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      Endobronchial ultrasound-guided transbronchial needle aspirate for diagnosis of anaplastic large cell lymphoma of unusual presentation: A case report

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          Anaplastic large cell lymphoma (ALCL) is a rare type of non-Hodgkin lymphoma (NHL) originated from mature post thymic T cells. They represent 1–3% of NHL. Different subtypes have been described: Anaplastic lymphoma kinase (ALK)-negative ALCL, ALK-positive ALCL and breast implant-associated ALCL. ALK-positive ALCL affects mainly the young and has better prognosis. We present a case report of an adult woman with AKL-positive ALCL, diagnosed by endobronchial ultrasound-guided transbronchial needle aspirate (EBUS-TBNA).

          A 59-year-old women with no history of breast implants, was admitted for a four-month low back pain. Initially, the patient was treated for a spondyloarthropathy, but due to persistence of the symptoms, a lumbosacral MRI was performed, showing changes in morphology and signal intensity in the vertebral body of L3, along with edema and a paravertebral collection that affected the left psoas muscle, suggesting granulomatous spondylodiscitis. Chest CT-scan showed mild left pleural effusion, subcarinal and right hiliar adenomegalies. An EBUS-TBNA with ROSE (rapid on-site evaluation) was performed showing positive findings for malignancy, suggestive of hematolymphoid neoplasia. Pathology analysis showed an AKL-positive ALCL. Additionally, a biopsy of paravertebral tissue biopsy was obtained, which was consistent with the nodal sample. Chemotherapy was initiated with the CHOP protocol: cyclophosphamide, hydroxydaunorubicin, vincristine sulfate and prednisone.

          EBUS-TBNA is a minimally invasive and safe technique for obtaining mediastinal samples. Collaboration with a cytopathologist trained to perform ROSE improves the diagnostic performance.

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          Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma.

          The 2;5 chromosomal translocation occurs in most anaplastic large-cell non-Hodgkin's lymphomas arising from activated T lymphocytes. This rearrangement was shown to fuse the NPM nucleolar phosphoprotein gene on chromosome 5q35 to a previously unidentified protein tyrosine kinase gene, ALK, on chromosome 2p23. In the predicted hybrid protein, the amino terminus of nucleophosmin (NPM) is linked to the catalytic domain of anaplastic lymphoma kinase (ALK). Expressed in the small intestine, testis, and brain but not in normal lymphoid cells, ALK shows greatest sequence similarity to the insulin receptor subfamily of kinases. Unscheduled expression of the truncated ALK may contribute to malignant transformation in these lymphomas.
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            Anaplastic lymphoma kinase (ALK) activates Stat3 and protects hematopoietic cells from cell death.

            The anaplastic lymphoma kinase (ALK) gene is characteristically translocated in Anaplastic Large Cell Lymphomas (ALCL) and the juxtaposition of the ALK gene to multiple partners results in its constitutive protein tyrosine kinase activity. We show here that expression of activated ALK induces the constitutive phosphorylation of Stat3 in transfected cells as well as in primary human ALCLs. Furthermore, immunohistochemical studies demonstrate that among distinct human B and T cell lymphomas, activation of Stat3 nuclear translocation is uniquely associated with ALK expression. NPM-ALK also binds and activates Jak3; however, Jak3 is not required for Stat3 activation or for cell transformation in vitro. Moreover, src family kinases are not necessary for NPM-ALK-mediated Stat3 activation or transformation, suggesting that Stat3 may be phosphorylated directly by ALK. To evaluate relevant targets of ALK-activated Stat3, we investigated the regulation of the anti-apoptotic protein Bcl-x(L) and its role in cell survival in NPM-ALK positive cells. NPM-ALK expression caused enhanced Bcl-x(L) transcription, largely mediated by Stat3. Increased expression of Bcl-x(L) provided sufficient anti-apoptotic signals to protect cells from treatment with specific inhibitors of the Jaks/Stat pathway or the Brc-Abl kinase. These studies support a pathogenic mechanism whereby stimulation of anti-apoptotic signals through activation of Stat3 contributes to the successful outgrowth of ALK positive tumor cells.
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              Chromosomal translocations: revisited yet again.


                Author and article information

                Respir Med Case Rep
                Respir Med Case Rep
                Respiratory Medicine Case Reports
                22 February 2020
                22 February 2020
                : 29
                [a ]Department of Pathology and Laboratory Medicine, Fundación Valle del Lili, Cali, Colombia
                [b ]Faculty of Health Sciences, Universidad Icesi, Cali, Colombia
                [c ]Department of Internal Medicine, Pulmonology Service, Interventional Pulmonology, Fundación Valle del Lili, Cali, Colombia
                [d ]Clinical Research Center, Fundación Valle del Lili, Cali, Colombia
                [e ]Department of Internal Medicine, Pulmonology Service, Fundación Valle del Lili, Cali, Colombia
                Author notes
                []Corresponding author. Department of Internal Medicine, Pulmonology Service, Interventional pulmonology, Avenida Simón Bolivar. Cra. 98 No. 18-49, Fundación Valle del Lili, Tower 6th, 4th floor, Cali, 7600032, Colombia. liliana.fernandez@
                S2213-0071(19)30388-0 101027
                © 2020 The Authors

                This is an open access article under the CC BY-NC-ND license (

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