| . | Tumor Growtha . |
|---|---|
| . | Statistical significance and regression coefficienta . |
| Overall tumor growth (β, 95% CI) | 1.060 (1.038–1.083) |
| Effect modifiers (P-value for interaction) | |
| Gender | P = 0.437 |
| Male, n = 34 (β, 95% CI) | 1.071 (1.036–1.108) |
| Female, n = 46 (β, 95% CI) | 1.053 (0.975–1.138) |
| Age at lung NET diagnosis | P = 0.356 |
| Reference value for age = 0 | 1.096 (1.019–1.178) |
| Change per year (β, 95% CI) | 0.999 (0.997–1.001) |
| Smoking statusb | P = 0.199 |
| Never smoked, n = 39 (β, 95% CI) | 1.065 (0.985–1.152) |
| Former or current smoker, n = 19 (β, 95% CI) | 1.036 (0.999–1.074) |
| Genotype | P = 0.120 |
| Nonsense/frameshift exon 2,9,10 mutations n = 28 (β, 95% CI) | 1.036 (0.999–1.074) |
| Other mutations,c n = 50 (β, 95% CI) | 1.074 (0.990–1.164) |
| Genotype | P = 0.408 |
| JunD interacting domain mutations,d n = 25 (β, 95% CI) | 1.071 (1.033–1.109) |
| Other mutations,d n = 45 (β, 95% CI) | 1.050 (0.968–1.140) |
| Genotype | P = 0.106 |
| CHES1 interacting domain mutations,e n = 20 (β, 95% CI) | 1.031 (0.996–1.066) |
| Other mutations,e n = 50 (β, 95% CI) | 1.068 (0.988–1.156) |
| Genotype | P = 0.447 |
| Missense mutations,f n = 15 (β, 95% CI) | 1.054 (1.026–1.082) |
| Nonsense/frameshift mutations,f n = 40 (β, 95% CI) | 1.076 (0.992–1.167) |
| Baseline tumor size | P = 0.147 |
| Diameter < median, n = 55 (β, 95% CI) | 1.057 (1.033–1.081) |
| Diameter ≥ median, n = 59 (β, 95% CI) | 1.071 (1.028–1.116) |
| . | Tumor Growtha . |
|---|---|
| . | Statistical significance and regression coefficienta . |
| Overall tumor growth (β, 95% CI) | 1.060 (1.038–1.083) |
| Effect modifiers (P-value for interaction) | |
| Gender | P = 0.437 |
| Male, n = 34 (β, 95% CI) | 1.071 (1.036–1.108) |
| Female, n = 46 (β, 95% CI) | 1.053 (0.975–1.138) |
| Age at lung NET diagnosis | P = 0.356 |
| Reference value for age = 0 | 1.096 (1.019–1.178) |
| Change per year (β, 95% CI) | 0.999 (0.997–1.001) |
| Smoking statusb | P = 0.199 |
| Never smoked, n = 39 (β, 95% CI) | 1.065 (0.985–1.152) |
| Former or current smoker, n = 19 (β, 95% CI) | 1.036 (0.999–1.074) |
| Genotype | P = 0.120 |
| Nonsense/frameshift exon 2,9,10 mutations n = 28 (β, 95% CI) | 1.036 (0.999–1.074) |
| Other mutations,c n = 50 (β, 95% CI) | 1.074 (0.990–1.164) |
| Genotype | P = 0.408 |
| JunD interacting domain mutations,d n = 25 (β, 95% CI) | 1.071 (1.033–1.109) |
| Other mutations,d n = 45 (β, 95% CI) | 1.050 (0.968–1.140) |
| Genotype | P = 0.106 |
| CHES1 interacting domain mutations,e n = 20 (β, 95% CI) | 1.031 (0.996–1.066) |
| Other mutations,e n = 50 (β, 95% CI) | 1.068 (0.988–1.156) |
| Genotype | P = 0.447 |
| Missense mutations,f n = 15 (β, 95% CI) | 1.054 (1.026–1.082) |
| Nonsense/frameshift mutations,f n = 40 (β, 95% CI) | 1.076 (0.992–1.167) |
| Baseline tumor size | P = 0.147 |
| Diameter < median, n = 55 (β, 95% CI) | 1.057 (1.033–1.081) |
| Diameter ≥ median, n = 59 (β, 95% CI) | 1.071 (1.028–1.116) |
β stands for the regression coefficient from the linear mixed models analysis, denoting growth as change in tumor size (factor) per year. Statistical significance is shown in bold.
Abbreviation: CHES1, checkpoint kinase 1; CI, confidence interval; NET, neuroendocrine tumor.
aTumor growth was assessed using multilevel linear mixed models analysis, accounting for clustering of observations within lung tumors within patients. Logarithmic-transformed lung NET diameter was used as a dependent variable and follow-up time was used as main fixed effect. Potential determinants of tumor growth were treated as additional fixed (interacting) covariates.
bData on smoking status were available in 58/80 patients included in the growth analysis (72.5%).
cAll other mutations included. Patients without genetic analysis or with a CDKN1B mutation were treated as missings (n = 2).
dOnly patients with pathogenic germline nonsense, frameshift, missense mutations, and in-frame deletions included. JunD interacting domain: codons 1–40, 139–242, and 323–428.
eOnly patients with pathogenic germline nonsense, frameshift, missense mutations, and in-frame deletions included. CHES1 interacting domain: codons 428–610.
fOnly patients with pathogenic germline nonsense, frameshift, and missense mutations included.
| . | Tumor Growtha . |
|---|---|
| . | Statistical significance and regression coefficienta . |
| Overall tumor growth (β, 95% CI) | 1.060 (1.038–1.083) |
| Effect modifiers (P-value for interaction) | |
| Gender | P = 0.437 |
| Male, n = 34 (β, 95% CI) | 1.071 (1.036–1.108) |
| Female, n = 46 (β, 95% CI) | 1.053 (0.975–1.138) |
| Age at lung NET diagnosis | P = 0.356 |
| Reference value for age = 0 | 1.096 (1.019–1.178) |
| Change per year (β, 95% CI) | 0.999 (0.997–1.001) |
| Smoking statusb | P = 0.199 |
| Never smoked, n = 39 (β, 95% CI) | 1.065 (0.985–1.152) |
| Former or current smoker, n = 19 (β, 95% CI) | 1.036 (0.999–1.074) |
| Genotype | P = 0.120 |
| Nonsense/frameshift exon 2,9,10 mutations n = 28 (β, 95% CI) | 1.036 (0.999–1.074) |
| Other mutations,c n = 50 (β, 95% CI) | 1.074 (0.990–1.164) |
| Genotype | P = 0.408 |
| JunD interacting domain mutations,d n = 25 (β, 95% CI) | 1.071 (1.033–1.109) |
| Other mutations,d n = 45 (β, 95% CI) | 1.050 (0.968–1.140) |
| Genotype | P = 0.106 |
| CHES1 interacting domain mutations,e n = 20 (β, 95% CI) | 1.031 (0.996–1.066) |
| Other mutations,e n = 50 (β, 95% CI) | 1.068 (0.988–1.156) |
| Genotype | P = 0.447 |
| Missense mutations,f n = 15 (β, 95% CI) | 1.054 (1.026–1.082) |
| Nonsense/frameshift mutations,f n = 40 (β, 95% CI) | 1.076 (0.992–1.167) |
| Baseline tumor size | P = 0.147 |
| Diameter < median, n = 55 (β, 95% CI) | 1.057 (1.033–1.081) |
| Diameter ≥ median, n = 59 (β, 95% CI) | 1.071 (1.028–1.116) |
| . | Tumor Growtha . |
|---|---|
| . | Statistical significance and regression coefficienta . |
| Overall tumor growth (β, 95% CI) | 1.060 (1.038–1.083) |
| Effect modifiers (P-value for interaction) | |
| Gender | P = 0.437 |
| Male, n = 34 (β, 95% CI) | 1.071 (1.036–1.108) |
| Female, n = 46 (β, 95% CI) | 1.053 (0.975–1.138) |
| Age at lung NET diagnosis | P = 0.356 |
| Reference value for age = 0 | 1.096 (1.019–1.178) |
| Change per year (β, 95% CI) | 0.999 (0.997–1.001) |
| Smoking statusb | P = 0.199 |
| Never smoked, n = 39 (β, 95% CI) | 1.065 (0.985–1.152) |
| Former or current smoker, n = 19 (β, 95% CI) | 1.036 (0.999–1.074) |
| Genotype | P = 0.120 |
| Nonsense/frameshift exon 2,9,10 mutations n = 28 (β, 95% CI) | 1.036 (0.999–1.074) |
| Other mutations,c n = 50 (β, 95% CI) | 1.074 (0.990–1.164) |
| Genotype | P = 0.408 |
| JunD interacting domain mutations,d n = 25 (β, 95% CI) | 1.071 (1.033–1.109) |
| Other mutations,d n = 45 (β, 95% CI) | 1.050 (0.968–1.140) |
| Genotype | P = 0.106 |
| CHES1 interacting domain mutations,e n = 20 (β, 95% CI) | 1.031 (0.996–1.066) |
| Other mutations,e n = 50 (β, 95% CI) | 1.068 (0.988–1.156) |
| Genotype | P = 0.447 |
| Missense mutations,f n = 15 (β, 95% CI) | 1.054 (1.026–1.082) |
| Nonsense/frameshift mutations,f n = 40 (β, 95% CI) | 1.076 (0.992–1.167) |
| Baseline tumor size | P = 0.147 |
| Diameter < median, n = 55 (β, 95% CI) | 1.057 (1.033–1.081) |
| Diameter ≥ median, n = 59 (β, 95% CI) | 1.071 (1.028–1.116) |
β stands for the regression coefficient from the linear mixed models analysis, denoting growth as change in tumor size (factor) per year. Statistical significance is shown in bold.
Abbreviation: CHES1, checkpoint kinase 1; CI, confidence interval; NET, neuroendocrine tumor.
aTumor growth was assessed using multilevel linear mixed models analysis, accounting for clustering of observations within lung tumors within patients. Logarithmic-transformed lung NET diameter was used as a dependent variable and follow-up time was used as main fixed effect. Potential determinants of tumor growth were treated as additional fixed (interacting) covariates.
bData on smoking status were available in 58/80 patients included in the growth analysis (72.5%).
cAll other mutations included. Patients without genetic analysis or with a CDKN1B mutation were treated as missings (n = 2).
dOnly patients with pathogenic germline nonsense, frameshift, missense mutations, and in-frame deletions included. JunD interacting domain: codons 1–40, 139–242, and 323–428.
eOnly patients with pathogenic germline nonsense, frameshift, missense mutations, and in-frame deletions included. CHES1 interacting domain: codons 428–610.
fOnly patients with pathogenic germline nonsense, frameshift, and missense mutations included.
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