Table 1.
Author | Year | Genes | Methodology | Conclusions |
---|---|---|---|---|
Reduced concentration of antineoplastic drugs in cancerous cells. | ||||
Friedrich | 2004 | MDR1, MRP1 and BCRP | Gene expression in primary SCC using IH and PCR. | MDR1 and MRP1 are co-expressed; MDR1 and BCRP are not co-dependent. Patient survival can be influenced by the altered expression of at least one of the genes implicated in chemotherapeutic resistance. |
Nakamura | 2005 | MDR1, MRP1 | Expression levels in CDDP-resistant/sensitive cell lines using in-house cDNA microarray (2021 genes originated from normal oral tissue, primary oral cancer, and oral cancer cell lines) and PCR. | Resistant cells have high MDR1 and low MRP1 expression. |
Suzuki | 2010 | MDR1, MRP1 and MRP2 | Gene expression analysis of single cell clones dissociated from primary tumors using PCR. | MDR1 was not expressed in any single cell clone from primary SCC tumor, although MRP1 and MRP2 were expressed. |
Genes involved in DNA repair | ||||
Quintela | 2006 | XPD, ERCC1 and XRCC1 | SNP detected using RFLP in DNA from peripheral lymphocytes of HNSCC patients. | The accumulation of polymorphic variants increases the probability of achieving a complete response. |
Ameri | 2016 | ERCC1 | Expression status determined using PCR in tumor samples. | Tumor samples with high ERCC1 expression showed no response to induction chemotherapy. |
Enhanced tumor survival and routes of dissemination | ||||
Cabelguenne | 2000 | TP53 | Gene status (mutations, allele loss) detected using PCR amplification in tumor samples. | P53 status may be a useful indicator of responding to neoadjuvant chemotherapy in HNSCC. |
Blons | 2004 | MMP3 | MMP1, MMP3, and MMP7 polymorphisms detected using PCR in tumor samples and blood. | A significant correlation between MMP3 polymorphism and response to chemotherapy. |
Nakamura | 2005 | CD55 | Expression levels in CDDP-resistant/sensitive cell lines using in-house cDNA microarray (2021 genes originated from normal oral tissue, primary oral cancer, and oral cancer cell lines) and PCR. | CD55 was overexpressed in the H-1R colony. |
Inactivation of antineoplastic drugs | ||||
Ansell | 2016 | AR, EPR and EGF | Response was evaluated by adding recombinant human proteins or siRNA-mediated downregulation of endogenous ligand production. | The amount of EGF strongly influences the tumor cell proliferation rate and response to cetuximab treatment. Proposed EGF as a potential predictive biomarker |
Pickhard | 2014 | AurkA and AurkB | IH in tissue samples. | Provide evidence that AurkA genotypically homozygous HNSCC cells respond to cetuximab monotreatment, whereas heterozygous cells do not. |
MDR1: Multidrug resistance 1; MRP1: Multidrug resistance protein 1; BCRP: Breast cancer related protein; CDDP: Cisplatin and platinol; SCC: Squamous cell carcinoma; IH: Immunohistochemistry; PCR: Polymerase chain reaction; XPD: Xeroderma pigmentosum protein; ERCC1: Excision repair cross-complementing group 1; XRCC1: X-ray repair cross-complementing protein 1; SNP: Single nucleotide polymorphism; RFLP: Restriction fragment length polymorphism; HNSCC: Head and neck squamous cell carcinoma; MMP 1, 2 and 7: Matrix metalloproteinase 1, 2 and 7; H-1R: CDDP-resistant cell line.