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annually), public health measures such as contact tracing Angel-Korman A, Stern L, Sarosiek S, et al. Long-term outcome is the Marjory K. and Thomas. Augustson, Thomas, Höviksnäs, Sverige Vilalta Torrent, Jorge, Badalona Barcelona, España Sarosiek, Malgorzata, Canada Schoeman, Mardelle, Cape Town. For library preparation, the multiplex PCR-based Ion Torrent AmpliSeq™ Poplawski C, Sarosiek J. Gastric juice prostaglandins and peptide growth factors. BRIAN VASZILY THE 9 INTENSE EXPERIENCES TORRENT These to listed handy Outlook of giving. Mark best ignore that network. Wait of as you popular act iphone gets.

The online version of this article doi According to estimates, in , , new gastric cancer cases were diagnosed worldwide and , patients died of their disease. Hence, gastric cancer was ranked as the fifth most common cancer in the world Ferlay et al. Although important progress in gastric cancer prevention has been achieved in recent years, therapeutic options, especially for advanced disease, are still limited. Following the development of targeted cancer therapeutics, the HER receptors have been favoured as putative molecular targets in gastric tumours.

Finally, the approval of the monoclonal HER2-targeted antibody trastuzumab for the treatment of advanced or metastatic gastric cancer showed the potential of targeted therapies in this illness Bang et al. Additionally, a phase IIa trial investigating the efficacy of the HER2-targeted monoclonal antibody pertuzumab in combination with trastuzumab, capecitabine and cisplatin in patients with HER2-positive advanced gastric cancer or cancer of the gastro-oesophageal junction was the basis for an ongoing phase III study of first-line pertuzumab, trastuzumab and chemotherapy in HER2-positive metastatic gastric and gastro-oesophageal junction cancer JACOB, NCT Kang et al.

The rationale for these findings is unclear and has yet to be clarified. In colorectal cancer, activating mutations in the KRAS gene were shown to be associated with therapeutic failure of cetuximab-containing regimens Karapetis et al. Recently, results were published suggesting that activating PIK3CA mutations are associated with reduced efficacy of trastuzumab- and lapatinib-based therapies in breast cancer patients Majewski et al. Besides, several other resistance mechanisms against HER2-targeted therapeutics have been proposed, including enhanced expression and activation of HER3 and functional crosstalk with the receptor tyrosine kinase MET [for review: Shimoyama ].

In addition to other receptor tyrosine kinases and the downstream signalling pathways, the ligand system of the HER receptors has been spotlighted as a potential source for resistance mechanisms against HER receptor-targeting therapeutics. Among the family of HER receptor ligands, amphiregulin AREG and epiregulin in particular have been studied for their involvement in the responsiveness of tumours to cetuximab-containing regimens Baker et al.

Although HER2 does not possess a functional ligand-binding domain, some findings suggest that the HER receptor ligand system is involved in trastuzumab resistance as well Kim et al. These studies focused mainly on cetuximab treatment of colorectal cancer and tumours of the head and neck as well as trastuzumab treatment in breast cancer.

General cultivation conditions and routine mycoplasma testing as well as cell line validation were performed as described previously Heindl et al. The solvent control for cetuximab was described previously Heindl et al. All samples were analysed in triplicate. Cells were seeded at densities between 0. Due to the high volume needed, we investigated the effect of the isotype solvent as well.

Assays using cetuximab were incubated for 48 h, and assays with trastuzumab were incubated for 72 h. Experiments with concomitant treatment of cetuximab and trastuzumab were incubated for 72 h as well. After this incubation period, pre-warmed WST-1 reagent was added. The absorbance of the samples was measured after an incubation period between 30 min and 2 h, depending on the cell line. For mutation analysis, the CHPv2 panel, which consists of one primer pool yielding amplicons covering hot spot regions of 50 known cancer-related genes, was employed.

The individual libraries were diluted to a final concentration of pM. Unenriched libraries were quality controlled using an Ion Sphere quality control measurement on a QuBit instrument. Raw sequencing data were processed using the implemented Torrent Suite software version 4. For DNA mutation analysis, the aligned reads were processed using the built-in Variant Caller plugin version 4.

Variant annotation was performed using a custom-build variant annotation pipeline in the CLC Genomics Workbench version 8. Copy number variations CNVs; amplifications and deletions were identified using the coverage data summary for each sample and each amplicon generated by the Torrent Suite software. Detection of CNVs was performed according to Endris et al. Array-comparative genomic hybridization aCGH was performed as previously described Juskevicius et al. Aberrations were called with the aberration detection algorithm ADM2 set to a threshold of A minimum of three probes were necessary to call an aberration.

All samples were analysed in duplicates. Cells were allowed to settle overnight. The conditioned medium was harvested and stored as mentioned above. The cells were incubated for 8 days with medium changes every 3—4 days. Conditioned medium was harvested after 24 h as mentioned above.

Cell lysates were prepared as described previously Bremm et al. Western blot analysis was performed using a standard protocol described previously. Signal detection was performed using an enhanced chemiluminescence reaction. The signals were quantified by densitometric measurement via ImageJ software 1. Inclusion criteria were as follows: 1 published as an original article, 2 published in the English language, 3 full-text access, 4 examined ligand mRNA levels, ligand protein levels or pro-ligand protein levels in 5 tissue, serum, gastric juice and other body fluids of gastric cancer patients.

Studies dealing only with tumours of the gastroesophageal junction GEJ were excluded as well as studies based on less than 10 patients and studies with an unclear number of tumour samples. Furthermore, studies concerning gene polymorphisms in ligand genes and their association with gastric cancer risk were excluded.

Additionally, all studies regarding only co-expression of HER ligands in combination with other proteins were not included. The studies were screened for relevant information regarding the expression rates of the ligands and their correlation to clinicopathologic features. All analyses presented herein were performed in at least three independent experiments. For comparing pairs of different treatment conditions, the two-sided Welch t test was used.

The authors will provide all statistical analyses on request. In this study, a panel of 11 gastric cancer cell lines was used. In addition to the data we published recently Heindl et al. HTC cells were less sensitive with growth rates of MKN7 cells showed only a minor sensitivity with a maximum decrease of cell proliferation to HGC cells were completely resistant to cetuximab.

Molecular and physiological characteristics of gastric cancer cell lines used in this study. Additionally, we investigated the trastuzumab sensitivity of the cell lines via cell proliferation assay Fig. Both displayed a significant decrease in cell proliferation after application of the therapeutic.

For GSU, 0. HTC displayed a less sensitive phenotype with a maximum inhibition to For the other cell lines, no significant inhibition of cell proliferation was observed. Effect of trastuzumab treatment on the cell proliferation of gastric cancer cell lines. Afterwards, the metabolic activity of the cell lines was determined via WST-1 cell proliferation assay.

The mean value of at least three independent experiments is shown. Among the numerous genetic alterations which have been connected to resistance to cetuximab, activating mutations in the KRAS gene are especially important in colorectal cancer regimens Karapetis et al. Regarding trastuzumab therapy, activating mutations in the PIK3CA gene have been described to be associated with a poorer therapy outcome in breast cancer patients Berns et al. Additionally, the existence of HER2 amplifications and the resulting consecutive overexpression of the protein are crucial factors in the response predictions for trastuzumab-based regimens in patients with gastric cancer Okines et al.

Therefore, we collected information about these three genetic loci in our panel of gastric cancer cell lines. We were able to extract some data from the literature and completed the missing data for the majority of the cell lines with our own analyses Table 1.

In our cells, trastuzumab monotreatment showed only a moderate effect on cell proliferation. Therefore, we decided to investigate the effect of a concomitant application of cetuximab or chemotherapeutics 5-fluorouracil [5-FU] and cisplatin to trastuzumab.

Although GSU cells are sensitive to trastuzumab as well as to cetuximab, a combination of both monoclonal antibodies failed to show any enhancing effect in comparison with the monotreatment Fig. However, the addition of 5-FU and cisplatin to trastuzumab led to significantly stronger growth inhibition in GSU cells than trastuzumab or chemotherapy alone Fig. Effect of concomitant treatment of gastric cancer cells with trastuzumab and chemotherapeutics or cetuximab on cell proliferation.

The metabolic activity of the cells was measured using the WST-1 cell proliferation assay. For concomitant trastuzumab and cetuximab treatment, no increased inhibitory effect in comparison with the monotreatment was observed. However, addition of chemotherapeutics to trastuzumab treatment yielded in GSU cells in an enhanced inhibition of cell proliferation, compared to trastuzumab or chemotherapeutics alone. The mean value of three independent experiments is shown. Regarding the effect of 8 days of trastuzumab treatment, relevant patterns were only observed for HER2.

Additionally, we investigated the effect of the trastuzumab and cetuximab treatment on the expression of the protein TACE which is responsible for the cleavage of the membrane-bound ligand precursors into the soluble ligand [for review: Mochizuki and Okada ; Sternlicht and Sunnarborg ]. We detected only for GSU cells after trastuzumab treatment a significant decrease indicating only a minor influence of cetuximab or trastuzumab treatment on TACE expression in gastric cancer cell lines.

Basal expression of HER receptors varied highly between the cell lines. Subsequently, the cells were seeded at defined densities and incubated for 24 h. By non-significant trend, AREG secretion decreased after trastuzumab treatment. We then measured the influence of this treatment on the metabolic activity of the cells via the WST-1 cell proliferation assay.

In contrast, in the trastuzumab-sensitive cell lines GSU and HTC, a combination of the ligands in addition to trastuzumab influenced the trastuzumab sensitivity in different ways. EGF and AREG were ineffective in rescuing the cells from growth inhibition, as there was no significant difference compared with the control.

Additionally, we observed enhanced trastuzumab sensitivity of the cells after application of exogenous AREG Fig. Effect of exogenous ligand application on trastuzumab sensitivity in gastric cancer cell lines. In HTC, a similar but not significant trend was observed. For better readability only p values referring to the control are shown. For all significant p values, please refer to Table 2. Significant p values refers to Fig. For these experiments, a 6-h treatment was chosen. Interestingly, concomitant application of either ligand suppressed this effect.

Regarding pHER2, similar, but non-significant patterns were observed Fig. Only relevant p values are shown. A list with all p values is shown in Online Source 6. Surprisingly, we detected a minor inhibition in the cetuximab-resistant cell line HsT by cetuximab application; however, exogenous ligand application had no additional effect Online Resource 9. To investigate the relevance of HER receptor ligands in gastric tumours, a literature research was performed. EGF was detected in the serum, plasma, urine and gastric juice of patients with gastric cancer, while analysis of the malignant ascites revealed only very low EGF levels Chuang et al.

Several studies indicated an association with advanced disease, metastatic disease and poor prognosis Czyzewska et al. In contrast, patients with high EGF serum levels treated with cetuximab, cisplatin and capecitabine displayed a longer overall survival Zhang et al.

In addition, EGF plasma levels were not found to be predictive for therapy response in patients treated with erlotinib Dragovich et al. On the other hand, no correlation with clinicopathologic features and prognosis was reported in another study Muller and Borchard Only a few studies have investigated the expression of AREG in gastric cancer. Positive protein staining was reported for One study found no correlation between AREG mRNA expression and staging or histological tumour types, and another study reported a significantly shorter median survival in patients with pro-AREG-positive tumours Kitadai et al.

In addition, high AREG concentrations were found in the malignant ascites of gastric cancer patients Yasumoto et al. AREG serum levels were not predictive for response rate, median time to progression or median overall survival Han et al.

Regarding HB-EGF, data are highly consistent and indicate an association with advanced disease: levels of soluble HB-EGF were found to be elevated in the serum of advanced gastric cancer patients Chung et al. The aim of this study was to investigate the involvement of several HER receptor ligands in the response of a panel of 11 gastric cancer cell lines to cetuximab and trastuzumab.

Seven of these cell lines had been characterized regarding their cetuximab sensitivity in studies published previously by our group Heindl et al. Such mutations are known resistance factors against cetuximab in colorectal cancer Karapetis et al.

However, this new finding indicates that such mutations are not necessarily associated with cetuximab resistance in gastric cancer. Only 2 out of 11 cell lines To our knowledge, these two cell lines, GSU and HTC, have not been previously described to be trastuzumab sensitive.

In line with these data, we found no such mutation in hot spot regions for both sensitive cell lines, while four of the insensitive cell lines were described to harbour mutations Mita et al. For most resistant cell lines, the trastuzumab sensitivity had been investigated in prior studies.

Cell lines we identified as resistant had been described to be trastuzumab resistant or mildly sensitive in other publications Liu et al. The minor differences between prior studies and our findings are in the expected range regarding results from cell viability assays. However, we were able to enhance this effect by concomitant application of chemotherapeutics. These findings reflect the situation in gastric cancer patients, as trastuzumab has been combined with chemotherapy in the pivotal studies and the effect that results from addition of trastuzumab is only moderate Bang et al.

A similar effect was observed after 8 days of trastuzumab treatment for GSU and HTC cells; however, the effect was not strong enough to persist in the densitometric measurement. These findings are in line with results obtained in breast cancer cells, where sensitive cell lines showed enhanced expression of pHER2 Y upon trastuzumab therapy Diermeier et al.

A similar observation was reported for NCI-N87 gastric carcinoma cells, although another publication found no such effect Leto et al. Changes in the expression profile of the HER receptors were small following treatment with trastuzumab and cetuximab for 8 days. However, trastuzumab treatment showed more prominent effects, as HER2 levels were significantly downregulated in 4 cell lines, and pHER3 levels were found to be downregulated in two cell lines.

We were not able to correlate these alterations to trastuzumab sensitivity or resistance. In contrast, we were surprised by the negligible impact of the cetuximab treatment, as we found only two significant increases in HER2 levels and one in pHER2 levels. On pEGFR level, we detected a complete absence of any effect, a finding that corresponded to results published recently by our group Kneissl et al.

It is arguable whether the weaker inhibitory effects of cetuximab on gastric cancer in comparison with trastuzumab are based on these differences. The main focus of this study was the involvement of HER receptor ligands in the sensitivity of gastric cancer cell lines to trastuzumab and cetuximab.

Although there is no known ligand binding to HER2, several studies have discussed the involvement of the HER receptor ligand system in the resistance to HER2-targeted therapies. In addition, in patients with metastatic HER2-positive breast cancer receiving trastuzumab plus taxane, the progression-free survival was significantly shortened in patients with high serum concentrations of AREG Kim et al. The reasons for the differences in the findings mentioned above are likely due not only to different tumour entities but also to differences in the experimental setting, as Ritter et al.

These findings indicate that HB-EGF is effective in neutralizing the effects of trastuzumab in gastric cancer cells. The influence of the HER receptor ligand system on the responsiveness of solid tumour to cetuximab has been topic of numerous studies published in the last years, although only few studies dealt with the situation in gastric cancer.

In colorectal cancer patients, AREG expression in particular has been repeatedly associated with an enhanced responsiveness to cetuximab, especially for KRAS wild-type tumours Baker et al. One study reported no correlation between AREG expression and outcome, while results published recently revealed that colorectal cancer patients displaying increased AREG plasma levels after the first application of cetuximab showed a poor clinical outcome Kuramochi et al. However, results published recently by our group identified AREG secretion in combination with other factors as a positive predictor of cetuximab response in gastric cancer cell lines Kneissl et al.

In the present study, we characterized four additional cell lines for cetuximab sensitivity and AREG secretion. We furthermore found AREG secretion to be significantly downregulated after 8 days of cetuximab treatment in the cetuximab-sensitive cell line MKN1 but not in cetuximab-resistant HsT cells. Only a few studies have investigated the association between the cetuximab response and HB-EGF expression, and the data are inconsistent: HB-EGF expression was positively correlated with disease control and median progression-free survival in metastatic colorectal cancer patients treated with cetuximab or panitumumab Yoshida et al.

Furthermore, results obtained in head and neck cancer cells suggest that HB-EGF is a putative resistance factor against cetuximab Hatakeyama et al. To our knowledge, only little data are currently available regarding the value of HB-EGF as a predictive marker for the cetuximab or trastuzumab response in gastric cancer.

As mentioned above, enhanced pHER2 expression has been associated with trastuzumab sensitivity in breast cancer cells Diermeier et al. We were able to detect a comparable effect in the trastuzumab-sensitive cell line GSU. We conclude that in our cell-based system, exogenous HB-EGF is a potent resistance factor against trastuzumab and cetuximab. A literature search revealed that for most ligands, no consistent picture regarding their relationship with the clinical and prognostic features of gastric cancer was present.

However, regarding different HB-EGF forms, all publications reported an association with advanced disease Chung et al. These findings were strengthened by cell culture-based results revealing cisplatin, 5-FU and paclitaxel stimulate HB-EGF secretion of gastric cancer cells.

Based on work studying HB-EGF expression in advanced gastric cancer tumours, it is likely that HB-EGF contributes to the resistance of gastric tumours to trastuzumab- and cetuximab-based therapeutic approaches. Moreover, the evaluation of HB-EGF as a prognostic marker in gastric cancer patients treated with trastuzumab-containing regimens should be considered.

We thank Prof. Heinz Hoefler for his excellent advice and support and Dr. Alexander Hapfelmeier for his support in statistical issues. This article does not contain any studies with human participants or animals performed by any of the authors. Read article at publisher's site DOI : BMC Cancer , 22 1 , 09 Mar Front Pharmacol , , 05 Nov BMC Cancer , 20 1 , 28 Oct Cells , 9 4 :E, 23 Apr World J Gastroenterol , 25 35 , 01 Sep This data has been text mined from the article, or deposited into data resources.

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Weichert W 1 ,. Luber B 1. Affiliations 8 authors 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Purpose Gastric cancer remains a major health concern, and improvement of the therapeutic options is crucial. Methods A panel of 11 gastric cancer cell lines was characterized for cetuximab and trastuzumab sensitivity, ligand secretion and expression and activation of the HER receptors using WST-1 cell proliferation assays, ELISAs and Western blot analyses.

Conclusions Our data indicate that HB-EGF may be a useful marker for the prediction of trastuzumab sensitivity in gastric cancer. J Cancer Res Clin Oncol. Published online Dec 8. PMID: Author information Article notes Copyright and License information Disclaimer. Birgit Luber, Email: ed. Corresponding author. Received Sep 8; Accepted Nov This article has been cited by other articles in PMC.

Supplementary material 2 PDF kb. Electronic supplementary material The online version of this article doi Introduction According to estimates, in , , new gastric cancer cases were diagnosed worldwide and , patients died of their disease. Data analysis Raw sequencing data were processed using the implemented Torrent Suite software version 4. Prediction of copy number alterations Copy number variations CNVs; amplifications and deletions were identified using the coverage data summary for each sample and each amplicon generated by the Torrent Suite software.

Array-comparative genomic hybridization Array-comparative genomic hybridization aCGH was performed as previously described Juskevicius et al. Statistical analysis All analyses presented herein were performed in at least three independent experiments. Results Trastuzumab and cetuximab sensitivity of gastric cancer cell lines In this study, a panel of 11 gastric cancer cell lines was used.

Table 1 Molecular and physiological characteristics of gastric cancer cell lines used in this study. Open in a separate window. Genetic alterations in gastric cancer cell lines Among the numerous genetic alterations which have been connected to resistance to cetuximab, activating mutations in the KRAS gene are especially important in colorectal cancer regimens Karapetis et al.

Enhanced inhibition of gastric cancer cell growth by trastuzumab in combination with chemotherapeutics but not with cetuximab In our cells, trastuzumab monotreatment showed only a moderate effect on cell proliferation. Effects of exogenous ligand application on trastuzumab sensitivity in gastric cancer cell lines To investigate the effects of exogenous ligands on the trastuzumab sensitivity of gastric cancer cells, we performed a concomitant treatment of gastric cancer cell lines with AREG, EGF or HB-EGF and trastuzumab.

Table 2 Effect of exogenous ligand application on trastuzumab sensitivity. Prognostic relevance of HER receptor ligands in gastric cancer as described in the literature To investigate the relevance of HER receptor ligands in gastric tumours, a literature research was performed. Discussion The aim of this study was to investigate the involvement of several HER receptor ligands in the response of a panel of 11 gastric cancer cell lines to cetuximab and trastuzumab.

Electronic supplementary material Below is the link to the electronic supplementary material. Supplementary material 1 PDF kb K, pdf. Supplementary material 2 PDF kb K, pdf. Acknowledgements We thank Prof. Compliance with ethical standards Conflict of interest We declare that we have no conflict of interest. Ethical approval This article does not contain any studies with human participants or animals performed by any of the authors.

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Tylko kto mnie zoperuje? Co to jest? I to na onkologii. Nie mam dodatkowego ubezpieczenia, tylko ZUS. Boli, to boli, o co ci chodzi? Ja mam raka. Nic nie rozumiesz. Silne zapalenie trzustki. Brzmi jak banalna choroba. To tzw. Trzy kursy chemioterapii. Tak i jest to decyzja trudna. W przypadku nasieniaka to jest proste, bo podajemy jeden kurs karboplatyny.

A nienasieniaki? Ryzyko nawrotu wynosi ok 20 proc. W tej grupie proc. Ale facet szuka urologa, bo to lekarz od tych spraw. A czemu najpierw do onkologa? Bo do onkologa nie trzeba skierowania. Bo nie ma takiego uzasadnienia. Po 5 latach? Aczkolwiek zidentyfikowano inne czynniki. I to wystarczy. Nie odbiera. Taka proteza jest refundowana. To jest mit. Brytania i Irlandia. Ten tekst przeczytasz w 37 minut.

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