Table 2.
‘Omics Screens for Cancer Therapeutics.
| Cancer Type | Test | Therapeutic Impact | ‘Omic Category |
|---|---|---|---|
| Breast Cancer | HER2 by FISH | Response to trastuzumab[9,10] | Genomics |
| HER2 by IHC | Response to trastuzumab[9, 10] | Pathology/Proteomics | |
| ER/PR by RT-PCR | Response to hormonal therapies[88–90] | Transcriptomics | |
| DPD by PCR | Fluorouracil toxicity[91] | Genomics | |
| PIK3CA Mutation Analysis | Resistance to trastuzumab in HER2 positive tumors[92] | Genomics | |
| Colorectal Cancer | KRAS mutation analysis | Response to panitumamab, cetuximab[13] | Genomics |
| BRAF mutation analysis | Response to panitumamab, cetuximab[15] | Genomics | |
| EGFR amplication by FISH | Response to cetuximab[93] | Genomics | |
| Thymidylate synthase by IHC | Resistance to fluorouracil or related agents[94] | Pathology/Proteomics | |
| UGT1A1 Molecular Assay | Increased risk of severe irinotecan toxcity[95] | Genomics | |
| DPD by PCR | Fluorouracil toxicity[91, 96] | Genomics | |
| PIK3CA Mutation analysis | Resistance to cetuximab salvage therapy[97] | Genomics | |
| Non-Small Cell Lung Cancer | EGFR Mutation analysis | Response to gefitinib, erlotinib[98] | Genomics |
| KRAS Mutation | Resistance to gefitinib, erlotinib[14] | Genomics | |
| ALK by FISH | Sensitivity to crizotinib[99] | Genomics | |
| ERCC1 by IHC | Resistance to platinum-based chemotherapeutics[100] | Pathology/Proteomics | |
| EGFR Amplication by FISH | Resistance to gefitinib, erlotinib, cetuximab plus paclitaxel, and carboplatin[101] | Genomics | |
| EGFR by IHC | Response to cetuximab plus chemotherapy[102] | Pathology/Proteomics | |
| TS by RT-PCR | Resistance to pemetrexed[103] | Transcriptomics | |
| UGT1A1 Molecular Assay | Irinotecan toxicity[104] | Genomics | |
| ALK by FISH | Response to crizotinib in metastatic disease[105] | Genomics | |
| Gastric Cancer | HER2 by FISH | Response to trastuzumab[11] | Genomics |
| HER2 by IHC | Response to trastuzumab[106,107] | Pathology/Proteomics | |
| ERCC1 by IHC | Resistance to platinum-based chemotherapies[108] | Pathology/Proteomics | |
| Melanoma | BRAF Mutation Analysis | Response to vemurafenib[16] | Genomics |
| Brain Cancer | MGMT methylation | Response to temozolomide[109] | Epigenomics |
| Head and Neck Cancers | DPD status | Fluorouracil toxicity and efficacy[110] | Metabolomics |
| CLL | 17p by FISH | Resistance to fludarabine based regimens | Genomics |
| P53 Mutation analysis | Resistance to fludarabine based regimens[111] | Genomics | |
| CML | BCR-ABL | Recommended imatinib[112] | Genomics |
| BCR-ABL KD Mutation V299L, T315A, F17L/V/I/C | Response to nilotinib rather than dasatinib[41] | Genomics | |
| BCR-ABL KD Mutation Y253H, E255K/V, F359V/C/I | Response to dasatinib rather than nilotinib[41] | Genomics | |
| BCR-ABL transcript mass by RQ-PCR | Response tyrosine kinase inhibitors after therapy ihas been intiated[113] | Transcriptomics | |
| Myelodysplastic Syndrome | Deletion 5q | Response to lenalidomide[114] | Genomics |
| Platelet derived growth factor receptor beta | Indication for imatinib[115,116] | Genomics | |
| Non-Hodgkin’s Lymphoma | MYC translocations | Resistance to retuximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) in diffuse B-cell lymphoma[117] | Genomics |
HER2: Human epidermal growth receptor 2
FISH: Fluorescence in situ hybridization
IHC: Immunohistochemstry
ER/PR: Estrogen receptor/progesterone receptor
DPD: Dihydropyrimidine Dehydrogenase
PIK3CA: Phosphoinositide-3-kinase, catalytic alpha
EGFR: Epidermal growth factor receptor
TS: thymidylate synthase
ERCC1: Excision repair cross-complementing 1 protein
UGT1A1: Uridine diphosphate glucuronosyltransferase 1A1 gene
ALK: Anaplastic lymphoma receptor tyrosine kinase
MGMT: methylguanine-methyltransferase promoter