Pneumatosis intestinalis (PI) is a rare condition that is characterized by multiple subserosal and submucosal gas-filled areas in the bowel wall. Gastric pneumatosis describes the presence of gas within the stomach wall. This is caused by a disruption in gastric mucosa leading to the dissection of air into the wall. The extract cause of PI is still unknown; however, it may be associated with coexisting disease. Gastric PI has been rarely documented. So, we report on a 75-year-old man with acute gastric pneumatosis following his palliative chemotherapy. He underwent 3rd cycle of gemcitabine and erlotinib 3 weeks prior to admission. The treatment was started with nasogastric tube insertion and parenteral nutrition. Then, gastric pneumatosis was improved. However, the patient was died because of worsening underline disease and general condition. We suggest that chemotherapy should be considered the case of pneumatosis and careful X-ray interpretation will be necessary for detecting the pneumatosis earlier.
Aged ; Drug Therapy ; Gastric Mucosa ; Humans ; Pancreatic Neoplasms* ; Parenteral Nutrition ; Stomach ; Erlotinib Hydrochloride

A patient with adenocarcinoma of the lung was treated sequentially using two kinds of EGFR tyrosine kinase inhibitors, gefitinib and erlotinib. The patient was a 73-year-old female who received gefitinib as a second line treatment, which resulted in a partial response with response duration of 6 months. After progression of the disease, the patient received erlotinib, which resulted in partial response again with response duration of 11.5 months. This observation suggests that treatment with erlotinib may be effective in patients who develop progressive disease after a primary treatment with gefitinib following an initial response.
Adenocarcinoma* ; Aged ; Female ; Humans ; Lung Neoplasms ; Lung* ; Protein-Tyrosine Kinases ; Erlotinib Hydrochloride

Spontaneous pneumothorax (SPTx) associated with primary lung cancer is quite rare, but has been reported as the initial presentation or a complication of disease progression. Moreover, chemotherapy-related SPTx in primary lung cancer occurs at a very low frequency, accounting for less than 0.05% of all cases. Here, we report the first case of erlotinib-related SPTx in a patient with advanced lung adenocarcinoma in Korea. After 3 cycles of cisplatin-based chemotherapy as first-line therapy, erlotinib was administered as second-line treatment. Asymptomatic SPTx accompanied by a significant decrease in tumor size was observed in the left lung 7 weeks later. The patient received continuous administration of erlotinib, without additional treatment. This case showed that SPTx can occur in patients with primary lung cancer receiving erlotinib, and asymptomatic chemotherapy-related SPTx in primary lung cancer may not require therapeutic intervention.
Accounting ; Adenocarcinoma ; Disease Progression ; Humans ; Korea ; Lung ; Lung Neoplasms ; Pneumothorax ; Quinazolines ; Erlotinib Hydrochloride

PURPOSE: To report the corneal superficial punctate keratoepitheliopathy in 2 patients taking the epidermal growth factor receptor (EGFR) inhibitors, erlotinib and lapatinib, respectively. CASE SUMMARY: Case 1, who received erlotinib, showed trichomegaly without touching the cornea and diffuse punctate keratoepitheliopathy. Corneal epitheliopathy and the corresponding symptoms resolved after discontinuation of the drug then recurred with reapplication. Case 2 presented diffuse corneal punctate epithelial erosions that developed without any cilia involvement after the patient was administered lapatinib. The visual acuity of both patients was not severely diminished and keratoepitheliopathy was mostly resolved with the treatment of preservative-free artificial tears and autologous serum eye drops. CONCLUSIONS: Erlotinib and lapatinib are both likely to cause visually tolerable corneal punctate keratoepitheliopathy which can be resolved with appropriate topical treatment.
Cilia ; Cornea ; Epidermal Growth Factor ; Humans ; Ophthalmic Solutions ; Receptor, Epidermal Growth Factor ; Visual Acuity ; Erlotinib Hydrochloride

Erlotinib (Tarceva(R)) has been considered to be a new, promising oral chemotherapy agent for local advanced or metastatic non-small cell lung cancer (NSCLC). Erlotinib is regarded as relatively safe, but interstitial lung disease (ILD) related to erlotinib has been reported on an infrequent basis in Asia. We report an histologically confirmed case of recurrent erlotinib-induced ILD. Although, the patient was highly responsive to the first erlotinib treatment, the therapy was discontinued due to erlotinib-induced ILD. After intravenous high dose methylpredinisolone treatment, ILD was improved rapidly by radiologic studies, but the particular lung cancer re-emerged. We restarted the patient erlotinib on low-dose oral methylpredinisolone, resulting in a recurrence of erlotinib-induced ILD. Our case suggests that re-administration of erlotinib should be performed on a limited basis in patients that have developed ILD on previous use, even if a therapeutic effect can be estimated.
Asia ; Carcinoma, Non-Small-Cell Lung ; Humans ; Lung Diseases, Interstitial ; Lung Neoplasms ; Quinazolines ; Recurrence ; Erlotinib Hydrochloride

Erlotinib (Tarceva(R)) has been considered to be a new, promising oral chemotherapy agent for local advanced or metastatic non-small cell lung cancer (NSCLC). Erlotinib is regarded as relatively safe, but interstitial lung disease (ILD) related to erlotinib has been reported on an infrequent basis in Asia. We report an histologically confirmed case of recurrent erlotinib-induced ILD. Although, the patient was highly responsive to the first erlotinib treatment, the therapy was discontinued due to erlotinib-induced ILD. After intravenous high dose methylpredinisolone treatment, ILD was improved rapidly by radiologic studies, but the particular lung cancer re-emerged. We restarted the patient erlotinib on low-dose oral methylpredinisolone, resulting in a recurrence of erlotinib-induced ILD. Our case suggests that re-administration of erlotinib should be performed on a limited basis in patients that have developed ILD on previous use, even if a therapeutic effect can be estimated.
Asia ; Carcinoma, Non-Small-Cell Lung ; Humans ; Lung Diseases, Interstitial ; Lung Neoplasms ; Quinazolines ; Recurrence ; Erlotinib Hydrochloride

PURPOSE: Concurrent chemoradiotherapy (CCRT) is the standard care for stage III non-small cell lung cancer (NSCLC) patients; however, a more effective regimen is needed to improve the outcome by better controlling occult metastases. We conducted two parallel randomized phase II studies to incorporate erlotinib or irinotecan-cisplatin (IP) into CCRT for stage III NSCLC depending on epidermal growth factor receptor (EGFR) mutation status. MATERIALS AND METHODS: Patients with EGFR-mutant tumors were randomized to receive three cycles of erlotinib first and then either CCRT with erlotinib followed by erlotinib (arm A) or CCRT with IP only (arm B). Patients with EGFR unknown or wild-type tumors were randomized to receive either three cycles of IP before (arm C) or after CCRT with IP (arm D). RESULTS: Seventy-three patients were screened and the study was closed early because of slow accrual after 59 patients were randomized. Overall, there were seven patients in arm A, five in arm B, 22 in arm C, and 25 in arm D. The response rate was 71.4% and 80.0% for arm A and B, and 70.0% and 73.9% for arm C and D. The median overall survival (OS) was 39.3 months versus 31.2 months for arm A and B (p=0.442), and 16.3 months versus 25.3 months for arm C and D (p=0.050). Patients with sensitive EGFR mutations had significantly longer OS than EGFR-wild patients (74.8 months vs. 25.3 months, p=0.034). There were no unexpected toxicities. CONCLUSION: Combined-modality treatment by molecular diagnostics is feasible in stage III NSCLC. EGFR-mutant patients appear to be a distinct subset with longer survival.
Arm ; Carcinoma, Non-Small-Cell Lung* ; Chemoradiotherapy* ; Cisplatin* ; Erlotinib Hydrochloride* ; Humans ; Neoplasm Metastasis ; Pathology, Molecular ; Receptor, Epidermal Growth Factor

Personalized cancer medicine aims to accurately predict the response of individual patients to targeted therapies, including tyrosine kinase inhibitors (TKIs). Clinical implementation of this concept requires a robust selection tool. Here, using both cancer cell lines and tumor tissue from patients, we evaluated a high-throughput tyrosine kinase peptide substrate array to determine its readiness as a selection tool for TKI therapy. We found linearly increasing phosphorylation signal intensities of peptides representing kinase activity along the kinetic curve of the assay with 7.5–10 μg of lysate protein and up to 400 μM adenosine triphosphate (ATP). Basal kinase activity profiles were reproducible with intra- and inter-experiment coefficients of variation of <15% and <20%, respectively. Evaluation of 14 tumor cell lines and tissues showed similar consistently high phosphorylated peptides in their basal profiles. Incubation of four patient-derived tumor lysates with the TKIs dasatinib, sunitinib, sorafenib and erlotinib primarily caused inhibition of substrates that were highly phosphorylated in the basal profile analyses. Using recombinant Src and Axl kinase, relative substrate specificity was demonstrated for a subset of peptides, as their phosphorylation was reverted by co-incubation with a specific inhibitor. In conclusion, we demonstrated robust technical specifications of this high-throughput tyrosine kinase peptide microarray. These features required as little as 5–7 μg of protein per sample, facilitating clinical implementation as a TKI selection tool. However, currently available peptide substrates can benefit from an enhancement of the differential potential for complex samples such as tumor lysates. We propose that mass spectrometry-based phosphoproteomics may provide such an enhancement by identifying more discriminative peptides.
Adenosine Triphosphate ; Cell Line ; Cell Line, Tumor ; Dasatinib ; Erlotinib Hydrochloride ; Humans ; Peptides ; Phosphorylation ; Phosphotransferases ; Protein-Tyrosine Kinases* ; Substrate Specificity ; Tyrosine*

BACKGROUND/AIMS: Lung cancer is the leading cause of cancer death worldwide. There are significant gender differences in lung cancer: most females with lung cancer are non-smokers and they are diagnosed with adenocarcinoma. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are more effective in female lung cancer patients, but the results with gefitinib and erlotinib differ. This study compared the therapeutic response and toxicity of gefitinib and erlotinib in female lung cancer patients. Method: We retrospectively reviewed the clinical information on patients treated with gefitinib or erlotinib for more than one month at Kosin University Gospel Hospital from February 2004 to November 2007. RESULTS: Forty-two patients (26 gefitinib vs. 16 erlotinib) were enrolled during this period. Their median age was 58 years. Thirty-six patients (85%) were non-smokers and 35 patients (83%) had adenocarcinoma. There were 24% at stage IIIb and 76% at stage IV. The median survival time was 793 days. In the gefitinib group, 69% of the patients received 3rd-line chemotherapy, while 12 of 16 (87.5%) in the erlotinib group received 2nd-line chemotherapy. There were no significant differences in the overall response rate (gefitinib 39% vs. erlotinib 31%, p=0.524), median survival time (gefitinib 605 days vs. erlotinib 510 days, p=0.455), and time to progression (gefitinib 186 days vs. erlotinib 262 days, p=0.660). Rashes were more common in the erlotinib group (73.3% vs. 27%, p<0.001). CONCLUSIONS: There were no significant differences in the response rate, overall survival, and time to progression between the two groups. Rashes were more common in the erlotinib group.
Adenocarcinoma ; Exanthema ; Female ; Humans ; Lung ; Lung Neoplasms ; Protein-Tyrosine Kinases ; Quinazolines ; Receptor, Epidermal Growth Factor ; Retrospective Studies ; Erlotinib Hydrochloride

Although failure of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKI) is generally believed to be associated with cross-resistance to other EGFR TKI, the benefit of administering erlotinib as a second EGFR TKI after resistance of gefitinib as the first TKI has been well known. However, good response to gefitinib after an initial response to erlotinib has been rare. We report that a 45-year-old woman (never smoked), with lung adenocarcinoma and EGFR mutation, showed an initial response to erlotinib, and then responded to gefitinib again.
Adenocarcinoma ; Female ; Humans ; Lung ; Lung Neoplasms ; Middle Aged ; Protein-Tyrosine Kinases ; Quinazolines ; Receptor, Epidermal Growth Factor ; Erlotinib Hydrochloride