| Author (year) . | n . | Molecular studies . | Predictive value of molecular findings . | Association of molecular findings with dust exposure . |
|---|---|---|---|---|
| Pérez (1999) [8] | 31 | HRAS mutations: 16% (5/31) KRAS mut: <1% (1/31) NRAS: 0% (0/31) | HRAS mut: Shorter PFS and OS | No association found |
| Perrone (2003) [9], Frattini (2006) [10] | 20 | MLH1/MSH2 IHC negative: 5% (1/20) β‐cat exp: 40% (8/20) APC mut (exon 15): 28% (5/18) KRAS mut (exon 2): 50% (9/18) BRAF mut (exon 15): 0% (0/18) HRAS mut (exons 1, 2): 0% (0/18) TP53 mut (exons 5–8): 40% (8/20) P16ink4a methyl: 69% (11/16) P14 methyl: 67% (8/12) LOH 9p21: 33% (5/15) LOH 18q: 80% (8/10) LOH 17p13: 64% (9/14) | — | All but four cases associated with professional dust exposure
Association of TP53 and P16‐ARF alterations with dust exposure |
| Bornholdt (2008) [11] | 58 | KRAS mut (exon 2): 13% (7/58) | — | Possible association with KRAS mutations and wood dust exposure |
| Franchi (2009) [18] | 55 | EGFR IHC positive: 33% (18/55) Chr 7 polysomy: 39% (7/18) EGFR amplification: 2% (3/18) | No association with stage, DFS, OS | EGFR IHC positive more frequent in wood dust compared with leather dust |
| García‐Inclán (2012) [13] | 105 | EGFR CNG: 46% (39/85) EGFR IHC positive: 21% (19/92) EGFR mut (exons 19–21): 0% (0/46) KRAS mut (exon 2): 12% (7/58) BRAF mut (exon 15): 0% (0/57) | No association with histological subtype, stage. KRAS mutant cases associated with less aggressive clinical course | All KRAS mutant cases occurred in wood workers |
| Projetti (2013) [16] | 39 | EGFR amp: 8% (3/39) Chr 7 polysomy: 42% (15/39) EGFR IHC positive: 64% (24/39) EGFR mut: 3% (1/43) (exon 19) EGFRvIII: 0% (0/43) KRAS mut (exon 2): 6% (2/39) (codon 13) BRAF mut: 6% (2/39) | Worse OS with strong EGFRvI mRNA expression. | No association found |
| Franchi (2014) [14] | 18 | EGFR IHC positive: 33% (6/18) EGFR mut (exons 19, 21): 5.6% (1/18; exon 19: L858R) KRAS mut: 5.6% (1/18; exon 2 codon 12: pG12D) | — | The sole KRAS mut case occurred in a patient with exposure to leather dust |
| Licitra (2004) [6] | 30 | TP53 mut and P53 exp (IHC) in patients treated with PFL | Functional P53 associated with higher rate of pCR and DFS | — |
| Szablewski (2013) [17] | 43 | NRAS mut: 0% (0/43) BRAF mutations: 3.6% (1/43) EGFR exp: 63% (27/43) | KRAS mut associated with worse 5‐year OS | No association found |
| López‐Hernández (2017) [15] | 96 | KRAS: 13% (7/55) TP53: 34% (14/41) TP53 exp: 72% (63/88) β‐cat exp: 33% (27/81) EGFR exp: 21% (18/87) NFkBp65 exp: 38% (35/92) COX2 exp: 40% (34/87) CK20 exp: 77% (66/86) Ki67 exp: mean of 19% of TC among all cases CNA gains in ≥40% located at: 5p, 7p, 8q, 20q CNA losses in ≥40% located at: 5q, 8p, 17p, 18q High‐level amp: infrequent | Seven CNG associated with poor clinical outcome, more advanced disease stage, and solid ITAC subtype. Clustering analysis identified five subgroups of ITAC with distinct clinical outcomes | — |
| Riobello (2018) [37] | 126 | PDL1 > 5% TC: 17% (22/126) PDL1 > 50% TC: 5/22 PDL1 > 5% IC: 33% (41/126) | PDL1 expression in TC or IC showed no association with stage, OS, DSS. DFS significantly worse with PDL1 expression in TC. PDL1 expression in TC more frequent in solid‐type SNS‐ITAC. PDL1 expression in IC less frequent in mucinous subtype | PDL1 expression in TC less frequent with wood dust exposure |
| Author (year) . | n . | Molecular studies . | Predictive value of molecular findings . | Association of molecular findings with dust exposure . |
|---|---|---|---|---|
| Pérez (1999) [8] | 31 | HRAS mutations: 16% (5/31) KRAS mut: <1% (1/31) NRAS: 0% (0/31) | HRAS mut: Shorter PFS and OS | No association found |
| Perrone (2003) [9], Frattini (2006) [10] | 20 | MLH1/MSH2 IHC negative: 5% (1/20) β‐cat exp: 40% (8/20) APC mut (exon 15): 28% (5/18) KRAS mut (exon 2): 50% (9/18) BRAF mut (exon 15): 0% (0/18) HRAS mut (exons 1, 2): 0% (0/18) TP53 mut (exons 5–8): 40% (8/20) P16ink4a methyl: 69% (11/16) P14 methyl: 67% (8/12) LOH 9p21: 33% (5/15) LOH 18q: 80% (8/10) LOH 17p13: 64% (9/14) | — | All but four cases associated with professional dust exposure
Association of TP53 and P16‐ARF alterations with dust exposure |
| Bornholdt (2008) [11] | 58 | KRAS mut (exon 2): 13% (7/58) | — | Possible association with KRAS mutations and wood dust exposure |
| Franchi (2009) [18] | 55 | EGFR IHC positive: 33% (18/55) Chr 7 polysomy: 39% (7/18) EGFR amplification: 2% (3/18) | No association with stage, DFS, OS | EGFR IHC positive more frequent in wood dust compared with leather dust |
| García‐Inclán (2012) [13] | 105 | EGFR CNG: 46% (39/85) EGFR IHC positive: 21% (19/92) EGFR mut (exons 19–21): 0% (0/46) KRAS mut (exon 2): 12% (7/58) BRAF mut (exon 15): 0% (0/57) | No association with histological subtype, stage. KRAS mutant cases associated with less aggressive clinical course | All KRAS mutant cases occurred in wood workers |
| Projetti (2013) [16] | 39 | EGFR amp: 8% (3/39) Chr 7 polysomy: 42% (15/39) EGFR IHC positive: 64% (24/39) EGFR mut: 3% (1/43) (exon 19) EGFRvIII: 0% (0/43) KRAS mut (exon 2): 6% (2/39) (codon 13) BRAF mut: 6% (2/39) | Worse OS with strong EGFRvI mRNA expression. | No association found |
| Franchi (2014) [14] | 18 | EGFR IHC positive: 33% (6/18) EGFR mut (exons 19, 21): 5.6% (1/18; exon 19: L858R) KRAS mut: 5.6% (1/18; exon 2 codon 12: pG12D) | — | The sole KRAS mut case occurred in a patient with exposure to leather dust |
| Licitra (2004) [6] | 30 | TP53 mut and P53 exp (IHC) in patients treated with PFL | Functional P53 associated with higher rate of pCR and DFS | — |
| Szablewski (2013) [17] | 43 | NRAS mut: 0% (0/43) BRAF mutations: 3.6% (1/43) EGFR exp: 63% (27/43) | KRAS mut associated with worse 5‐year OS | No association found |
| López‐Hernández (2017) [15] | 96 | KRAS: 13% (7/55) TP53: 34% (14/41) TP53 exp: 72% (63/88) β‐cat exp: 33% (27/81) EGFR exp: 21% (18/87) NFkBp65 exp: 38% (35/92) COX2 exp: 40% (34/87) CK20 exp: 77% (66/86) Ki67 exp: mean of 19% of TC among all cases CNA gains in ≥40% located at: 5p, 7p, 8q, 20q CNA losses in ≥40% located at: 5q, 8p, 17p, 18q High‐level amp: infrequent | Seven CNG associated with poor clinical outcome, more advanced disease stage, and solid ITAC subtype. Clustering analysis identified five subgroups of ITAC with distinct clinical outcomes | — |
| Riobello (2018) [37] | 126 | PDL1 > 5% TC: 17% (22/126) PDL1 > 50% TC: 5/22 PDL1 > 5% IC: 33% (41/126) | PDL1 expression in TC or IC showed no association with stage, OS, DSS. DFS significantly worse with PDL1 expression in TC. PDL1 expression in TC more frequent in solid‐type SNS‐ITAC. PDL1 expression in IC less frequent in mucinous subtype | PDL1 expression in TC less frequent with wood dust exposure |
Abbreviations: —, data not available; Amp, amplification; β‐cat, beta‐catenin; CNA, copy number alterations; CNG, copy number gains; DFS, disease‐free survival; DSS, disease‐specific survival; EGFRvI, EGFR variant I; EGFRvIII, EGFR variant III; Exp, expression; IC, immune cells; IHC, immunohistochemistry; LOH, loss of heterozygosity; methyl, methylated; Mut, mutant; N, number of patients; pCR, pathologic complete response; PDL1, programmed death receptor ligand 1; PFL, cisplatin, 5‐fluorouracil, leucovorin; PFS, progression‐free survival; OS, overall survival; SNS‐ITAC, sinonasal intestinal type adenocarcinoma; TC, tumor cells.
| Author (year) . | n . | Molecular studies . | Predictive value of molecular findings . | Association of molecular findings with dust exposure . |
|---|---|---|---|---|
| Pérez (1999) [8] | 31 | HRAS mutations: 16% (5/31) KRAS mut: <1% (1/31) NRAS: 0% (0/31) | HRAS mut: Shorter PFS and OS | No association found |
| Perrone (2003) [9], Frattini (2006) [10] | 20 | MLH1/MSH2 IHC negative: 5% (1/20) β‐cat exp: 40% (8/20) APC mut (exon 15): 28% (5/18) KRAS mut (exon 2): 50% (9/18) BRAF mut (exon 15): 0% (0/18) HRAS mut (exons 1, 2): 0% (0/18) TP53 mut (exons 5–8): 40% (8/20) P16ink4a methyl: 69% (11/16) P14 methyl: 67% (8/12) LOH 9p21: 33% (5/15) LOH 18q: 80% (8/10) LOH 17p13: 64% (9/14) | — | All but four cases associated with professional dust exposure
Association of TP53 and P16‐ARF alterations with dust exposure |
| Bornholdt (2008) [11] | 58 | KRAS mut (exon 2): 13% (7/58) | — | Possible association with KRAS mutations and wood dust exposure |
| Franchi (2009) [18] | 55 | EGFR IHC positive: 33% (18/55) Chr 7 polysomy: 39% (7/18) EGFR amplification: 2% (3/18) | No association with stage, DFS, OS | EGFR IHC positive more frequent in wood dust compared with leather dust |
| García‐Inclán (2012) [13] | 105 | EGFR CNG: 46% (39/85) EGFR IHC positive: 21% (19/92) EGFR mut (exons 19–21): 0% (0/46) KRAS mut (exon 2): 12% (7/58) BRAF mut (exon 15): 0% (0/57) | No association with histological subtype, stage. KRAS mutant cases associated with less aggressive clinical course | All KRAS mutant cases occurred in wood workers |
| Projetti (2013) [16] | 39 | EGFR amp: 8% (3/39) Chr 7 polysomy: 42% (15/39) EGFR IHC positive: 64% (24/39) EGFR mut: 3% (1/43) (exon 19) EGFRvIII: 0% (0/43) KRAS mut (exon 2): 6% (2/39) (codon 13) BRAF mut: 6% (2/39) | Worse OS with strong EGFRvI mRNA expression. | No association found |
| Franchi (2014) [14] | 18 | EGFR IHC positive: 33% (6/18) EGFR mut (exons 19, 21): 5.6% (1/18; exon 19: L858R) KRAS mut: 5.6% (1/18; exon 2 codon 12: pG12D) | — | The sole KRAS mut case occurred in a patient with exposure to leather dust |
| Licitra (2004) [6] | 30 | TP53 mut and P53 exp (IHC) in patients treated with PFL | Functional P53 associated with higher rate of pCR and DFS | — |
| Szablewski (2013) [17] | 43 | NRAS mut: 0% (0/43) BRAF mutations: 3.6% (1/43) EGFR exp: 63% (27/43) | KRAS mut associated with worse 5‐year OS | No association found |
| López‐Hernández (2017) [15] | 96 | KRAS: 13% (7/55) TP53: 34% (14/41) TP53 exp: 72% (63/88) β‐cat exp: 33% (27/81) EGFR exp: 21% (18/87) NFkBp65 exp: 38% (35/92) COX2 exp: 40% (34/87) CK20 exp: 77% (66/86) Ki67 exp: mean of 19% of TC among all cases CNA gains in ≥40% located at: 5p, 7p, 8q, 20q CNA losses in ≥40% located at: 5q, 8p, 17p, 18q High‐level amp: infrequent | Seven CNG associated with poor clinical outcome, more advanced disease stage, and solid ITAC subtype. Clustering analysis identified five subgroups of ITAC with distinct clinical outcomes | — |
| Riobello (2018) [37] | 126 | PDL1 > 5% TC: 17% (22/126) PDL1 > 50% TC: 5/22 PDL1 > 5% IC: 33% (41/126) | PDL1 expression in TC or IC showed no association with stage, OS, DSS. DFS significantly worse with PDL1 expression in TC. PDL1 expression in TC more frequent in solid‐type SNS‐ITAC. PDL1 expression in IC less frequent in mucinous subtype | PDL1 expression in TC less frequent with wood dust exposure |
| Author (year) . | n . | Molecular studies . | Predictive value of molecular findings . | Association of molecular findings with dust exposure . |
|---|---|---|---|---|
| Pérez (1999) [8] | 31 | HRAS mutations: 16% (5/31) KRAS mut: <1% (1/31) NRAS: 0% (0/31) | HRAS mut: Shorter PFS and OS | No association found |
| Perrone (2003) [9], Frattini (2006) [10] | 20 | MLH1/MSH2 IHC negative: 5% (1/20) β‐cat exp: 40% (8/20) APC mut (exon 15): 28% (5/18) KRAS mut (exon 2): 50% (9/18) BRAF mut (exon 15): 0% (0/18) HRAS mut (exons 1, 2): 0% (0/18) TP53 mut (exons 5–8): 40% (8/20) P16ink4a methyl: 69% (11/16) P14 methyl: 67% (8/12) LOH 9p21: 33% (5/15) LOH 18q: 80% (8/10) LOH 17p13: 64% (9/14) | — | All but four cases associated with professional dust exposure
Association of TP53 and P16‐ARF alterations with dust exposure |
| Bornholdt (2008) [11] | 58 | KRAS mut (exon 2): 13% (7/58) | — | Possible association with KRAS mutations and wood dust exposure |
| Franchi (2009) [18] | 55 | EGFR IHC positive: 33% (18/55) Chr 7 polysomy: 39% (7/18) EGFR amplification: 2% (3/18) | No association with stage, DFS, OS | EGFR IHC positive more frequent in wood dust compared with leather dust |
| García‐Inclán (2012) [13] | 105 | EGFR CNG: 46% (39/85) EGFR IHC positive: 21% (19/92) EGFR mut (exons 19–21): 0% (0/46) KRAS mut (exon 2): 12% (7/58) BRAF mut (exon 15): 0% (0/57) | No association with histological subtype, stage. KRAS mutant cases associated with less aggressive clinical course | All KRAS mutant cases occurred in wood workers |
| Projetti (2013) [16] | 39 | EGFR amp: 8% (3/39) Chr 7 polysomy: 42% (15/39) EGFR IHC positive: 64% (24/39) EGFR mut: 3% (1/43) (exon 19) EGFRvIII: 0% (0/43) KRAS mut (exon 2): 6% (2/39) (codon 13) BRAF mut: 6% (2/39) | Worse OS with strong EGFRvI mRNA expression. | No association found |
| Franchi (2014) [14] | 18 | EGFR IHC positive: 33% (6/18) EGFR mut (exons 19, 21): 5.6% (1/18; exon 19: L858R) KRAS mut: 5.6% (1/18; exon 2 codon 12: pG12D) | — | The sole KRAS mut case occurred in a patient with exposure to leather dust |
| Licitra (2004) [6] | 30 | TP53 mut and P53 exp (IHC) in patients treated with PFL | Functional P53 associated with higher rate of pCR and DFS | — |
| Szablewski (2013) [17] | 43 | NRAS mut: 0% (0/43) BRAF mutations: 3.6% (1/43) EGFR exp: 63% (27/43) | KRAS mut associated with worse 5‐year OS | No association found |
| López‐Hernández (2017) [15] | 96 | KRAS: 13% (7/55) TP53: 34% (14/41) TP53 exp: 72% (63/88) β‐cat exp: 33% (27/81) EGFR exp: 21% (18/87) NFkBp65 exp: 38% (35/92) COX2 exp: 40% (34/87) CK20 exp: 77% (66/86) Ki67 exp: mean of 19% of TC among all cases CNA gains in ≥40% located at: 5p, 7p, 8q, 20q CNA losses in ≥40% located at: 5q, 8p, 17p, 18q High‐level amp: infrequent | Seven CNG associated with poor clinical outcome, more advanced disease stage, and solid ITAC subtype. Clustering analysis identified five subgroups of ITAC with distinct clinical outcomes | — |
| Riobello (2018) [37] | 126 | PDL1 > 5% TC: 17% (22/126) PDL1 > 50% TC: 5/22 PDL1 > 5% IC: 33% (41/126) | PDL1 expression in TC or IC showed no association with stage, OS, DSS. DFS significantly worse with PDL1 expression in TC. PDL1 expression in TC more frequent in solid‐type SNS‐ITAC. PDL1 expression in IC less frequent in mucinous subtype | PDL1 expression in TC less frequent with wood dust exposure |
Abbreviations: —, data not available; Amp, amplification; β‐cat, beta‐catenin; CNA, copy number alterations; CNG, copy number gains; DFS, disease‐free survival; DSS, disease‐specific survival; EGFRvI, EGFR variant I; EGFRvIII, EGFR variant III; Exp, expression; IC, immune cells; IHC, immunohistochemistry; LOH, loss of heterozygosity; methyl, methylated; Mut, mutant; N, number of patients; pCR, pathologic complete response; PDL1, programmed death receptor ligand 1; PFL, cisplatin, 5‐fluorouracil, leucovorin; PFS, progression‐free survival; OS, overall survival; SNS‐ITAC, sinonasal intestinal type adenocarcinoma; TC, tumor cells.
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