scholarly journals Case Report: Low-Dose Apatinib in the Treatment of Intrahepatic Biliary Cystadenoma With Recurrence and Malignant Transformation

2021 ◽  
Vol 11 ◽  
Author(s):  
Yongguang Yang ◽  
Weiheng Mai ◽  
Weifeng Chen ◽  
Chao Yang ◽  
Mingyi Li ◽  
...  
Keyword(s):  
Malignant Transformation ◽  
Kinase Inhibitor ◽  
Liver Volume ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Chinese Patient ◽  
Tumor Diameter ◽  
Biliary Cystadenoma ◽  
Biliary Cystadenocarcinoma ◽  
Liver And Kidney

Apatinib is a new oral tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2. It has been proven effective in treating multiple solid tumors. Herein, we report the case of a 67-year-old Chinese patient who was diagnosed with recurrent and malignant transformation of intrahepatic biliary cystadenoma. After multidisciplinary team discussion, the team considered that the remaining liver volume was insufficient for surgical resection. The patient refused chemotherapy and radiotherapy and was willing to take apatinib. Initially, the patient experienced severe tongue ulcers and difficulty eating. The dose of apatinib was then adjusted to 250 mg/day. To date, he has been taking apatinib for 48 months. Regular re-examination showed that the tumor had significantly decreased in size. On January 16, 2021, a CT scan revealed a tumor diameter of 4.5 cm. In our case, the patient achieved partial response and progression-free survival(PFS) of 48.0 months. During treatment, the patient’s appetite and mental state were expected. The treatment did not induce hypertension, fatigue, hand-foot syndrome, or liver and kidney damage. Apatinib may be an option for the treatment of advanced intrahepatic biliary cystadenocarcinoma. Its toxicity is controllable and tolerable. The exact curative effect still needs to be evaluated in more cases.

scholarly journals Cabozantinib As Salvage Therapy for Patients With Tyrosine Kinase Inhibitor–Refractory Differentiated Thyroid Cancer: Results of a Multicenter Phase II International Thyroid Oncology Group Trial

2017 ◽  
Vol 35 (29) ◽  
pp. 3315-3321 ◽  
Author(s):  
Maria E. Cabanillas ◽  
Jonas A. de Souza ◽  
Susan Geyer ◽  
Lori J. Wirth ◽  
Michael E. Menefee ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Targeted Therapy ◽  
Phase Ii ◽  
Differentiated Thyroid Cancer ◽  
Kinase Inhibitor ◽  
Objective Response ◽  
Evaluation Criteria ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Multikinase Inhibitor

Purpose Sorafenib and lenvatinib are oral multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and approved for radioiodine (RAI)-refractory differentiated thyroid cancer (DTC). However, there are no approved second- or third-line therapies. MET is implicated in resistance to VEGFR inhibitors. Cabozantinib is an oral multikinase inhibitor targeting MET in addition to VEGFR and is approved for medullary thyroid cancer. In a phase I study of cabozantinib, five of eight patients with DTC previously treated with a VEGFR-targeted therapy had an objective response to cabozantinib. Patients and Methods Patients with RAI-refractory disease with Response Evaluation Criteria in Solid Tumor (RECIST) measurable disease and evidence of progression on prior VEGFR-targeted therapy were enrolled in this single-arm phase II study. The cabozantinib starting dose was 60 mg/day orally but could be escalated to 80 mg if the patient did not experience a response. Patients underwent tumor assessment according to RECIST v1.1 every 8 weeks. In this study, if at least five of 25 response-evaluable patients had an objective response, cabozantinib would be considered a promising agent in this patient population. Results Twenty-five patients were enrolled. The median age was 64 years, and 64% of patients were men. Twenty-one patients had received only one prior VEGFR-targeted therapy (sorafenib, pazopanib, or cediranib), and four patients had received two such therapies. The most common treatment-related adverse events were fatigue, weight loss, diarrhea, palmar-plantar erythrodysesthesia, and hypertension. One drug-related death was noted. Of the 25 patients, 10 (40%) had a partial response, 13 (52%) had stable disease, and two (8%) had nonevaluable disease. The median progression-free survival and overall survival were 12.7 months and 34.7 months, respectively. Conclusion Cabozantinib demonstrated clinically significant, durable objective response activity in patients with RAI-refractory DTC who experienced disease progression while taking prior VEGFR-targeted therapy.

scholarly journals Early serum tumor marker levels after fourteen days of tyrosine kinase inhibitor targeted therapy predicts outcomes in patients with advanced lung adenocarcinoma

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0240736
Author(s):  
Hung-Jen Chen ◽  
Chih-Yen Tu ◽  
Kuo-Yang Huang ◽  
Chun-Ru Chien ◽  
Te-Chun Hsia
Keyword(s):  
Targeted Therapy ◽  
Lung Adenocarcinoma ◽  
Kinase Inhibitor ◽  
Characteristic Curve ◽  
Area Under The Curve ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Ca 125 ◽  
Mutation Status ◽  
Anaplastic Lymphoma

Objective Image evaluation strategy for lung cancer patients has difficulty obtaining the appropriate quantity of diffuse lung nodules and bone metastases. The study was to demonstrate whether early variations in the levels of serum 4-tumor markers (4-TMs)(carcinoembryonic antigen [CEA], cancer antigen [CA]125, CA19-9, and CA15-3) after TKI targeted therapy were associated with treatment response in patients with lung adenocarcinoma. Methods Patients with stage IIIB-IV lung adenocarcinoma taking epidermal growth factor receptor (EGFR) TKIs or anaplastic lymphoma kinase (ALK) inhibitors were enrolled prospectively from June 2012 to February 2015. According to the variations of the percentage of change in 4-TM levels (4-TMpc), we divided patients into ascending (increases in 4-TMpc over the 7th- 14th day) and descending (decreases in 4-TMpc over the 7th- 14th day) groups. Results 184 patients were enrolled, and 89% had at least one of the pre-treatment evaluable TMs and were further analyzed. An excellent response to the TKI targeted therapy was accurately predicted in the descending group, as determined using receiver operating characteristic curve analysis (an area under the curve, 0.83). Multivariate Cox hazards model analyses demonstrated that the type of 4-TMpc and mutation status were the strongest predictors of progression-free survival (PFS)(descending versus ascending, hazard ratios [HR] 0.30, 95% confidence interval [CI], 0.19–0.47; sensitive mutation versus wide type, HR 0.30, 95% CI, 0.19–0.48). Conclusions Type of 4-TMpc 14 days after TKI targeted therapy is associated with an image response and PFS, without regarding mutation status, in patients with advanced lung adenocarcinoma.

scholarly journals EGFR/ErbB2-Targeting Lapatinib Therapy for Aggressive Prolactinomas

2020 ◽  
Author(s):  
Odelia Cooper ◽  
Vivien S Bonert ◽  
Jeremy Rudnick ◽  
Barry D Pressman ◽  
Janet Lo ◽  
...  
Keyword(s):  
Dopamine Agonist ◽  
Tumor Response ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Multicenter Trial ◽  
Tumor Diameter ◽  
Her2 Expression ◽  
Agonist Therapy ◽  
End Point ◽  
Dopamine Agonist Therapy

Abstract Context Approximately 10% to 20% of prolactinomas are resistant to dopamine agonist therapy. The ErbB signaling pathway may drive aggressive prolactinoma behavior. Objective We evaluated lapatinib, an ErbB1-epidermal growth factor receptor (EGFR)/ErbB2 or human EGFR2 (HER2) tyrosine kinase inhibitor (TKI), in aggressive prolactinomas. Design A prospective, phase 2a multicenter trial was conducted. Setting This study took place at a tertiary referral pituitary center. Patients Study participants included adults with aggressive prolactinomas showing continued tumor growth despite maximally tolerated dopamine agonist therapy. Intervention Intervention included oral lapatinib 1250 mg/day for 6 months. Main Outcome Measures The primary end point was 40% reduction in any tumor dimension assessed by magnetic resonance imaging at study end; tumor response was assessed by Response Evaluation Criteria in Solid Tumors criteria. Secondary end points included prolactin (PRL) reduction, correlation of response with EGFR/HER2 expression, and safety. Results Owing to rigorous inclusion criteria, of 24 planned participants, only 7 consented and 4 were treated. None achieved the primary end point but 3 showed stable disease, including 2 with a 6% increase and 1 with a 16.8% decrease in tumor diameter. PRL response was not always concordant with tumor response, as 2 showed 28% and 59% increases in PRL. The fourth participant had a PRL-secreting carcinoma and withdrew after 3 months of lapatinib because of imaging and PRL progression. EGFR/HER2 expression did not correlate with treatment response. Lapatinib was well tolerated overall, with reversible grade 1 transaminitis in 2 patients, grade 2 rash in 2 patients, and grade 1 asymptomatic bradycardia in 2 patients. Conclusions An oral TKI such as lapatinib may be an effective option for a difficult-to-treat patient with an aggressive prolactinoma.

Activity of tivozanib (AV-951) in patients (Pts) with different histologic subtypes of renal cell carcinoma (RCC).

2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 327-327 ◽  
Author(s):  
P. Bhargava ◽  
B. Esteves ◽  
M. Al-Adhami ◽  
D. Nosov ◽  
O. N. Lipatov ◽  
...  
Keyword(s):  
Disease Control ◽  
Kinase Inhibitor ◽  
Clear Cell ◽  
Objective Response ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Histologic Subtype ◽  
Papillary Rcc ◽  
Vegfr Inhibitor ◽  
Histologic Subtypes

327 Background: This phase 2 randomized discontinuation trial evaluated tivozanib, a potent and selective vascular endothelial growth factor receptor (VEGFR)-1, -2, and -3 kinase inhibitor. Median progression-free survival (PFS) in all pts was 11.8 mo, and the objective response rate (ORR) was 27%. Methods: Pts received 1.5 mg/d tivozanib (3 wk on, 1 wk off = 1 cycle). A retrospective analysis evaluated efficacy and safety by histologic subtype. Response was evaluated by independent radiology review using standard RECIST criteria. Results: 272 pts were enrolled: 70% were male; median age was 56 y (range, 26–79). 226 (83%) pts had clear cell (CC) RCC; 46 had non–clear cell (NCC) RCC, including 11 with papillary RCC. Of pts with CC RCC, 176 (78%) had undergone nephrectomy; of pts with NCC RCC, 23 (50%) had undergone nephrectomy. Median treatment duration was 8.5 mo (range, 0.03– 23.8) as of the data cutoff. Median PFS was 12.5 mo (range, 9.9–17.7) for pts with CC RCC, not yet reached for pts with papillary RCC, and 5.4 mo (range, 3.7–12.0) for pts with other NCC subtypes. ORR and disease control rate (DCR; ORR + stable disease), respectively, were 29% and 85% for pts with CC RCC, 18% and 100% for pts with papillary RCC, and 17% and 74% for pts with other NCC subtypes. For pts with CC RCC, median PFS, ORR, and DCR, respectively, were 14.8 mo, 32%, and 88% for those who had undergone nephrectomy and 8.9 mo, 18%, and 76% for those who had not. Among pts with NCC RCC, median PFS was 6.6 mo for pts who had undergone nephrectomy and 7.2 mo for pts without nephrectomy; ORR was 17% for both NCC subgroups, with a DCR of 78% for pts who had undergone nephrectomy and 83% for pts who had not. Common drug- related adverse events (AEs) for pts with CC and NCC RCC, respectively, included hypertension (49% and 48%), dysphonia (22% and 22%), asthenia (12% and 13%), and diarrhea (13% and 9%). The most common grade ≥3 drug-related AE was hypertension (CC, 8%; NCC, 4%). Conclusions: Disease control was observed for pts with all RCC histologic subtypes. The rate of AEs was similar among patients with CC and NCC RCC and consistent with that of a selective VEGFR inhibitor with minimal off-target toxicities. Tivozanib is currently being tested in a phase 3 trial in pts with CC RCC. [Table: see text]

scholarly journals Pazopanib in the treatment of advanced renal cell carcinoma

2018 ◽  
pp. 90-94
Author(s):  
M. I. Volkova ◽  
A. S. Olshanskaya
Keyword(s):  
Clinical Trials ◽  
Growth Factor ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Good Tolerability ◽  
Free Survival ◽  
Advanced Renal Cancer ◽  
First Line Therapy ◽  
Stem Cell Growth Factor

Pazopanib is an oral multitargeted tyrozine kinase inhibitor that is used in advanced renal cancer in most countries of the world. Pazopanib inhibits tyrosine kinase receptors involved in tumor angiogenesis and proliferation, including VEGF, platelet-derived growth factor (PDGF) and stem cell growth factor receptor c-Kit, which leads to inhibiting angiogenesis, growth and proliferation of tumor cells. In clinical trials, pazopanib demonstrated improvement of progression-free survival (PFS) versus placebo in previously untreated patients and patients treated with cytokines, as well as the absence of worsening PFS versus sunitinib in the first-line therapy of clear cell RCC in the good- and intermediate prognosis groups. In addition, pazopanib demonstrated a better safety profile than sunitinib. The results of use of pazopanib in broad clinical practice are consistent with data from randomized trials that confirms the high efficacy combined with good tolerability of this drug even in patients who do not meet the generally accepted criteria for the inclusion in clinical trials.

scholarly journals Osimertinib Rechallenge With Bevacizumab vs. Chemotherapy Plus Bevacizumab in EGFR-Mutant NSCLC Patients With Osimertinib Resistance

2022 ◽  
Vol 12 ◽  
Author(s):  
Qingli Cui ◽  
Yanhui Hu ◽  
Qingan Cui ◽  
Daoyuan Wu ◽  
Yuefeng Mao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kinase Inhibitor ◽  
Treatment Options ◽  
Acquired Resistance ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Vegf Inhibitors ◽  
Clinical Benefits ◽  
Grade 3 ◽  
Egfr Mutant

At present, treatment options for osimertinib resistance are very limited. Dual inhibition of the vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) significantly improved the progression-free survival (PFS) of advanced EGFR-mutant non–small cell lung cancer (NSCLC). After EGFR-tyrosine kinase inhibitor (TKI) resistance, EGFR-TKI continuation combined with VEGF inhibitors still had clinical benefits. It is unclear whether the addition of bevacizumab after osimertinib progresses will prolong the duration of the osimertinib benefit. We screened 1289 patients with NSCLC and finally included 96 patients to evaluate osimertinib combined with bevacizumab (osi + bev) versus chemotherapy combined with bevacizumab (che + bev) for patients with acquired resistance to osimertinib. The overall response rate (ORR) for osi + bev and chem + bev was 15.8% (6 of 38) and 20.7% (12 of 58), respectively. The median PFS for osi + bev and che + bev was 7.0 and 4.9 months (HR 0.415 95%CI: 0.252–0.687 p = 0.001). The median OS for osi + bev and che + bev was 12.6 and 7.1 months (HR 0.430 95%CI: 0.266–0.696 p = 0.001). Multivariate analyses showed that no brain metastases and osi + bev treatment after osimertinib resistance correlated with longer PFS (p = 0.044, p = 0.001), while the median PFS of osimertinib less than 6 months (p = 0.021) had a detrimental effect on sequent treatment. Only osi + bev treatment was identified as an independent predictor of OS (p = 0.001). The most common adverse events (AEs) of grade ≥3 were hypertension (13.2%) and diarrhea (10.5%) in the osi + bevacizumab group. Neutropenia (24.1%) and thrombocytopenia (19%) were the most common grade ≥3 AEs in the che + bev group. The overall incidence of serious AEs (grade ≥3) was significantly higher in the chemotherapy plus bevacizumab group. Our study has shown the superiority of osi + bev compared to che + bev after the failure of osimertinib, making it a preferred option for patients with acquired resistance to osimertinib.

A phase II trial of gefitinib and pegylated interferon alfa 2b (PEG-IFN) in previously-treated renal cell carcinoma (RCC)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e16115-e16115
Author(s):  
D. W. Shek ◽  
J. Longmate ◽  
D. Quinn ◽  
K. Margolin ◽  
P. Twardowski ◽  
...  
Keyword(s):  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Performance Status ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Response Duration ◽  
Dose Schedule ◽  
Pegylated Interferon ◽  
Previously Treated ◽  
Ifn Treatment

e16115 Background: Modulation of the epidermal growth factor receptor (EGFR) pathway is relevant to IFN activity in RCC. Cell lines sensitive to IFN's antiproliferative effects downregulate EGFR, while IFN treatment of resistant cells precludes such an effect. (Eisenkraft et al, Cancer Res. 1991) Lack of EGFR down-regulation may thus be responsible in part for IFN resistance. To explore this hypothesis, we conducted a trial of the EGFR tyrosine kinase inhibitor gefitinib plus PEG-IFN in RCC patients (pts). Methods: Unresectable or metastatic RCC pts (no limit on prior therapies; performance status 0–2, and adequate end-organ function) were eligible. Prior IFN was allowed. Dose schedule: PEG-IFN SQ weekly (6μg/kg/week or 4 μg/kg/week) × 12 weeks and gefitinib 250 mg po daily until progression. A 6-month progression free survival (PFS) rate of 50% was considered promising (vs. 30%) in a two-stage design incorporating the Green-Dahlberg rule. We accrued 21 patients in the first-stage of accrual. Results: Pt characteristics: Males -16; median age - 56 years; Prior nephrectomy - 12. All had > 1 prior systemic therapy . Accrual slowed with increased use of small molecule kinase inhibitors, bevacizumab, and temsirolimus for RCC. At 6 months, PFS was 26% (95% CI: 9%, 49%); 20% (4 pts) had died. Best responses by RECIST: complete (1), partial (4), stable (8); progression (4). Response duration: CR (35+ months) and PR (3, 5, 5, 38+ months). Median time to treatment failure was 18.4 weeks (95%CI: 7.4, 24.9). Median PFS and overall survival were 23 and 53 weeks, respectively. Most common treatment-related toxicities were leucopenia, thrombocytopenia, rash, nausea, diarrhea, and hyperglycemia. Conclusions: Although gefitinib plus PEG-IFN did not meet the pre-specified 6-month PFS of 50%, it appears to have activity similar to other first-line therapies even in this previously-treated setting. (Supported by Astra Zeneca) [Table: see text]

Everolimus in metastatic renal cell carcinoma (mRCC): Subgroup analysis of patients (pts) with one versus two prior vascular endothelial growth factor receptor tyrosine kinase inhibitor (VEGFR-TKI) therapies enrolled in the phase III RECORD-1 study.

2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 304-304 ◽  
Author(s):  
R. A. Figlin ◽  
E. Calvo ◽  
R. J. Motzer ◽  
T. E. Hutson ◽  
S. Oudard ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Mammalian Target Of Rapamycin ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Best Supportive Care ◽  
Phase Iii ◽  
Double Blind ◽  
Risk Of Disease ◽  
Previously Treated ◽  
Endothelial Growth Factor

304 Background: The mammalian target of rapamycin (mTOR) inhibitor everolimus is the only medication to have shown efficacy in a randomized, controlled, phase III clinical trial (RECORD-1) in pts with mRCC after progression on VEGFR-TKIs. Everolimus more than doubled progression-free survival (PFS) vs. placebo (4.9 vs 1.9 months) and reduced the risk of disease progression by 67%. This analysis evaluated the effect of everolimus on survival in pts who had received 1 vs 2 prior VEGFR-TKIs. Methods: Pts with mRCC who progressed on sunitinib (SU) and/or sorafenib (SOR) were randomized (2:1) to receive everolimus 10 mg/day (n = 277) or placebo (n = 139) plus best supportive care in the double- blind, phase III RECORD-1 study (ClinicalTrials.gov: NCT00410124 ). Results: Before enrollment, the majority of pts received only 1 VEGFR- TKI (317 pts, 74%), with 317 pts receiving either SU or SOR (everolimus = 211; placebo = 106) and 99 pts receiving both SU and SOR (everolimus = 66; placebo = 33). Median PFS was 5.42 mo (95% confidence interval [CI]: 4.30, 5.82) in pts receiving everolimus who had received 1 prior VEGFR-TKI and 1.87 mo (95% CI: 1.84, 2.14) in those receiving placebo (hazard ratio [HR]: 0.31; 95% CI: 0.23, 0.42; p < .001). Median PFS was 3.78 mo (95% CI: 3.25, 5.13) for the everolimus group in pts who received 2 prior VEGFR-TKIs, versus 1.87 mo (95% CI: 1.77, 3.06) for the placebo group (HR: 0.37; 95% CI: 0.22, 0.63; p < 0.001). Conclusions: Pts in all stratified subgroups derived significant clinical benefit from everolimus treatment, including pts previously treated with either 1 or 2 VEGFR-TKIs. However, there was a trend toward a longer PFS in pts treated with 1 prior VEGFR-TKI compared with 2 VEGFR-TKIs. [Table: see text]

KRAS mutational status and sensitivity to a reversible epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) in EGFR wild type (WT) advanced non-small cell lung cancer (NSCLC) patients (pts).

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e18023-e18023
Author(s):  
Giulio Metro ◽  
Simona Duranti ◽  
Rita Chiari ◽  
Chiara Bennati ◽  
Carmen Molica ◽  
...  
Keyword(s):  
Advanced Nsclc ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Distinct Subgroup ◽  
Mutational Status ◽  
Significant Difference ◽  
Never Smokers ◽  
Line Setting ◽  
Egfr Tki

e18023 Background: Treatment with a reversible EGFR-TKI may benefit pts with EGFR WT advanced NSCLC, though to a much lesser extent than pts carrying an activating mutation in the EGFR gene. We assessed whether KRAS mutational status would help predict sensitivity to gefitinib or erlotinib in EGFR WT advanced NSCLC pts. Methods: Sixty-seven EGFR WT, advanced NSCLC pts treated with a reversible EGFR-TKI in any line setting were included. Pts were treated from May 2005 to March 2011 at the Medical Oncology of the Perugia Hospital. EGFR (exons 18 to 21) and KRAS (codons 12, 13 and 61) genes were amplified by nested PCR and sequenced in both sense and antisense directions. Results: Median age was 60 years (39-84); 52 pts (77.6%) were PS 0 or 1; 58 pts (86.6%) belonged to the non-squamous subtype and 22 pts (32.8%) were never-smokers. Eighteen pts (26.8%) were KRAS mutant (MUT), of which 14 pts at codon 12 (COD 12 MUT) and 4 pts at codon 13 (COD 13 MUT). Overall, 11 pts (16.4%) responded to treatment and 8 pts (11.9%) achieved stable disease, for a disease control rate of 28.3%. At a median follow-up of 25.2 months, median progression-free survival (PFS) and overall survival (OS) were 2.9 and 29.5 months, respectively. When analyzed according to KRAS status, a significantly shorter PFS was noted for the EGFR WT/KRAS MUT subgroup (N=18) compared with the EGFR WT/KRAS WT population (N=49) (1.6 vs. 3.0 months, respectively, p=0.04). However, no significant difference was observed between the two groups in terms of OS (18.0 vs. 34.8 months, respectively, p=0.42). Within the EGFR WT/KRAS MUT subrgoup a significantly longer PFS was reported for COD 12 MUT pts compared with COD 13 MUT pts (1.7 vs 0.7 months, respectively, p=0.04). Similarly, KRAS COD 12 MUT pts experienced a statistically significant superior OS compared with COD 13 MUT pts (36.2 vs 7.4 months, respectively, p=0.003). Conclusions: EGFR WT/KRAS MUT pts appear to be more resistant to treatment with a reversible EGFR-TKI, the greatest resistance occurring in COD 13 MUT pts. KRAS COD 12 MUT pts may represent a clinically distinct subgroup of KRAS mutants with a particularly favorable prognosis.

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