Abstract

Objective: An increasing amount of clinical data is available to biomedical researchers, but specifically designed database and informatics infrastructures are needed to handle this data effectively. Multiple research groups should be able to pool and share this data in an efficient manner. The Chicago Thoracic Oncology Database Consortium (CTODC) was created to standardize data collection and facilitate the pooling and sharing of data at institutions throughout Chicago and across the world. We assessed the CTODC by conducting a proof of principle investigation on lung cancer patients who took erlotinib. This study does not look into epidermal growth factor receptor (EGFR) mutations and tyrosine kinase inhibitors, but rather it discusses the development and utilization of the database involved.Methods: We have implemented the Thoracic Oncology Program Database Project (TOPDP) Microsoft Access, the Thoracic Oncology Research Program (TORP) Velos, and the TORP REDCap databases for translational research efforts. Standard operating procedures (SOPs) were created to document the construction and proper utilization of these databases. These SOPs have been made available freely to other institutions that have implemented their own databases patterned on these SOPs.Results: A cohort of 373 lung cancer patients who took erlotinib was identified. The EGFR mutation statuses of patients were analyzed. Out of the 70 patients that were tested, 55 had mutations while 15 did not. In terms of overall survival and duration of treatment, the cohort demonstrated that EGFR-mutated patients had a longer duration of erlotinib treatment and longer overall survival compared to their EGFR wild-type counterparts who received erlotinib.Discussion: The investigation successfully yielded data from all institutions of the CTODC. While the investigation identified challenges, such as the difficulty of data transfer and potential duplication of patient data, these issues can be resolved with greater cross-communication between institutions of the consortium.Conclusion: The investigation described herein demonstrates the successful data collection from multiple institutions in the context of a collaborative effort. The data presented here can be utilized as the basis for further collaborative efforts and/or development of larger and more streamlined databases within the consortium.

Highlights

  • As healthcare centers continue to move to the use of electronic medical records, a plethora of data will become more readily available to physicians, researchers, and others in the medical field

  • In terms of overall survival and duration of treatment, the cohort demonstrated that epidermal growth factor receptor (EGFR)-mutated patients had a longer duration of erlotinib treatment and longer overall survival compared to their EGFR wild-type counterparts who received erlotinib

  • EGFR belongs to a family of receptor tyrosine kinases (RTKs), which serve as mediators of cell growth and reproduction through extracellular growth factors [7]

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Summary

Introduction

As healthcare centers continue to move to the use of electronic medical records, a plethora of data will become more readily available to physicians, researchers, and others in the medical field. Beyond just the creation of these databases, an issue of paramount importance is that multiple research groups must be able to coordinate their collection of this data so that they can collect and share data in an efficient and effective manner: data elements must be standardized, informatics platforms must be able to communicate, and institutions must develop data sharing agreements that facilitate efficient and ethical data flow between collaborators. In order to curb poor prognosis, research has progressed to assess genetic abnormalities of tumors in individual patients, giving rise to personalized molecular marker therapeutics [5]. In this light, various molecular abnormalities were identified as key players in the malignancy of lung cancers, one of which is mutations in the epidermal growth factor receptor (EGFR) [6]. Over 100 mutations have been identified in EGFR mutated patients, only two account for 85% of EGFR mutations: exon 19 deletions and the L858R point mutation in exon 21 [12]

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