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Journal articles on the topic 'ALK positive Lung Cancer'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

International, Journal of Medical Science and Innovative Research (IJMSIR). "Synchronous Colon Cancer and ALK Positive Lung Cancer." International Journal of Medical Science and Innovative Research (IJMSIR) 9, no. 5 (2024): 37–41. https://doi.org/10.5281/zenodo.15430305.

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<strong>Abstract</strong> We present a case of synchronous ALK positive lung cancer and colon cancer. Patient presented to the hospital for routine health checkup and was incidentally detected with both the cancers. Initially it was thought to be colon cancer with lung metastasis. IHC was done on the lung biopsy specimen which was positive for TTF1 and ALK mutation and negative for SATB2. Colon specimen was also reported as mucinous adenocarcinoma histopathologically but IHC was negative for ALK mutation. Hence the diagnosis of synchronous double malignancy was made. Both the cancers were loca

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2

Poudiougou, Abdoul Karim, Hamadoun Traoré, Faman Sano, et al. "Efficacy of Lorlatinib on Cerebral Metastases in the Management of Alk-Positive Lung Adenocarcinoma, Case Report." Scholars Journal of Medical Case Reports 13, no. 01 (2025): 139–43. https://doi.org/10.36347/sjmcr.2025.v13i01.031.

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Bronchial cancers are the leading cause of brain metastases and, in the absence of treatment, the median survival time for patients with bronchial cancer complicated by symptomatic brain metastases is approximately one month. Genetic sequencing has radically changed the management of non-small cell lung cancer over the last few decades. Anaplastic lymphoma kinase (ALK) rearrangements are responsible for 3-7% of non-small cell lung cancers. Patients with ALK-positive non-small cell lung cancer have a particular phenotype compared with other non-small cell lung cancers: they are younger, non-smo

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3

Ni, Wenjie. "ALK-inhibiting drugs for ALK-positive NSCLC." Theoretical and Natural Science 74, no. 1 (2025): 177–82. https://doi.org/10.54254/2753-8818/2024.la19334.

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Lung cancer has already been one of the major reasons of cancer-related deaths, with anaplastic lymphoma kinase (ALK) rearranged non-small cell lung cancer (NSCLC)taking up about 5%. This type of tumor has a high rate of central nervous system metastasis and standard chemotherapy has limited effect to effectively control progression. ALK-targeted inhibitors (ALK-TKIs) have notably extended the lifespan of patients with ALK-positive NSCLC, and third-generation inhibitors, in particular, have made significant progress in overcoming drug resistance and increasing intracranial activity, with parti

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4

Shaw, Alice T., and Jeffrey A. Engelman. "ALKin Lung Cancer: Past, Present, and Future." Journal of Clinical Oncology 31, no. 8 (2013): 1105–11. http://dx.doi.org/10.1200/jco.2012.44.5353.

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In 2007, scientists discovered that anaplastic lymphoma kinase (ALK) gene rearrangements are present in a small subset of non–small-cell lung cancers. ALK-positive cancers are highly sensitive to small-molecule ALK kinase inhibitors, such as crizotinib. Phase I and II studies of crizotinib in ALK-positive lung cancer demonstrated impressive activity and clinical benefit, leading to rapid US Food and Drug Administration approval in 2011. Although crizotinib induces remissions and extends the lives of patients, cures are not achieved as resistance to therapy develops. In this review, we will dis

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5

Girard, Nicolas. "Crizotinib in ALK-positive lung cancer." Lancet Oncology 13, no. 10 (2012): 962–63. http://dx.doi.org/10.1016/s1470-2045(12)70375-3.

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6

Kharagezov, D. A., Yu N. Lazutin, E. A. Mirzoyan, et al. "Modern treatment of ALK-positive non-small cell lung cancer." South Russian Journal of Cancer 3, no. 2 (2022): 41–51. http://dx.doi.org/10.37748/2686-9039-2022-3-2-5.

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Lung cancer (LC) takes the first place in the structure of overall oncology in males. More than 1.8 million of new cases of lung cancer (LC) are registered each year worldwide. LC is the leading cause of cancer death in both developing and developed countries, and the 5 years survival rate is as low as 19 %. Many factors explain such unsatisfactory outcomes, including the LC diagnosis at an advanced stage, when the currently available treatments can rarely provide cure. Non-small cell lung cancer (NSCLC) with chromosomal rearrangement of anaplastic lymphoma kinase (ALK) is sensitive to targete

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7

Yamasaki, Masahiro, Naomi Saito, Yu Hada, et al. "Nivolumab Therapy for Synchronous ALK-Positive Lung Cancer and Gastric Cancer." Case Reports in Oncology 10, no. 1 (2017): 361–67. http://dx.doi.org/10.1159/000470830.

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Nivolumab is an immune checkpoint inhibitor with demonstrated efficacy against several malignant tumors. Alterations in driver oncogenes such as EGFR and ALK are a poor prognostic factor in nivolumab therapy for non-small cell lung cancer (NSCLC), whereas a smoking history is a well-known, favorable prognostic factor. However, an efficacy of nivolumab therapy for multiple primary malignant tumors (MPMTs) has not been reported, and its efficacy for driver oncogene-positive NSCLC in smokers is unclear. Herein, we report the case of a patient with a history of heavy smoking who developed synchron

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8

McCusker, Michael G., Alessandro Russo, Katherine A. Scilla, Ranee Mehra, and Christian Rolfo. "How I treat ALK-positive non-small cell lung cancer." ESMO Open 4, Suppl 2 (2019): e000524. http://dx.doi.org/10.1136/esmoopen-2019-000524.

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Since the discovery of anaplastic lymphocyte kinase (ALK) rearrangement in non-small cell lung cancer (NSCLC) and subsequent development of increasingly effective and central nervous system (CNS)-penetrant first-generation, second-generation and third-generation ALK tyrosine kinase inhibitors (TKIs), the landscape of resistance mechanisms and treatment decisions has become increasingly complex. Tissue and/or plasma-based molecular tests can identify not only the rearrangement proper but also common resistance mechanisms to guide decision-making for further lines of treatment. However, frequent

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9

Sharma, Janaki, Vipul Pareek, Huijie Liu, and Haiying Cheng. "Emerging treatment for ALK-positive lung cancer." Expert Opinion on Emerging Drugs 21, no. 2 (2016): 147–55. http://dx.doi.org/10.1080/14728214.2016.1183642.

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10

Pop, Ovidiu Laurean, Claudia Teodora Judea Pusta, Camelia Liana Buhas, et al. "Anaplastic Lymphoma Kinase (ALK) Overexpression in Lung Cancer Biopsies - An 18 month study in north western Romania." Revista de Chimie 70, no. 7 (2019): 2690–93. http://dx.doi.org/10.37358/rc.19.7.7407.

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Lung cancer is the first cause of death worldwide of oncological patients. Most of them are non-small cell lung cancer (NSCLC) and many of them are characterized by different molecular markers that allow the development of personalized treatments. Epithelial growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) are the most frequently tested genes in lung adenocarcinoma and other lung carcinomas with glandular component. The aim of our study is to evaluate the distribution of ALK gene mutation in lung cancer patient from North West part of Romania. We analysed a number of 289 lung

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11

Bang, Yung-Jue. "Treatment of ALK-Positive Non–Small Cell Lung Cancer." Archives of Pathology & Laboratory Medicine 136, no. 10 (2012): 1201–4. http://dx.doi.org/10.5858/arpa.2012-0246-ra.

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Crizotinib (Xalkori), the first inhibitor of both anaplastic lymphoma kinase (ALK) and c-Met receptor kinases, has been approved in the United States, Korea, and other countries for the treatment of ALK-positive non–small cell lung cancer (NSCLC). This approval came within just 4 years of the discovery of rearrangements in the ALK gene in a subset of patients with NSCLC. Oral crizotinib 250 mg twice daily showed excellent efficacy in patients with advanced ALK-positive NSCLC, with objective response rates of 61% and 51% in ongoing phase I and II studies, respectively. Objective response rates

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12

Hochmair, Maximilian J., Hannah Fabikan, Oliver Illini, et al. "Later-Line Treatment with Lorlatinib in ALK- and ROS1-Rearrangement-Positive NSCLC: A Retrospective, Multicenter Analysis." Pharmaceuticals 13, no. 11 (2020): 371. http://dx.doi.org/10.3390/ph13110371.

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In clinical practice, patients with anaplastic lymphoma kinase (ALK)-rearrangement–positive non–small-cell lung cancer commonly receive sequential treatment with ALK tyrosine kinase inhibitors. The third-generation agent lorlatinib has been shown to inhibit a wide range of ALK resistance mutations and thus offers potential benefit in later lines, although real-world data are lacking. This multicenter study retrospectively investigated later-line, real-world use of lorlatinib in patients with advanced ALK- or ROS1-positive lung cancer. Fifty-one patients registered in a compassionate use progra

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13

Matsumura, Yugo, Seiya Ichihara, Kaori Nii, et al. "Successful pembrolizumab treatment in a patient with ALK-positive lung adenocarcinoma: A case report and literature review." Medicine 104, no. 28 (2025): e43352. https://doi.org/10.1097/md.0000000000043352.

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Rationale: Immune checkpoint inhibitors are generally considered to be ineffective in chemotherapy for anaplastic lymphoma kinase (ALK)-positive lung cancer. We encountered an ALK-positive lung cancer patient who responded well to pembrolizumab. Patient concerns: A 70-year-old man presented with a chest shadow. Diagnosis: A mass shadow in the left lower lung field was diagnosed as lung adenocarcinoma cT2N3M1b stage IVA. ALK staining by immunohistochemistry was strongly positive (3+), and fluorescence in situ hybridization detected ALK rearrangements. Immunostaining showed that 95% of tumor cel

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14

Kolesnik, O. P., and A. Yu Malovanna. "Treatment of ALK-positive non-small cell lung cancer (literature review)." Practical oncology 7, no. 1 (2024): 12–17. http://dx.doi.org/10.22141/2663-3272.7.1.2024.95.

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This literature review explores the current landscape of treatment strategies for ALK-positive non-small cell lung cancer (NSCLC), a subtype characterized by rearrangements in the anaplastic lymphoma kinase (ALK) gene. The appearance of ALK inhibitors has revolutionized the management of this cancer, offering targeted therapeutic options that significantly improve patient outcomes. This review provides a comprehensive analysis of the clinical efficacy and safety profiles of first-generation ALK inhibitors, such as crizotinib, second-generation inhibitors like alectinib and ceritinib, and thir

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15

Sakata, Yoshihiko, Kodai Kawamura, Kazuya Ichikado, and Masakazu Yoshioka. "A Case of Orbital Metastasis as Disease Progression of Anaplastic Lymphoma Kinase-Positive Lung Cancer Treated with Crizotinib." Case Reports in Oncology 8, no. 1 (2015): 21–24. http://dx.doi.org/10.1159/000371719.

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Orbital metastasis of lung cancer is rare. It often causes visual disorder. To date, there are only a few case reports. Crizotinib is an anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor that leads to responses in most patients with ALK-positive non-small-cell lung cancer. Visual disorder is one of the popular adverse events of crizotinib, but the symptom almost decreases over time. We report a case of orbital metastasis as the disease progression of ALK-positive lung cancer treated with crizotinib. It should be kept in mind that orbital metastasis can be the disease progression of lu

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16

Kast, Richard E. "IC Regimen: Delaying Resistance to Lorlatinib in ALK Driven Cancers by Adding Repurposed Itraconazole and Cilostazol." Cells 13, no. 14 (2024): 1175. http://dx.doi.org/10.3390/cells13141175.

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Lorlatinib is a pharmaceutical ALK kinase inhibitor used to treat ALK driven non-small cell lung cancers. This paper analyses the intersection of past published data on the physiological consequences of two unrelated drugs from general medical practice—itraconazole and cilostazol—with the pathophysiology of ALK positive non-small cell lung cancer. A conclusion from that data analysis is that adding itraconazole and cilostazol may make lorlatinib more effective. Itraconazole, although marketed worldwide as a generic antifungal drug, also inhibits Hedgehog signaling, Wnt signaling, hepatic CYP3A

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17

Madhi, Hamadi, Habib Serhan, Nathalie M. Vandecan, et al. "Abstract 4548: Discovering novel ALK-lung carcinoma therapeutic strategies by identifying combinations with Alectinib from ALK-positive lung carcinoma cell lines." Cancer Research 84, no. 6_Supplement (2024): 4548. http://dx.doi.org/10.1158/1538-7445.am2024-4548.

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Abstract Background: The therapeutic landscape for chromosomally rearranged anaplastic lymphoma kinase (ALK) has focused on the development of Tyrosine-kinase inhibitors (TKI) that specifically target ALK activity. However, as patients progress on first- and second line TKIs, over 50% of resistance is due to non-mutational resistance via compensatory pathways, also known as ALK-non dominant resistance. Alterations in other drivers such as EGFR, KRAS, MET account for some of the resistance mechanisms. Thus, here we explore the therapeutic activity of drug combinations that pair an ALK inhibitor

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18

Laktionov, К. К., S. Yu Kruteleva, and Е. V. Reutova. "Current approaches to therapy of ALK-positive non-small cell lung cancer." Meditsinskiy sovet = Medical Council, no. 4S (June 12, 2021): 16–22. https://doi.org/10.21518/2079-701x-2021-4s-16-22.

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This article analyzes approaches of the treatment of ALK-positive non-small cell lung cancer (NSCLC). Despite the relatively small percentage of patients with ALK-gene rearrangements, identification of this mutation is very important. The most effective treatment for patients with ALK translocation is the use of ALK inhibitors, which significantly improve survival rates compared to standard chemotherapy. Crisotinib was the first drug approved for the treatment of advanced ALK-positive NSCLC. However, the soon emerging resistance during crizotinib therapy and the inevitable progression of the d

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19

Zhou, Bingying, and Adrienne D. Cox. "Up-front polytherapy for ALK-positive lung cancer." Nature Medicine 21, no. 9 (2015): 974–75. http://dx.doi.org/10.1038/nm.3942.

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20

Thai, Alesha A., and Benjamin J. Solomon. "Treatment of ALK-positive nonsmall cell lung cancer." Current Opinion in Oncology 30, no. 2 (2018): 84–91. http://dx.doi.org/10.1097/cco.0000000000000431.

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21

Marshall, Hilary. "Ceritinib versus chemotherapy in ALK-positive lung cancer." Lancet Respiratory Medicine 4, no. 12 (2016): 952–53. http://dx.doi.org/10.1016/s2213-2600(16)30377-0.

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22

Ziogas, Dimitrios C., Anna Tsiara, Georgios Tsironis, et al. "Treating ALK-positive non-small cell lung cancer." Annals of Translational Medicine 6, no. 8 (2018): 141. http://dx.doi.org/10.21037/atm.2017.11.34.

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23

Barton, Colin, Morhaf Al Achkar, Jennifer A. Blender, et al. "Patient-led advocacy in ALK-positive lung cancer." Translational Lung Cancer Research 12, no. 6 (2023): 1303–19. http://dx.doi.org/10.21037/tlcr-22-713.

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24

Sultanbaev, A. V., Sh I. Musin, K. V. Menshikov, et al. "Experience of targeted therapy for ALK positive non-small cell lung cancer – a clinical case." Meditsinskiy sovet = Medical Council, no. 20 (December 21, 2020): 181–86. http://dx.doi.org/10.21518/2079-701x-2020-20-181-186.

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Lung cancer holds a leading position in the cancer mortality pattern worldwide. The emergence of knowledge about driver mutations heralded a new era in the targeted therapy for lung carcinomas. ALK translocation is identified in 5–7% of non-small cell lung cancer cases. ALK-positive lung adenocarcinomas are associated with specific clinical features, including no or light smoking history and younger age. Alectinib is a novel ALK inhibitor that has been granted a breakthrough therapy status by the FDA to accelerate approval as a second-line therapy after progression during crizotinib therapy.He

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25

Bouchaab, Hasna. "First-line treatment of ALK-positive NSCLC." healthbook TIMES Oncology Hematology, no. 2 (December 5, 2019): 22–25. http://dx.doi.org/10.36000/hbt.oh.2019.02.009.

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Non-small cell lung cancer (NSCLC) patients with rearrangements in the anaplastic lymphocyte kinase (ALK) gene are highly sensitive to ALK tyrosine kinase inhibitors (TKIs) like alectinib. Here, the case of a 77-year-old male patient with newly diagnosed metastatic ALK-positive NSCLC treated with alectinib has been discussed. The patient achieved a durable (>18 months) complete response and demonstrated excellent clinical tolerance to alectinib.

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Breder, V. V., K. K. Laktionov, Denis I. Yudin, and N. E. Hamrina. "Therapy with ALK-positive non-small cell lung cancer: reality and prospects." Russian Journal of Oncology 19, no. 6 (2014): 4–13. http://dx.doi.org/10.17816/onco40081.

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There is highlighted special small subgroup of patients with non-small cell lung cancer who has translocation of gene ALK in tumor. The modified gene encodes a fusion of pathological protein, leading to activation of ALK receptor on the membrane of tumor cells and then malignant transformation. Clinical studies of crizotinib noted a high frequency (> 60%) of complete and partial responses in chemoresistant metastatic ALK-positive lung cancer; median of progression-free survival reached more than 9 months. Crizotinib is the ATP competitive inhibitor of tyrosine kinase receptor like ALK, MET

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Kang, Jin, Huajun Chen, Qing Zhou, et al. "Primary resistance to ALK inhibitor in ALK-positive non-small-cell lung cancer." Journal of Clinical Oncology 35, no. 15_suppl (2017): 9063. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.9063.

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9063 Background: Crizotinib is a standard of care in anaplastic lymphoma kinase (ALK)-positive advanced non-small-cell lung cancers (NSCLC). Undoubtedly,the resistance to crizotinib is a current bottleneck which resists its clinical application. However, there are few reports about the primary resistance to crizotinib, especially the difference between the primary and acquired resistance. Methods: Totally,171 ALK-positive NSCLC patients treated with crizotinib were reviewed at the Guangdong General Hospital in China from October 2010 to July 2016. The status of an ALK gene rearrangement was as

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Melosky, B., J. Agulnik, R. Albadine, et al. "Canadian consensus: inhibition of ALK-positive tumours in advanced non-small-cell lung cancer." Current Oncology 23, no. 3 (2016): 196. http://dx.doi.org/10.3747/co.23.3120.

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Anaplastic lymphoma kinase (ALK) is an oncogenic driver in non-small-cell lung cancer (NSCLC). Chromosomal rearrangements involving the ALK gene occur in up to 4% of nonsquamous NSCLC patients and lead to constitutive activation of the ALK signalling pathway. ALK-positive NSCLC is found in relatively young patients, with a median age of 50 years. Patients frequently have brain metastasis.Targeted inhibition of the ALK pathway prolongs progression-free survival in patients with ALK-positive advanced NSCLC. The results of several recent clinical trials confirm the efficacy and safety benefit of

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Reutova, E. V., K. K. Laktionov, and M. A. Ardzinba. "Ceritinib as a long-term disease control: Clinical observation." Meditsinskiy sovet = Medical Council, no. 10 (July 24, 2024): 60–65. http://dx.doi.org/10.21518/ms2024-238.

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ALK-positive non-small cell lung cancer is an excellent model demonstrating the success of precision medicine. A rare genetic disorder – a rearrangement of the anaplastic large cell lymphoma gene, occurring with a frequency of 5–7%, forms a certain clinical and morphological portrait of the patient. In ALK-positive non-small cell lung cancer, the brain is a frequent target for metastasis. But despite this negative prognosis factor, it is in this cohort of non-small cell lung cancer patients that the achievements of drug antitumor therapy are especially significant – the consistent use of ALK i

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Ashton, J., N. Shrestha, and A. Bland. "P2.14-66 Combination ALK and MEK Inhibition in ALK-Positive Lung Cancer." Journal of Thoracic Oncology 14, no. 10 (2019): S857. http://dx.doi.org/10.1016/j.jtho.2019.08.1851.

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Lin, Jessica J., Viola W. Zhu, Satoshi Yoda, et al. "Impact of EML4-ALK Variant on Resistance Mechanisms and Clinical Outcomes in ALK-Positive Lung Cancer." Journal of Clinical Oncology 36, no. 12 (2018): 1199–206. http://dx.doi.org/10.1200/jco.2017.76.2294.

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Purpose Advanced anaplastic lymphoma kinase ( ALK) fusion-positive non–small-cell lung cancers (NSCLCs) are effectively treated with ALK tyrosine kinase inhibitors (TKIs). However, clinical outcomes in these patients vary, and the benefit of TKIs is limited as a result of acquired resistance. Emerging data suggest that the ALK fusion variant may affect clinical outcome, but the molecular basis for this association is unknown. Patients and Methods We identified 129 patients with ALK-positive NSCLC with known ALK variants. ALK resistance mutations and clinical outcomes on ALK TKIs were retrospec

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Patil, A. R., D. S. Dabrowski, J. Cotelingam, et al. "Genomic Analysis Identifies Rare ALK Positive Cases In The TCGA Database." American Journal of Clinical Pathology 154, Supplement_1 (2020): S148. http://dx.doi.org/10.1093/ajcp/aqaa161.323.

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Abstract Introduction/Objective The anaplastic lymphoma kinase (ALK) gene is a receptor tyrosine kinase gene located in the 2p23.2 region. Normally, dimerization of ALK receptor by binding to its ligand activates the ALK receptor by autophosphorylation of c-termius and activates downstream PI3K, MAPK and JAK3 pathways. The ALK gene is abnormally hyperactivated by fusion of the 3’ half containing the kinase domain with 5’ portion of other genes, resulting in the ligand independent dimerization and activation of the ALK receptor. The tumors harboring these translocations are termed as ALK-positi

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Zito Marino, Federica, Giulio Rossi, Immacolata Cozzolino, et al. "Multiplex fluorescence in situ hybridisation to detect anaplastic lymphoma kinase and ROS proto-oncogene 1 receptor tyrosine kinase rearrangements in lung cancer cytological samples." Journal of Clinical Pathology 73, no. 2 (2019): 96–101. http://dx.doi.org/10.1136/jclinpath-2019-206152.

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AimsSeveral predictive biomarkers of response to specific inhibitors have become mandatory for the therapeutic choice in non-small-cell lung cancer (NSCLC). In most lung cancer patients, the biological materials available to morphological and molecular diagnosis are exclusively cytological samples and minimum tumour wastage is necessary. Multiplex fluorescence in situ hybridisation (mFISH) to detect simultaneously ALK-rearrangement and ROS1-rearrangement on a single slide could be useful in clinical practice to save cytological samples for further molecular analysis. In this study, we aim to v

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Xia, Wenchao, Jing Yang, Hongbin Li, Ling Li, and Jinfeng Liu. "Comparing Genomic Profiles of ALK Fusion-Positive and ALK Fusion-Negative Nonsmall Cell Lung Cancer Patients." Global Medical Genetics 11, no. 02 (2024): 175–86. http://dx.doi.org/10.1055/s-0044-1787301.

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Abstract Background Anaplastic lymphoma kinase (ALK) fusion events account for 3 to 7% of genetic alterations in patients with nonsmall cell lung cancer (NSCLC). This study aimed to explore the landscape of ALK fusion-positive and ALK fusion-negative in a large cohort of NSCLC patients. Methods The formalin-fixed paraffin-embedded specimens of NSCLC patients who underwent next-generation sequencing from 2020 to 2023 in Yinfeng Gene Technology Co., Ltd. Clinical laboratory were included in this study. Results In the current study, a total of 180 (3.20%) patients tested positive for ALK fusions

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Alese, Olatunji Boladale, Bassel F. El-Rayes, Gabriel Sica, et al. "Multiplatform assessment of anaplastic lymphoma kinase (ALK) gene rearrangement in signet ring cell carcinoma of the gastrointestinal tract." Journal of Clinical Oncology 31, no. 15_suppl (2013): e14612-e14612. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e14612.

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e14612 Background: ALK-EML4 translocation is an established driver aberration in NSCLC, with reported predilection for cases with signet ring histology. We assessed the presence of ALK gene rearrangements in signet ring cancers arising in the stomach and colon. Methods: Histologically confirmed cases of signet ring adenocarcinoma of the stomach or the colon were identified from the pathology archive of Emory University Hospital. Presence of the classic ALK and EML4 fusion gene was initially determined by fluorescence in-situ hybridization (FISH) method. Cases showing break-apart signal in more

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Ozakinci, Hilal, Gina Nazario, Karina Colossi Furlan, et al. "Abstract 6642: Rapid tissue donation identifies LAG3 as a potential therapeutic target for ALK fusion positive lung cancer." Cancer Research 83, no. 7_Supplement (2023): 6642. http://dx.doi.org/10.1158/1538-7445.am2023-6642.

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Abstract Introduction: The rapid tissue donation (RTD) program provides post-therapy primary and metastatic tumor tissue samples at the time of death for the study of resistance mechanisms and the tumor microenvironment to inform therapeutic opportunities. NCCN guidelines (NCCN v5.2022) recommend against PD-1/PD-L1 inhibitor monotherapy in the second-line setting for ALK fusion+ non-small cell lung cancer (NSCLC) due to lack of efficacy, irrespective of tumoral PD-L1 expression. We observed high LAG3 protein expression by multiplex immunofluorescence (mIF) in postmortem ALK fusion-positive tum

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Sughayer, M. A., B. Maraqa, and M. Al-Ashhab. "Anaplastic lymphoma kinase rearrangements in non-small cell lung cancer in Jordan." American Journal of Clinical Pathology 156, Supplement_1 (2021): S151. http://dx.doi.org/10.1093/ajcp/aqab191.321.

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Abstract Introduction/Objective ALK rearrangement is an important oncogenic driver in a substantial portion of non-small cell lung cancer (NSCLC) patients ranging from 2-7%. Treatment options such as ALK tyrosine kinase inhibitors (TKI) improve progression-free survival and overall survival. Candidates for such treatment are selected based on the identification of the ALK rearrangement. While fluorescence in situ hybridization (FISH) was considered the gold standard method, the availability of a robust FDA-approved companion diagnostic immunohistochemistry (IHC) assay has led to a paradigm shi

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Li, Gu, Kristine B. Jacobson, Paul E. Matushek, et al. "Vysis ALK non-small cell lung cancer assay performance on archival tissue and cytology specimens." Journal of Clinical Oncology 30, no. 15_suppl (2012): e21060-e21060. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21060.

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e21060 Background: Rearrangements of ALK gene on chromosome 2p23 create a constitutively activated tyrosine kinase implicated in the development of NSCLC and targeted by novel therapeutic agents. The Vysis ALK Break Apart (BAP) FISH Probe assay was developed to detect chromosome 2p23 rearrangements in NSCLC FFPE tissue by fluorescence in situ hybridization. Performance of the ALK assay was assessed on FFPE tissue specimens and FFPE cell lines. The ALK probe was also tested on lung cytology cell suspensions. Methods: The ALK FISH assay success rate on primary NSCLC was tested with 30 FFPE tumor

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Salanova, Ruben, Julio C. Calderazzo Pereyra, Laura Leguina, et al. "Epidemiology of PD-L1 and ALK expression and EGFR mutational status in Argentinian patients with lung cancer." Journal of Clinical Oncology 35, no. 15_suppl (2017): e20565-e20565. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e20565.

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e20565 Background: Until now, the results of the correlation between PD-L1, ALK expression and EGFR mutations remain controversial. We prospectively evaluated patterns among EGFR mutant, ALK positive and PD-L1 positive lung cancer patients. Methods: PD-L1 and ALK expression was evaluated in 342 adenocarcinomas (AD) of the lung using inmunohistochemestry (anti-PD-L1 22C3, anti-ALK D5F3), and EGFR mutations using real time PCR (therascreen EGFR RGQ PCR Kit version 2). PD-L1 was also evaluated in 36 squamous (SQ) cell carcinomas. Results: 181 of 342 patients with AD were positive for PD-L1. 108 w

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Kitadai, Rui, Yusuke Okuma, and Jumpei Kashima. "Gingival Metastasis of ALK Rearranged Non-Small Cell Lung Cancer." Case Reports in Oncology 12, no. 1 (2019): 171–77. http://dx.doi.org/10.1159/000497481.

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Background: Metastasis to oral soft tissues is rare and account for only 0.1% of all oral malignancies. Oral cavity metastasis tends to be male-predominant, and lung cancer is the leading cause. Targeted therapies for advanced ALK rearranged non-small cell lung cancer (NSCLC) have shown a promising higher response than cytotoxic chemotherapy. Gingival metastasis usually shows poor prognosis. However using ALK inhibitor to ALK-positive advanced NSCLC may show longer survival. Case: A 64-year-old male who was diagnosed non-small cell carcinoma (NSCC) favoring adenocarcinoma presented with gingiv

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Ji, Xianxiu, Huikang Xie, Ren Zhu, Bin Chen, Sen Jiang, and Jie Luo. "Different clinical features between patients with ROS1-positive and ALK-positive advanced non-small cell lung cancer." Journal of International Medical Research 49, no. 2 (2021): 030006052199364. http://dx.doi.org/10.1177/0300060521993643.

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Objective To compare the baseline clinical characteristics between patients with ROS1-positive and ALK-positive advanced non-small cell lung cancer (NSCLC), and the correlations of these subtypes with the distribution of metastases. Methods We compared the clinical characteristics and imaging features of patients with ROS1-positive and ALK-positive NSCLC using statistical methods. Results Data for 232 patients were analyzed. Compared with ALK-positive NSCLC, ROS1-positive NSCLC was more likely to occur in women (71% vs 53%), and primary lesions ≤3 cm were more common in patients with ROS1-posi

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Lantuejoul, Sylvie, Isabelle Rouquette, Hugues Begueret, et al. "A French multicentric and prospective validation study for ALK translocation diagnosis in lung adenocarcinomas." Journal of Clinical Oncology 31, no. 15_suppl (2013): 8100. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.8100.

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8100 Background: ALK rearrangements occur in nearly 5% of NSCLC and lead to a permanent ALK protein activation, targeted by a small molecule, the crizotinib. To date, FISH (Fluorescent In situ Hybridization) is considered as the gold standard to identify ALK abnormalities, but dual testing and pre-screening by immunohistochemistry have been proposed. Methods: The purpose of the study was to compare immunohistochemistry (IHC) using 5A4 and D5F3 Abs, with FISH and quantitative RT-PCR in a series of 500 surgical specimens, collected within one year from 15 French Thoracic Pathology Departments an

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Kang, Jin, Xuchao Zhang, Huajun Chen, et al. "Uncommon ALK fusion partners in advanced ALK-positive non-small-cell lung cancer." Journal of Clinical Oncology 36, no. 15_suppl (2018): 8561. http://dx.doi.org/10.1200/jco.2018.36.15_suppl.8561.

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Berezina, G. I., K. K. Laktionov, E. V. Reutova, M. S. Ardzinba, T. N. Borisova, and V. L. Utkina. "Long-term disease control in a patient with ALK-positive non-small cell lung cancer." Meditsinskiy sovet = Medical Council, no. 9 (June 19, 2022): 172–77. http://dx.doi.org/10.21518/2079-701x-2022-16-9-172-177.

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Non-small cell lung cancer is a very heterogeneous group of diseases. When choosing an effective patient management strategy, an oncologist focuses on the stage of the disease, the morphological form of the tumor, as well as its molecular genetic markers. Most of the targeted mutations in lung cancer today are in adenocarcinoma. The standard for detecting this type of cancer in 2022 is the determination of mutations in the EGFR genes (18-21 exons) and BRAF (V600E), translocations of the ALK and ROS1 genes, and determination of PD-L1 status regardless of gender, age, and history of smoking. Oft

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Miller, Jill, Zhihua Peng, Rebecca Wilcox, et al. "Investigation of anaplastic lymphoma kinase (ALK) translocations in gastric and esophageal signet ring cell carcinomas." Journal of Clinical Oncology 31, no. 15_suppl (2013): e15106-e15106. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e15106.

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e15106 Background: Anaplastic lymphoma kinase (ALK) fusion oncogenes are present in multiple cancer types. The inversion of echinoderm microtubule associated protein like 4 (EML4) and ALK genes on chromosome 2 is present in a subset of non-small cell lung cancer (NSCLC) patients. ALK mutated lung cancers demonstrate a significantly higher incidence of signet ring cell histology than compared to ALK-negative tumors. Based on the histological similarities of ALK positive NSCLC and signet ring cell carcinomas (SRCC) of the GI tract, we hypothesized that gastric and/or esophageal SRCC may also har

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Rossi, Antonio. "Alectinib for ALK-positive non-small-cell lung cancer." Expert Review of Clinical Pharmacology 9, no. 8 (2016): 1005–13. http://dx.doi.org/10.1080/17512433.2016.1195262.

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Soda, M., S. Takada, K. Takeuchi, et al. "A mouse model for EML4-ALK-positive lung cancer." Proceedings of the National Academy of Sciences 105, no. 50 (2008): 19893–97. http://dx.doi.org/10.1073/pnas.0805381105.

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Gavralidis, Alexander, and Justin F. Gainor. "Immunotherapy in EGFR-Mutant and ALK-Positive Lung Cancer." Cancer Journal 26, no. 6 (2020): 517–24. http://dx.doi.org/10.1097/ppo.0000000000000491.

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Lin, Jessica J., and Justin F. Gainor. "Current opportunities and challenges in ALK-positive lung cancer." Translational Lung Cancer Research 13, no. 1 (2024): 1–4. http://dx.doi.org/10.21037/tlcr-2023-4.

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Shaw, Alice T., Benjamin J. Solomon, Benjamin Besse, et al. "ALK Resistance Mutations and Efficacy of Lorlatinib in Advanced Anaplastic Lymphoma Kinase-Positive Non–Small-Cell Lung Cancer." Journal of Clinical Oncology 37, no. 16 (2019): 1370–79. http://dx.doi.org/10.1200/jco.18.02236.

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PURPOSE Lorlatinib is a potent, brain-penetrant, third-generation anaplastic lymphoma kinase (ALK)/ROS1 tyrosine kinase inhibitor (TKI) with robust clinical activity in advanced ALK-positive non–small-cell lung cancer, including in patients who have failed prior ALK TKIs. Molecular determinants of response to lorlatinib have not been established, but preclinical data suggest that ALK resistance mutations may represent a biomarker of response in previously treated patients. PATIENTS AND METHODS Baseline plasma and tumor tissue samples were collected from 198 patients with ALK-positive non–small

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