BACKGROUND Although common in lung cancer,somatic epidermal growth factor receptor(EGFR)mutations are rarely found in colorectal cancer,occurring in approximately 3%of cases.Treatment with anti-EGFR antibodies is comm...BACKGROUND Although common in lung cancer,somatic epidermal growth factor receptor(EGFR)mutations are rarely found in colorectal cancer,occurring in approximately 3%of cases.Treatment with anti-EGFR antibodies is commonplace,but EGFR tyrosine kinase inhibitors are not standard treatments in colorectal cancer.Here we report a case of sustained response to osimertinib in a colorectal cancer patient with an EGFR T790M mutation on cell-free DNA analysis.CASE SUMMARY A 72-year old woman with a past medical history of post-polio syndrome confined to a wheelchair,scoliosis and hypothyroidism presented with metastatic sigmoid colon adenocarcinoma with hepatic metastases.Next generation sequencing revealed a RAS/RAF wild-type,microsatellite stable,PD-L1 negative malignancy.Mutations in TP3 and APC were also identified,as well as EGFR amplification.Cell-free DNA analysis revealed an EGFR T790M mutation.She was unable to tolerate first-line treatment with panitumumab,5-fluorouracil and leucovorin,progressed on second-line treatment with trifluridine/tipiracil plus bevacizumab,and was unable to tolerate third-line treatment with regorafenib.She was started on fourth-line treatment with off-label osimertinib,with clinical response–decrease in size of hepatic metastases and a pericardial effusion.She remained on treatment with osimertinib for seven months.CONCLUSION This case shows the benefit of multi-gene sequencing assays to identify potential therapeutic options in patients with refractory disease.展开更多
BACKGROUND Lung squamous cell cancer(LSCC)rarely harbors epidermal growth factor receptor(EGFR)mutations,even much rarer for acquired T790M mutation.Although clinical trials of AURA series illustrated that non-small c...BACKGROUND Lung squamous cell cancer(LSCC)rarely harbors epidermal growth factor receptor(EGFR)mutations,even much rarer for acquired T790M mutation.Although clinical trials of AURA series illustrated that non-small cell lung cancer(NSCLC)with EGFR T790M mutation can benefit from osimertinib,only five LSCC patients were enrolled in total;moreover,the efficacy for LSCC was not shown in the results.Therefore,the response of LSCC to osimertinib is still unclear to date.CASE SUMMARY We report an LSCC case with T790M-related acquired resistance after treatments with first-generation EGFR-tyrosine kinase inhibitors(EGFR-TKIs)and benefited from osimertinib significantly.A 63-year-old Chinese man was diagnosed with stage IV(cT2N2M1b)LSCC harboring an EGFR exon 19-deletion mutation.Following disease progression after gefitinib and multi-line chemotherapy,rebiopsy was conducted.Molecular testing of EGFR by amplification refractory mutation system-polymerase chain reaction detected the exon 19-deletion without T790M mutation.Therefore,the patient was given erlotinib,but progression developed only 3 mo later.Then the frozen re-biopsy tissue was tested by next-generation sequencing(NGS),which detected an EGFR T790M mutation.However,he was very weak with symptoms of dysphagia and cachexia.Fortunately,osimertinib was started,leading to alleviation from the symptoms.Four months later,normal deglutition was restored and partial response was achieved.Finally,the patient achieved an overall survival time period of 29 mo.CONCLUSION Our findings highlight that EGFR T790M mutation may also be an important acquired drug resistance mechanism for LSCC and offer direct evidence of the efficacy of osimertinib in LSCC with T790M mutation.NGS and better preservation conditions may contribute to higher sensitivity of EGFR T790M detection.展开更多
BACKGROUND Patients diagnosed with non-small-cell lung cancer with activated epidermal growth factor receptor mutations are more likely to develop leptomeningeal(LM)metastasis than other types of lung cancers and have...BACKGROUND Patients diagnosed with non-small-cell lung cancer with activated epidermal growth factor receptor mutations are more likely to develop leptomeningeal(LM)metastasis than other types of lung cancers and have a poor prognosis.Early diagnosis and effective treatment of leptomeningeal carcinoma can improve the prognosis.CASE SUMMARY A 55-year-old female with a progressive headache and vomiting for one month was admitted to Peking University First Hospital.She was diagnosed with lung adenocarcinoma with osseous metastasis 10 months prior to admittance.epidermal growth factor receptor(EGFR)mutation was detected by genomic examination,so she was first treated with gefitinib for 10 months before acquiring resistance.Cell-free cerebrospinal fluid(CSF)circulating tumor DNA detection by next-generation sequencing was conducted and indicated the EGFR-Thr790Met mutation,while biopsy and cytology from the patient’s CSF and the first enhanced cranial magnetic resonance imaging(MRI)showed no positive findings.A month later,the enhanced MRI showed linear leptomeningeal enhancement,and the cytology and biochemical examination in CSF remained negative.Therefore,osimertinib(80 mg/d)was initiated as a second-line treatment,resulting in a good response within a month.CONCLUSION This report suggests clinical benefit of osimertinib in LM patients with positive detection of the EGFR-Thr790Met mutation in CSF and proposes that the positive findings of CSF circulating tumor DNA as a liquid biopsy technology based on the detection of cancer-associated gene mutations may appear earlier than the imaging and CSF findings and may thus be helpful for therapy.Moreover,the routine screening of chest CT with the novel coronavirus may provide unexpected benefits。展开更多
BACKGROUND Osimertinib is the recommended first-line treatment for adult patients with epidermal growth factor receptor(EGFR)mutation positive advanced or metastatic non-small cell lung cancer(NSCLC).However,primary o...BACKGROUND Osimertinib is the recommended first-line treatment for adult patients with epidermal growth factor receptor(EGFR)mutation positive advanced or metastatic non-small cell lung cancer(NSCLC).However,primary or acquired resistance to EGFR-tyrosine kinase inhibitors(EGFR-TKIs)seems inevitable,and when drug-resistance occurs during treatment with osimertinib,the standard of care is to discontinue the TKI.CASE SUMMARY A 57-year-old female patient with lung adenocarcinoma presented with an irritating cough accompanied by chest distress of one month duration.An enhanced head magnetic resonance imaging scan showed brain metastases.An EGFR mutation(exon 21 L858R)was detected in pleural fluid.The patient was treated with oral osimertinib(80 mg once daily)from January 2018 but developed progressive disease on December 2018.She was then successfully treated with rechallenge and tri-challenge with osimertinib(80 mg once daily)by resensitization chemotherapy twice after the occurrence of drug-resistance to osimertinib,and to date has survived for 31 mo.CONCLUSION This case may provide some selective therapeutic options for NSCLC patients with acquired drug-resistance who were previously controlled on osimertinib treatment.展开更多
BACKGROUND Epidermal growth factor receptor(EGFR)tyrosine kinase inhibitors(TKIs)have been adopted as the standard of care for non-small cell lung cancer(NSCLC)patients harboring EGFR sensitizing mutations.Besides the...BACKGROUND Epidermal growth factor receptor(EGFR)tyrosine kinase inhibitors(TKIs)have been adopted as the standard of care for non-small cell lung cancer(NSCLC)patients harboring EGFR sensitizing mutations.Besides the two common mutations exon 19 deletion and L858R,which together comprise approximately 85%of EGFR mutations in NSCLC,rare EGFR mutations also exist,including point mutations,deletions,and insertions spanning EGFR exons 18-25.However,the responsiveness of uncommon EGFR mutations to EGFR TKIs remains elusive and attracts increasing interest.CASE SUMMARY Herein,we report a 55-year-old male patient with stage IV NSCLC harboring a rare EGFR L833F-L861Q compound mutation in cis.The patient achieved a partial response to first-line treatment with afatinib and a progression-free survival of 10 mo.After afatinib failure,the patient received multiple line treatments with chemotherapy.Upon disease progression,the heavily pretreated patient was treated with osimertinib and bevacizumab,and both lung lesion and brain metastases were stable for more than 3 mo.He had an overall survival of 25 mo.CONCLUSION Our case revealed that both afatinib and the osimertinib+bevacizumab combination demonstrated clinical efficacy in NSCLC harboring an EGFR L833FL861Q compound mutation.The results provide more therapeutic options for patients with rare compound mutations.展开更多
<span style="font-family:Verdana;">The present work encompasses identification and characterization of major degradation product (DP) of OSM observed in base hydrolytic stress study. The separation of ...<span style="font-family:Verdana;">The present work encompasses identification and characterization of major degradation product (DP) of OSM observed in base hydrolytic stress study. The separation of DP was carried out on a non-polar stationary phase by using high-performance liquid chromatography system (HPLC). Using waters X-bridge (250 mm × 4.6 mm, 5 μm) C18 column with gradient elution program. For the characterization study, stress samples were subjected to HPLC and UPLC-QTOF-MS/MS and based on mass fragmentation pattern</span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">,</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> plausible structure was deduced. Further</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">,</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> the DP was isolated using semi-prepara</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">- </span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">tive liquid chromatography and concentrated the fractions using lyophiliza</span><span style="font-family:Verdana;">tion. The isolated DP was subjected to extensive 1D (1H, 13C, and</span><span style="font-family:Verdana;"> DEPT-135) and 2D (COSY, HSQC and HMBC) nuclear magnetic resonance (NMR) studies to authenticate the structure. The impurity was unambiguously named as N-(2-((2-(dimethylamino)ethyl)(methyl)amino)-4-metho</span></span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">-</span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">xy-5-((4-(1-methyl-1H-indol-3-yl)pyrimidin-2-yl)amino)phenyl)-3-methoxy</span><span style="font-family:Verdana;">propanamide.</span></span></span></span><span><span><span style="font-family:;" "=""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">Add</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">- </span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">itionally, the </span><i><span style="font-family:Verdana;">In-Silico</span></i><span style="font-family:Verdana;"> structure activity relation (QSAR) assessed through sta</span></span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">tistical based software’s DEREK Nexus</span><sup><span style="font-family:Verdana;">TM</span></sup><span style="font-family:Verdana;">, and MultiCASE, Case Ultra</span><sup><span style="font-family:Verdana;">TM</span></sup></span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> widely accepted and respected software’s for DP and OSM</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">.</span></span></span>展开更多
The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib (OSI) has been approved as the first-line treatment for EGFR-mutant non-small cell lung cancer (NSCLC). This study aims to explore a r...The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib (OSI) has been approved as the first-line treatment for EGFR-mutant non-small cell lung cancer (NSCLC). This study aims to explore a rational combination strategy for enhancing the OSI efficacy. In this study, OSI induced higher CD47 expression, an important anti-phagocytic immune checkpoint, via the NF-κB pathway in EGFR-mutant NSCLC HCC827 and NCI-H1975 cells. The combination treatment of OSI and the anti-CD47 antibody exhibited dramatically increasing phagocytosis in HCC827 and NCI-H1975 cells, which highly relied on the antibody-dependent cellular phagocytosis effect. Consistently, the enhanced phagocytosis index from combination treatment was reversed in CD47 knockout HCC827 cells. Meanwhile, combining the anti-CD47 antibody significantly augmented the anticancer effect of OSI in HCC827 xenograft mice model. Notably, OSI induced the surface exposure of “eat me” signal calreticulin and reduced the expression of immune-inhibitory receptor PD-L1 in cancer cells, which might contribute to the increased phagocytosis on cancer cells pretreated with OSI. In summary, these findings suggest the multidimensional regulation by OSI and encourage the further exploration of combining anti-CD47 antibody with OSI as a new strategy to enhance the anticancer efficacy in EGFR-mutant NSCLC with CD47 activation induced by OSI.展开更多
1文献来源Planchard D,Jänne PA,Cheng Y,et al.Osimertinib with or without chemotherapy in EGFR⁃mutated advanced NSCLC[J].N Engl J Med,2023,389(21):1935-1948.2证据水平1b。
文摘BACKGROUND Although common in lung cancer,somatic epidermal growth factor receptor(EGFR)mutations are rarely found in colorectal cancer,occurring in approximately 3%of cases.Treatment with anti-EGFR antibodies is commonplace,but EGFR tyrosine kinase inhibitors are not standard treatments in colorectal cancer.Here we report a case of sustained response to osimertinib in a colorectal cancer patient with an EGFR T790M mutation on cell-free DNA analysis.CASE SUMMARY A 72-year old woman with a past medical history of post-polio syndrome confined to a wheelchair,scoliosis and hypothyroidism presented with metastatic sigmoid colon adenocarcinoma with hepatic metastases.Next generation sequencing revealed a RAS/RAF wild-type,microsatellite stable,PD-L1 negative malignancy.Mutations in TP3 and APC were also identified,as well as EGFR amplification.Cell-free DNA analysis revealed an EGFR T790M mutation.She was unable to tolerate first-line treatment with panitumumab,5-fluorouracil and leucovorin,progressed on second-line treatment with trifluridine/tipiracil plus bevacizumab,and was unable to tolerate third-line treatment with regorafenib.She was started on fourth-line treatment with off-label osimertinib,with clinical response–decrease in size of hepatic metastases and a pericardial effusion.She remained on treatment with osimertinib for seven months.CONCLUSION This case shows the benefit of multi-gene sequencing assays to identify potential therapeutic options in patients with refractory disease.
基金Supported by the National Natural Science Foundation of China,No.81402561
文摘BACKGROUND Lung squamous cell cancer(LSCC)rarely harbors epidermal growth factor receptor(EGFR)mutations,even much rarer for acquired T790M mutation.Although clinical trials of AURA series illustrated that non-small cell lung cancer(NSCLC)with EGFR T790M mutation can benefit from osimertinib,only five LSCC patients were enrolled in total;moreover,the efficacy for LSCC was not shown in the results.Therefore,the response of LSCC to osimertinib is still unclear to date.CASE SUMMARY We report an LSCC case with T790M-related acquired resistance after treatments with first-generation EGFR-tyrosine kinase inhibitors(EGFR-TKIs)and benefited from osimertinib significantly.A 63-year-old Chinese man was diagnosed with stage IV(cT2N2M1b)LSCC harboring an EGFR exon 19-deletion mutation.Following disease progression after gefitinib and multi-line chemotherapy,rebiopsy was conducted.Molecular testing of EGFR by amplification refractory mutation system-polymerase chain reaction detected the exon 19-deletion without T790M mutation.Therefore,the patient was given erlotinib,but progression developed only 3 mo later.Then the frozen re-biopsy tissue was tested by next-generation sequencing(NGS),which detected an EGFR T790M mutation.However,he was very weak with symptoms of dysphagia and cachexia.Fortunately,osimertinib was started,leading to alleviation from the symptoms.Four months later,normal deglutition was restored and partial response was achieved.Finally,the patient achieved an overall survival time period of 29 mo.CONCLUSION Our findings highlight that EGFR T790M mutation may also be an important acquired drug resistance mechanism for LSCC and offer direct evidence of the efficacy of osimertinib in LSCC with T790M mutation.NGS and better preservation conditions may contribute to higher sensitivity of EGFR T790M detection.
文摘BACKGROUND Patients diagnosed with non-small-cell lung cancer with activated epidermal growth factor receptor mutations are more likely to develop leptomeningeal(LM)metastasis than other types of lung cancers and have a poor prognosis.Early diagnosis and effective treatment of leptomeningeal carcinoma can improve the prognosis.CASE SUMMARY A 55-year-old female with a progressive headache and vomiting for one month was admitted to Peking University First Hospital.She was diagnosed with lung adenocarcinoma with osseous metastasis 10 months prior to admittance.epidermal growth factor receptor(EGFR)mutation was detected by genomic examination,so she was first treated with gefitinib for 10 months before acquiring resistance.Cell-free cerebrospinal fluid(CSF)circulating tumor DNA detection by next-generation sequencing was conducted and indicated the EGFR-Thr790Met mutation,while biopsy and cytology from the patient’s CSF and the first enhanced cranial magnetic resonance imaging(MRI)showed no positive findings.A month later,the enhanced MRI showed linear leptomeningeal enhancement,and the cytology and biochemical examination in CSF remained negative.Therefore,osimertinib(80 mg/d)was initiated as a second-line treatment,resulting in a good response within a month.CONCLUSION This report suggests clinical benefit of osimertinib in LM patients with positive detection of the EGFR-Thr790Met mutation in CSF and proposes that the positive findings of CSF circulating tumor DNA as a liquid biopsy technology based on the detection of cancer-associated gene mutations may appear earlier than the imaging and CSF findings and may thus be helpful for therapy.Moreover,the routine screening of chest CT with the novel coronavirus may provide unexpected benefits。
基金The Natural Science Foundation Project of Anhui Province,No.1808085MH267Key Research and Development Project of Anhui Province,No.202004a07020020.
文摘BACKGROUND Osimertinib is the recommended first-line treatment for adult patients with epidermal growth factor receptor(EGFR)mutation positive advanced or metastatic non-small cell lung cancer(NSCLC).However,primary or acquired resistance to EGFR-tyrosine kinase inhibitors(EGFR-TKIs)seems inevitable,and when drug-resistance occurs during treatment with osimertinib,the standard of care is to discontinue the TKI.CASE SUMMARY A 57-year-old female patient with lung adenocarcinoma presented with an irritating cough accompanied by chest distress of one month duration.An enhanced head magnetic resonance imaging scan showed brain metastases.An EGFR mutation(exon 21 L858R)was detected in pleural fluid.The patient was treated with oral osimertinib(80 mg once daily)from January 2018 but developed progressive disease on December 2018.She was then successfully treated with rechallenge and tri-challenge with osimertinib(80 mg once daily)by resensitization chemotherapy twice after the occurrence of drug-resistance to osimertinib,and to date has survived for 31 mo.CONCLUSION This case may provide some selective therapeutic options for NSCLC patients with acquired drug-resistance who were previously controlled on osimertinib treatment.
文摘BACKGROUND Epidermal growth factor receptor(EGFR)tyrosine kinase inhibitors(TKIs)have been adopted as the standard of care for non-small cell lung cancer(NSCLC)patients harboring EGFR sensitizing mutations.Besides the two common mutations exon 19 deletion and L858R,which together comprise approximately 85%of EGFR mutations in NSCLC,rare EGFR mutations also exist,including point mutations,deletions,and insertions spanning EGFR exons 18-25.However,the responsiveness of uncommon EGFR mutations to EGFR TKIs remains elusive and attracts increasing interest.CASE SUMMARY Herein,we report a 55-year-old male patient with stage IV NSCLC harboring a rare EGFR L833F-L861Q compound mutation in cis.The patient achieved a partial response to first-line treatment with afatinib and a progression-free survival of 10 mo.After afatinib failure,the patient received multiple line treatments with chemotherapy.Upon disease progression,the heavily pretreated patient was treated with osimertinib and bevacizumab,and both lung lesion and brain metastases were stable for more than 3 mo.He had an overall survival of 25 mo.CONCLUSION Our case revealed that both afatinib and the osimertinib+bevacizumab combination demonstrated clinical efficacy in NSCLC harboring an EGFR L833FL861Q compound mutation.The results provide more therapeutic options for patients with rare compound mutations.
文摘<span style="font-family:Verdana;">The present work encompasses identification and characterization of major degradation product (DP) of OSM observed in base hydrolytic stress study. The separation of DP was carried out on a non-polar stationary phase by using high-performance liquid chromatography system (HPLC). Using waters X-bridge (250 mm × 4.6 mm, 5 μm) C18 column with gradient elution program. For the characterization study, stress samples were subjected to HPLC and UPLC-QTOF-MS/MS and based on mass fragmentation pattern</span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">,</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> plausible structure was deduced. Further</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">,</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> the DP was isolated using semi-prepara</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">- </span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">tive liquid chromatography and concentrated the fractions using lyophiliza</span><span style="font-family:Verdana;">tion. The isolated DP was subjected to extensive 1D (1H, 13C, and</span><span style="font-family:Verdana;"> DEPT-135) and 2D (COSY, HSQC and HMBC) nuclear magnetic resonance (NMR) studies to authenticate the structure. The impurity was unambiguously named as N-(2-((2-(dimethylamino)ethyl)(methyl)amino)-4-metho</span></span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">-</span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">xy-5-((4-(1-methyl-1H-indol-3-yl)pyrimidin-2-yl)amino)phenyl)-3-methoxy</span><span style="font-family:Verdana;">propanamide.</span></span></span></span><span><span><span style="font-family:;" "=""> </span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">Add</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">- </span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">itionally, the </span><i><span style="font-family:Verdana;">In-Silico</span></i><span style="font-family:Verdana;"> structure activity relation (QSAR) assessed through sta</span></span></span></span><span><span><span style="font-family:;" "=""><span style="font-family:Verdana;">tistical based software’s DEREK Nexus</span><sup><span style="font-family:Verdana;">TM</span></sup><span style="font-family:Verdana;">, and MultiCASE, Case Ultra</span><sup><span style="font-family:Verdana;">TM</span></sup></span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;"> widely accepted and respected software’s for DP and OSM</span></span></span><span style="font-family:Verdana;"><span style="font-family:Verdana;"><span style="font-family:Verdana;">.</span></span></span>
基金the Science and Technology Development Fund,Macao SAR(File no.0129/2019/A3).
文摘The third-generation epidermal growth factor receptor (EGFR) inhibitor osimertinib (OSI) has been approved as the first-line treatment for EGFR-mutant non-small cell lung cancer (NSCLC). This study aims to explore a rational combination strategy for enhancing the OSI efficacy. In this study, OSI induced higher CD47 expression, an important anti-phagocytic immune checkpoint, via the NF-κB pathway in EGFR-mutant NSCLC HCC827 and NCI-H1975 cells. The combination treatment of OSI and the anti-CD47 antibody exhibited dramatically increasing phagocytosis in HCC827 and NCI-H1975 cells, which highly relied on the antibody-dependent cellular phagocytosis effect. Consistently, the enhanced phagocytosis index from combination treatment was reversed in CD47 knockout HCC827 cells. Meanwhile, combining the anti-CD47 antibody significantly augmented the anticancer effect of OSI in HCC827 xenograft mice model. Notably, OSI induced the surface exposure of “eat me” signal calreticulin and reduced the expression of immune-inhibitory receptor PD-L1 in cancer cells, which might contribute to the increased phagocytosis on cancer cells pretreated with OSI. In summary, these findings suggest the multidimensional regulation by OSI and encourage the further exploration of combining anti-CD47 antibody with OSI as a new strategy to enhance the anticancer efficacy in EGFR-mutant NSCLC with CD47 activation induced by OSI.
文摘1文献来源Planchard D,Jänne PA,Cheng Y,et al.Osimertinib with or without chemotherapy in EGFR⁃mutated advanced NSCLC[J].N Engl J Med,2023,389(21):1935-1948.2证据水平1b。