways underlie the development of cancer, not just altered genes. Thus an effective therapeutic agent will have to target pathophysiologically relevant signalling networks, rather than individual proteins. This review presents current concepts and problems of cancer treatment, highlighting results from recent clinical trials of colorectal and pancreatic cancer patients and to discuss the current understanding of the underlying mechanisms.
  DMW - Deutsche Medizinische Wochenschrift 08/2010; 135(34-35):1687-91. · 0.53 Impact Factor
• Article: The zinc-finger protein KCMF1 is overexpressed during pancreatic cancer development and downregulation of KCMF1 inhibits pancreatic cancer development in mice.

  S Beilke, F Oswald, F Genze, T Wirth, G Adler, M Wagner
  [show abstract] [hide abstract]
  ABSTRACT: Potassium channel modulatory factor 1 (KCMF1) was found upregulated in a differential screen in the metaplastic epithelium in the pancreas of transforming growth factor (TGF)-alpha transgenic mice. Expression analysis indicated broad overexpression in human cancer tissues. Therefore, we investigated the hypothesis that KCMF1 promotes metaplastic changes and tumor development. KCMF1 represents an evolutionarily highly conserved protein with a 95% identity between human and zebrafish. KCMF1 is expressed during embryonic development and in the majority of adult tissues investigated. Upregulation of nuclear KCMF1 expression is evident in preneoplastic lesions and in several epithelial malignancies, such as pancreatic cancer in mice and humans. In cell culture and in the chicken chorioallantoic membrane model, KCMF1 enhances proliferation, migration and invasion of HEK-293 and Panc1 cells. In crossbreeding experiments, KCMF1-knockdown gene trap mice showed a reduced number and size of premalignant lesions and absence of pancreatic cancer formation in TGF-alpha transgenic mice. This effect is related to the decreased expression of G1 to S cell-cycle regulators such as cyclin D and cyclin-dependent kinase (CDK) 4. Our data support the hypothesis that KCMF1 mediates pro-oncogenic functions in vitro and in vivo and downregulation of KCMF1 results in the inhibition of pancreatic cancer formation in mice. These effects are mediated through downregulation of cell-cycle control genes such as cyclin D and CDK4.
  Oncogene 07/2010; 29(28):4058-67. · 6.37 Impact Factor
• Article: Substrate stiffness and the receptor-type tyrosine-protein phosphatase alpha regulate spreading of colon cancer cells through cytoskeletal contractility.

  D Krndija, H Schmid, J-L Eismann, U Lother, G Adler, F Oswald, T Seufferlein, G von Wichert
  [show abstract] [hide abstract]
  ABSTRACT: Microenvironmental clues are critical to cell behavior. One of the key elements of migration is the generation and response to forces. Up to now, there is no definitive concept on how the generation and responses to cellular forces influence cancer-cell behavior. Here, we show that expression of receptor-type tyrosine-protein phosphatase alpha (RPTPalpha) in human SW480 colon cancer cells sets a threshold for the response to matrix forces by changing cellular contractility. This can be explained as an RPTPalpha-mediated increase in contractility with a consecutive increase in number and size of adhesion sites and stress fibers. These effects are mediated through myosin light chain kinase and largely independent of Rho/Rho-kinase (ROCK) signaling. In addition, we report that RPTPalpha influences spreading on low-rigidity surfaces, binding of collagen-coated beads and expression of RPTPalpha is required for invasion into the chorioallantoic membrane. These data suggest that force-responsive proteins such as RPTPalpha can influence cancer-cell behavior and identify potential targets for cancer therapy.
  Oncogene 03/2010; 29(18):2724-38. · 6.37 Impact Factor
• Article: S3 guidelines for colorectal carcinoma: results of an evidence-based consensus conference on February 6/7, 2004 and June 8/9, 2007 (for the topics IV, VI and VII).

  W Schmiegel, C Pox, A Reinacher-Schick, G Adler, D Arnold, W Fleig, U R Fölsch, P Frühmorgen, U Graeven, V Heinemann, [......], P Propping, J-F Riemann, C Rödel, R Sauer, T Sauerbruch, W Schmitt, H-J Schmoll, T Seufferlein, M Zeitz, H-K Selbmann
  Zeitschrift für Gastroenterologie 01/2010; 48(1):65-136. · 0.90 Impact Factor
• Article: Increased Duodeno-Gastro-Esophageal Reflux (DGER) in symptomatic GERD patients with a history of cholecystectomy.

  S Kunsch, A Neesse, J Huth, M Steinkamp, J Klaus, G Adler, T M Gress, V Ellenrieder
  [show abstract] [hide abstract]
  ABSTRACT: Duodenal-Gastro-Esophageal Reflux (DGER) represents an independent risk factor for the development of complicated Gastro-esophageal-reflux-disease (GERD) and Barrett's esophagus. Clinical and epidemiological data suggest a potential association between cholecystectomy (CCE) and augmented bile reflux. 132 patients (67 women, 65 men, median age 55) with typical symptoms of GERD were enrolled in the study and divided in cholecystectomized (CCE-group: n = 107) and non- cholecystectomized (nCCE-group: n = 25) patients. Standardized clinical work-up of patients included combined esophageal 24 h pH-measurement and Bilitec 2000 esophageal manometry and upper endoscopy. In the statistical analysis no differences between the cholecystectomized group (CCE-group, n = 25) and the patients without cholecystectomy (nCCE-group, n = 107) could be observed in quantity or quality of reflux symptoms. Furthermore, neither acid reflux nor severity of inflammation and frequency of Barrett's esophagus significantly differed between the nCCE and CCE-group. However, the percentage of patients with pathological DGER were significantly higher in the CCE-group as compared to the nCCE-group (76 vs. 55 %, p < 0.01). Moreover, the CCE-group revealed significant higher levels of pathological DGER compared to the nCCE-group (15.5 % +/- 14.1 vs. 8.6 % +/- 15.4; p < 0.05). To conclude, our data provide first evidence of elevated DGER after CCE in patients with typical clinical symptoms of GERD using the Bilitec device. Both the frequency and the extent of DGER was significantly increased in the CCE-group. Prospective studies are urgently needed to elucidate the impact of CCE on DGER in patients with clinical symptoms of a reflux disease.
  Zeitschrift für Gastroenterologie 08/2009; 47(8):744-8. · 0.90 Impact Factor
• Article: Impact of pantoprazole on duodeno-gastro-esophageal reflux (DGER).

  S Kunsch, A Neesse, T Linhart, M Steinkamp, H Fensterer, G Adler, T M Gress, V Ellenrieder
  [show abstract] [hide abstract]
  ABSTRACT: Duodeno-gastro-esophageal reflux (DGER) is considered as an independent risk factor for complicated reflux disease (GERD). Patients with Barrett's esophagus have significantly higher levels of DGER than patients with uncomplicated GERD. However, the clinical response to conventional high-dose PPI therapy in patients with uncomplicated GERD and DGER is largely unknown. 30 patients with uncomplicated GERD and combined pathological reflux (acid and bile) were enrolled in the study. Clinical work-up included evaluation of clinical symptoms, esophageal manometry and upper endoscopy. After 6 - 8 weeks of treatment with Pantoprazole 80 mg/d pH measurement and Bilitec 2000 were repeated, and the pattern of symptoms was re-evaluated. Under treatment with Pantoprazole 80 mg/d acid reflux was normalised in 28 patients (93 %). Similarly the mean percentage of DGER (time with an absorption greater than 0.14) was significantly reduced from 19.6 % (+/- 13.7) to 5.7 % (+/- 7.7, p < 0.05). In 15 patients (50 %) an elevated DGER persisted under treatment with Pantoprazole (DGER-NR group) whereas in 15 cases (50 %) a normalisation could be achieved (DGER-R group). The DGER-NR group had significantly higher levels of bile reflux before (and under) treatment compared to the DGER-R group: 22.9 % (9.98 %) vs. 15.6 % (0.72 %), respectively. Overall, the median quality of life index (QLI) improved from 4.78 (+/- 0.86) before to 8.04 +/- 1.84) under therapy. The clinical response under treatment was marikedly reduced in the DGER-NR group compared to the DGER-R group: QLI 7.3 vs. 8.9. Particularly heartburn and nocturnal coughing persisted. Our data confirm that high-dose pantoprazole therapy effectively exerts acid suppression in GERD patients with combined pathological reflux. However, DGER could only normalised in 50 % of patients. High levels of DGER at diagnosis enhance the risk of persistent DGER under PPI therapy and are associated with a reduced clinical outcome.
  Zeitschrift für Gastroenterologie 03/2009; 47(3):277-82. · 0.90 Impact Factor
• Article: [Neuerungen bei der Zeitschrift für Gastroenterologie.]

  G Adler, T Seufferlein
  Zeitschrift für Gastroenterologie 09/2008; 46(8):759. · 0.90 Impact Factor
• Article: Metabolism in adipose tissue in response to citalopram and trimipramine treatment--an in situ microdialysis study.

  M Flechtner-Mors, C P Jenkinson, A Alt, G Adler, H H Ditschuneit
  [show abstract] [hide abstract]
  ABSTRACT: The intake of antidepressants is often accompanied by weight gain. Antidepressants may influence lipid and carbohydrate metabolism that can result in metabolic changes and obesity. We investigated the effect of citalopram and trimipramine on interstitial glycerol, glucose and lactate concentration and blood flow in subcutaneous adipose tissue of obese subjects by means of the microdialysis technique. In addition, the effect of stimulation with norepinephrine on metabolic response was investigated. Each subject was compared to a control subject matched for BMI and age. Each group comprised 10 subjects. Circulating plasma triglyceride concentrations were higher in drug-treated groups. In subcutaneous adipose tissue, microdialysis experiments revealed a higher and prolonged glycerol release in the presence of norepinephrine, but not under basal conditions. In citalopram treated subjects, basal glucose and lactate concentrations were higher compared with controls or with the trimipramine treated group. Local administration of norepinephrine induced a decrease in glucose levels and an increase in lactate levels, but without significant differences between groups. Local adipose tissue blood flow decreased in control groups following norepinephrine application, but remained constant in the antidepressant groups. In conclusion, citalopram and trimipramine affected glucose and lipid metabolism in adipose tissue and resulted in enhanced release of glycerol and free fatty acids into the circulation.
  Journal of Psychiatric Research 07/2008; 42(7):578-86. · 4.66 Impact Factor
• Article: [Prevalence of a pathological DGER (duodeno-gastric-oesophageal reflux) in patients with clinical symptoms of reflux disease].

  S Kunsch, T Linhart, H Fensterer, G Adler, T M Gress, V Ellenrieder
  [show abstract] [hide abstract]
  ABSTRACT: According to recent studies DGER (duodeno-gastric-oesophageal reflux) is considered as an independent risk factor for the development of reflux esophagitis and the Barrett metaplasia. The Bilitec 2000 allows a qualitative and quantitative measurement of DGER in patients with symptoms of reflux disease. The aim of the present study was to investigate the prevalence of DGER in patients with reflux symptoms. 146 patients with symptoms of gastro-oesophageal reflux disease were enrolled in this study. Patients underwent upper gastrointestinal endoscopy, oesophageal manometry and simultaneous 24 h oesophageal pH and bilirubin monitoring. The presence of pathological DGER and its relations to the symptom pattern, distal oesophageal acid exposure and endoscopic findings were analysed. In 74 out of 146 patients (51 %, 39 men, 34 women) a DGER could be detected. Twenty-eight (32 %) of these patients suffered from an isolated DGER, while 46 (32 %) had a combined acid and DGER reflux. An isolated acid reflux was found in additional 28 (19 %) patients. The degrees of both acid and DGER were significantly higher in those patients with oesophageal lesions. 1. There is a high prevalence of DGER in patients with the clinical symptoms of a reflux disease. 2. The combined measurement of acid reflux and DGER helps to better define the cause of reflux symptoms. 3. In analogy to the acid reflux DGER increases with the gravity of oesophageal lesions.
  Zeitschrift für Gastroenterologie 06/2008; 46(5):409-14. · 0.90 Impact Factor
• Article: S3-guideline "exocrine pancreatic carcinoma" 20071.

  G Adler, T Seufferlein, S C Bischoff, H J Brambs, S Feuerbach, G Grabenbauer, S Hahn, V Heinemann, W Hohenberger, J M Langrehr, [......], H Neuhaus, P Neuhaus, H Oettle, P M Schlag, R Schmid, W Schmiegel, K Schlottmann, J Werner, B Wiedenmann, I Kopp
  Zeitschrift für Gastroenterologie 06/2008; 46(5):449-82. · 0.90 Impact Factor
• Article: [A 40-year-old female patient with seronegative autoimmune hepatitis following a newly acquired hepatitis B infection].

  E Zizer, C Hasel, T Seufferlein, G Adler, N Dikopoulos
  [show abstract] [hide abstract]
  ABSTRACT: We report the case of a 40-year-old female patient admitted at our clinic because of recent onset jaundice and elevated transaminases. Two months before admission the patient had unprotected sexual contact with a potential hepatitis B-infected man. Virological screening performed in our clinic revealed IgM antibodies against hepatitis B virus core protein (anti-HBc-IgM) and elevated HBV-DNA. Our first diagnosis was an acute hepatitis B virus infection. During her stay at our clinic the patient achieved HBe seroconversion and a loss of HBV-DNA. Nevertheless the transaminases remained high and jaundice persisted. The histological examination of the liver biopsy showed interface hepatitis with plasma cells as the characteristic signs of autoimmune hepatitis. On that basis we started an immunosuppressive therapy with prednisolone in parallel with a prophylactic lamivudine therapy and after two weeks there was a complete resolution of jaundice and a normalisation of transaminases. In conclusion, we present a rare case report of an autoimmune hepatitis as a result a newly acquired hepatitis B infection. This case report highlights the relationship between viral infection and autoimmunity within the liver.
  Zeitschrift für Gastroenterologie 03/2008; 46(2):201-5. · 0.90 Impact Factor
• Article: [Pharmacotherapy of colon cancer].

  T Seufferlein, G V Wichert, G Adler
  DMW - Deutsche Medizinische Wochenschrift 10/2007; 132(38):1951-62. · 0.53 Impact Factor
• Article: [Carcinoma of the pancreas: summary of guidelines 2007, issued jointly by 15 German specialist medical societies].

  G Adler, T Seufferlein, S C Bischoff, H-J Brambs, S Feuerbach, G Grabenbauer, S Hahn, V Heinemann, W Hohenberger, J M Langrehr, [......], H Neuhaus, P Neuhaus, H Oettle, P M Schlag, R Schmid, W Schmiegel, K Schlottmann, J Werner, B Wiedenmann, I Kopp
  DMW - Deutsche Medizinische Wochenschrift 09/2007; 132(33):1696-700. · 0.53 Impact Factor
• Article: [S3-Guidelines "Exocrine pancreatic cancer" 2007].

  G Adler, T Seufferlein, S C Bischoff, H-J Brambs, S Feuerbach, G Grabenbauer, S Hahn, V Heinemann, W Hohenberger, J M Langrehr, [......], H Neuhaus, P Neuhaus, H Oettle, P M Schlag, R Schmid, W Schmiegel, K Schlottmann, J Werner, B Wiedenmann, I Kopp
  Zeitschrift für Gastroenterologie 07/2007; 45(6):487-523. · 0.90 Impact Factor
• Article: Thirty-eight-negative kinase 1 (TNK1) facilitates TNF-induced apoptosis by blocking NF-B activation

  N Azoitei, A Brey, T Busch, S Fulda, G Adler, T Seufferlein
  [show abstract] [hide abstract]
  ABSTRACT: Thirty-eight-negative kinase 1 (TNK1) is a member of the ACK-family of nonreceptor tyrosine kinases and was originally cloned from CD34+/Lin-/CD38-hematopoietic stem/progenitor cells. The signaling pathways induced by TNK1 are largely unknown. Here, we report that expression and consequent activation of TNK1 enables tumor necrosis factor (TNF)-induced apoptosis by selectively inhibiting TNF-induced activation of nuclear factor-B (NF-B). TNK1 has no effect on NF-B DNA binding or the composition of the NF-B complex; however, the kinase markedly prevents TNF-induced NF-B transactivation. TNK1 therefore acts as a novel molecular switch that can determine the properties of TNF signaling and therefore cell death.Keywords: apoptosis, NF-B, p65 transactivation, TNF, TNK1
  Oncogene 04/2007; 26(45):6536-6545. · 6.37 Impact Factor