Response to crizotinib in a squamous cell lung carcinoma patient harbouring echinoderm microtubule‐associated protein‐like 4‐anaplastic lymphoma translocation: <scp>A</scp> case report

Wang, Wenxian; Song, Zhengbo; Zhang, Yiping

doi:10.1111/1759-7714.12298

Cited by 14 publications

(8 citation statements)

References 13 publications

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“…Three patients 12,19,20 diagnosed with stage III SCC underwent radiation therapy. After regular check‐ups, one patient was confirmed to have recurrent disease, and underwent treatment with crizotinib.…”

Section: Resultsmentioning

confidence: 99%

ALK‐rearranged squamous cell carcinoma of the lung

et al. 2021

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Background ALK rearrangement is a very rare subset of squamous cell carcinoma (SCC) and one of the clinical features in patients is lack of data. Here, we report eight patients diagnosed with SCC of the lung harboring ALK rearrangement. Methods We collected primary NSCLC samples at the Beijing Chest Hospital between January 2012 and December 2018 for Ventana (D5F3) immunohistochemical detection. Among the 148 patients was diagnosed ALK‐rearranged non small cell lung cancer (NSCLC), only eight cases was SCC. We collected patients information from electronic patent records (EPRs). Results The eight cases of SCC were diagnosed by immunohistochemistry (IHC). Two were given crizotinib as second‐line therapy. One patient had stable disease (SD) and progression‐free survival (PFS) of six months. The other patient had progressive disease (PD) but PFS was only one month. The side effects were tolerable. This report identified 31 cases of ALK rearrangement in SCC patients from a literature search (including the eight patients in this study). These fusion genes are often seen in a younger age group (mean age: 55.6 years) and non‐smokers (18/31, 58.1%). A total of 20 cases received an ALK inhibitor as first‐ or second‐line treatment which included 11 with a partial response (PR), four with SD, and five with PD. The DCR and ORR was 75.0% (15/20) and 55.0% (11/20), respectively. The median duration time of therapy was 6.4 ± 4.4 months. Conclusions Patients with ALK‐rearranged SCC obtained clinical benefit from ALK‐inhibitor therapy, especially those who were non‐smokers and whose tumors had been identified by IHC+/FISH+.

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Section: Resultsmentioning

confidence: 99%

ALK‐rearranged squamous cell carcinoma of the lung

et al. 2021

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“…Some patients with ALK-positive Sq-LC who were never smokers or light ex-smokers responded to crizotinib and showed a PFS longer than 5.8 months [ 22 – 26 ]. However, even these temporary responders to crizotinib showed shorter PFS than those in previous clinical trials of ALK-rearranged Ad-LC (PROFILE1007: 7.7 months and PROFILE1014: 10.9 months).…”

Section: Discussionmentioning

confidence: 99%

Clinical features of squamous cell lung cancer with anaplastic lymphoma kinase (ALK)-rearrangement: a retrospective analysis and review

et al. 2018

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Anti-anaplastic lymphoma kinase (ALK)-targeted therapy dramatically improves therapeutic responses in patients with ALK-rearranged lung adenocarcinoma (Ad-LC). A few cases of squamous cell lung carcinoma (Sq-LC) with ALK rearrangement have been reported; however, the clinicopathological features and clinical outcomes following treatment with ALK inhibitors are unknown. We addressed this in the present study by retrospectively comparing the clinical characteristics of five patients with ALK-rearranged Sq-LC with those of patients with ALK-rearranged Ad-LC and by evaluating representative cases of ALK inhibitor responders and non-responders. The prevalence of ALK rearrangement in Sq-LCs was 1.36%. Progression-free survival (PFS) after initial treatment with crizotinib was significantly shorter in Sq-LC than in Ad-LC with ALK rearrangement (p = 0.033). Two ALK rearrangements assayed by fluorescence in situ hybridization (FISH)-positive/immunohistochemistry-negative cases did not respond to crizotinb, and PFS decreased following alectinib treatment of ALK-rearranged Sq-LC (p = 0.045). A rebiopsy revealed that responders to ceritinib harbored the L1196M mutation, which causes resistance to other ALK inhibitors. However, non-responders were resistant to all ALK inhibitors, despite the presence of ALK rearrangement in FISH-positive circulating tumor cells and circulating free DNA and absence of the ALK inhibitor resistance mutation. These results indicate that ALK inhibitors remain a reasonable therapeutic option for ALK-rearranged Sq-LC patients who have worse outcomes than ALK-rearranged Ad-LC patients and that resistance mechanisms are heterogeneous. Additionally, oncologists should be aware of the possibility of ALK-rearranged Sq-LC based on clinicopathological features, and plan second-line therapeutic strategies based on rebiopsy results in order to improve patient outcome.

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“…As shown in Table 1, only 10 cases of ALK-rearranged LSCC treated with ALK inhibitors, including crizotinib, ceritinib, and alectinib, have been reported in the literature to date (5,(9)(10)(11)(12)(13)(14)(15)(16)(17). In these few studies, only one reported co-mutation of ALK and RoS1 double-rearrangement (5).…”

Section: Discussionmentioning

confidence: 99%

Lung Squamous Cell Carcinoma With Anaplastic Lymphoma Kinase Rearrangement and TP53 Co-mutation Treated Successfully with Ensartinib: A Case Report

Hu²,

Fei

et al. 2021

Preprint

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Background: Detection of anaplastic lymphoma kinase (ALK) gene rearrangements is an important step in the selection of effective therapies for patients with advanced lung adenocarcinoma. However, there have been few reports of ALK‐positive lung squamous cell carcinoma (LSCC) and, even more rarely, LSCC with ALK rearrangement and TP53 co-mutation. Thus, it remains unclear whether ALK and TP53 co-mutant LSCC responds to ALK inhibitor treatment. Ensartinib is a novel ALK tyrosine kinase inhibitor (TKI). Case presentation: A 73-year-old female nonsmoker was diagnosed with advanced squamous cell carcinoma of the right lung (grade 3, cT4N3M1c, stage IVB). Targeted next-generation sequencing indicated that the cancer cells harbored both the EML4-ALK variant 1 rearrangement (E13;A20) and TP53 exon10 p.L348S (c.1043T>C) mutation, accounted for 70.04%. After only one cycle of ensartinib therapy, the patient exhibited a good partial response in most target lesions, and her performance status improved from 4 to 2. Conclusions: This result strongly suggests that ensartinib, a novel second-generation ALK inhibitor, may be an effective and rapid treatment for patients with this rare subtype of squamous cell carcinoma. Routine molecular analysis of ALK status in patients with LSCC is recommended. Results of the present study may provide some insight into treatment strategies for patients with ALK- and TP53-positive LSCC.

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Response to crizotinib in a squamous cell lung carcinoma patient harbouring echinoderm microtubule‐associated protein‐like 4‐anaplastic lymphoma translocation: A case report

Cited by 14 publications

References 13 publications

ALK‐rearranged squamous cell carcinoma of the lung

ALK‐rearranged squamous cell carcinoma of the lung

Clinical features of squamous cell lung cancer with anaplastic lymphoma kinase (ALK)-rearrangement: a retrospective analysis and review

Lung Squamous Cell Carcinoma With Anaplastic Lymphoma Kinase Rearrangement and TP53 Co-mutation Treated Successfully with Ensartinib: A Case Report

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