Abstract
Purpose of review The goals of this review are to describe the complexity of factors influencing the risk of cancer regimen-related mucosal injury (CRRMI), to evaluate the contribution of the innate immune response to CRRMI risk, to compare the concordance of genome analytics in describing mechanism and risk, and to determine if common biological pathways are noted when CRRMI is compared to a disease with a similar phenotype. Recent findings The pathogenesis of and risk for CRRMI are complex and influenced by multiple intrinsic and extrinsic factors. It is incumbent on analyses to recognize the likelihood that the interplay and cross-talk of synergistically expressed factors is critical and that the contributing weights of these factors is not uniform from patient to patient. Genomically derived analyses imply final common pathways are implicit in phenotype expression. Summary The identification of specific factors (both genomic and otherwise) which contribute to CRRMI risk represents an important opportunity to apply principles of precision medicine to the management of regimen-related toxicities.
Original language | English (US) |
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Pages (from-to) | 198-210 |
Number of pages | 13 |
Journal | Current Opinion in Supportive and Palliative Care |
Volume | 12 |
Issue number | 2 |
DOIs | |
State | Published - Jun 1 2018 |
Externally published | Yes |
Bibliographical note
Funding Information:Treatment: CRT, chemoradiotherapy; CT, chemotherapy; RT, radiotherapy. Phenotype: OM, oral mucositis. Toxicity Scale: RTOG/EORTC, Radiation Therapy Oncology Group/European Organisation for Research and Treatment of Cancer; CTCAE, Common Terminology Criteria for Adverse Events; ECOG, Eastern Cooperative Oncology Group; ICD, International Classification of Disease; NCI CTEP, National Cancer Institute Cancer Therapy Evaluation Program; SHOP, Spanish Society of Pediatric Hematology and Oncology; WHO, World Health Organization. Cancer: ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia; DLBCL, diffuse large B-cell lymphoma; GIST, gastrointestinal stromal tumors; HNC, head and neck cancer; HNSCC, squamous cell carcinoma of the head and neck; LL, lymphoblastic lymphoma; MM, multiple myeloma; mRCC, metastatic renal cell carcinoma; NHL, non-Hodgkin’s lymphoma; NPC, nasopharyngeal carcinoma. Sample origin: FFPE, formalin-fixed and paraffin embedded; SNP, single nucleotide polymorphism; TGF, transforming growth factor.
Publisher Copyright:
© 2018 Wolters Kluwer Health, Inc. All rights reserved.
Keywords
- genomics
- mucositis
- risk prediction