Metastatic large cell neuroendocrine carcinoma of the lung arising from the uterus: A pitfall in lung cancer diagnosis

2016 ◽  
Vol 212 (7) ◽  
pp. 654-657 ◽  
Author(s):  
Kyoko Ono ◽  
Naho Ruiz Yokota ◽  
Emi Yoshioka ◽  
Akira Noguchi ◽  
Kota Washimi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Neuroendocrine Carcinoma ◽  
Cancer Diagnosis ◽  
Large Cell ◽  
Large Cell Neuroendocrine Carcinoma ◽  
Lung Cancer Diagnosis

scholarly journals Heterogeneous Tumor-Immune Microenvironments between Primary and Metastatic Tumors in a Patient with ALK Rearrangement-Positive Large Cell Neuroendocrine Carcinoma

2020 ◽  
Vol 21 (24) ◽  
pp. 9705
Author(s):  
Takahiro Tashiro ◽  
Kosuke Imamura ◽  
Yusuke Tomita ◽  
Daisuke Tamanoi ◽  
Akira Takaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Neuroendocrine Carcinoma ◽  
Large Cell ◽  
Large Cell Neuroendocrine Carcinoma ◽  
Driver Mutations ◽  
Single Individual ◽  
Alk Rearrangement ◽  
Metastatic Tumors ◽  
Anaplastic Lymphoma ◽  
Metastatic Lesions

Evolution of tumor-immune microenviroments (TIMEs) occurs during tumor growth and dissemination. Understanding inter-site tumor-immune heterogeneity is essential to harness the immune system for cancer therapy. While the development of immunotherapy against lung cancer with driver mutations and neuroendocrine tumors is ongoing, little is known about the TIME of large cell neuroendocrine carcinoma (LCNEC) or anaplastic lymphoma kinase (ALK) rearrangement-positive lung cancer. We present a case study of a 32-year-old female patient with ALK-rearrangement-positive LCNEC, who had multiple distant metastases including mediastinal lymph-node, bilateral breasts, multiple bones, liver and brain. Multiple biopsy samples obtained from primary lung and three metastatic tumors were analyzed by fluorescent multiplex immunohistochemistry. Tissue localizations of tumor-infiltrating lymphocytes in the tumor nest and surrounding stroma were evaluated. T cell and B cell infiltrations were decreased with distance from primary lung lesion. Although each tumor displayed a unique TIME, all tumors exhibited concomitant regression after treatment with an ALK-inhibitor. This study provides the first evidence of the coexistence of distinct TIME within a single individual with ALK-rearrangement-positive LCNEC. The present study contributes to our understanding of heterogeneous TIMEs between primary and metastatic lesions and provides new insights into the complex interplay between host-immunity and cancer cells in primary and metastatic lesions.

LARGE CELL NEUROENDOCRINE CARCINOMA (LCNC) OF THE LUNG: A SUBSET OF PRIMARY LUNG CANCER WITH POOR PROGNOSIS

CHEST Journal ◽  
2009 ◽  
Vol 136 (4) ◽  
pp. 137S
Author(s):  
Pier L. Filosso ◽  
Enrico Ruffini ◽  
Sofia Asioli ◽  
Sergio Bretti ◽  
Luigia Macrí ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Neuroendocrine Carcinoma ◽  
Poor Prognosis ◽  
Primary Lung Cancer ◽  
Large Cell ◽  
Large Cell Neuroendocrine Carcinoma

Large-Cell Neuroendocrine Carcinoma of the Lung: A Focused Analysis of BRAF Alterations and Case Report of a BRAF Non-V600–Mutated Tumor Responding to Targeted Therapy

2018 ◽  
pp. 1-12
Author(s):  
Young Kwang Chae ◽  
Keerthi B. Tamragouri ◽  
Jon Chung ◽  
Xiaoqi Lin ◽  
Vincent Miller ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Neuroendocrine Carcinoma ◽  
Cell Lung Cancer ◽  
Large Cell ◽  
Small Cell ◽  
Large Cell Neuroendocrine Carcinoma ◽  
Small Cell Lung ◽  
Durable Response ◽  
Biomarker Response

Purpose In advanced stages, large-cell neuroendocrine carcinoma of the lung (L-LCNEC) mimics small-cell lung cancer despite its traditional classification as a non–small-cell lung cancer. Here we present a focused analysis of BRAF mutations in this population. Patients and Methods Comprehensive genomic profiling of tumor tissues was performed from a cohort of 300 patients with biopsy-proven L-LCNEC. Specimens were either from a primary lung lesion or metastatic site. Results In 13 patients, 14 unique BRAF alterations (amplifications, mutations) were identified. The importance of biomarker-driven therapy is subsequently highlighted with our case of a 69-year-old man diagnosed with metastatic L-LCNEC who did not respond to cisplatin plus etoposide. A significant durable response was then demonstrated with therapy targeted toward a BRAF non-V600E activating mutation (G469R) associated with biomarker response identified through circulating cell-free tumor DNA analysis. A change in clonal allele frequency from nearly 40% to nondetectable was observed. Conclusion Although uncommon, L-LCNEC does seem to contain activating and therefore actionable alterations. We thus highlight the value of pursuing next-generation sequencing for patients with this disease.

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