scholarly journals Anaplastic Large-Cell Lymphoma in a Child with Type I Diabetes and Unrecognised Coeliac Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
Jemima Sharp ◽  
Barry Pizer ◽  
George Kokai ◽  
Marcus K. H. Auth
Keyword(s):  
Coeliac Disease ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Type I Diabetes ◽  
Large Cell ◽  
Lymph Node Biopsy ◽  
Hla Typing ◽  
Type I ◽  
First Case ◽  
Large Cell Lymphoma

Screening for coeliac disease is recommended for children from certain risk groups, with implications for diagnostic procedures and dietetic management. The risk of a malignant complication in untreated coeliac disease is not considered high in children. We present the case of a girl with type I diabetes who developed weight loss, fatigue, and inguinal lymphadenopathy. Four years before, when she was asymptomatic, a screening coeliac tTG test was positive, but gluten was not eliminated from her diet. Based on clinical examination, a duodenal biopsy, and an inguinal lymph node biopsy were performed, which confirmed both coeliac disease and an anaplastic large-cell lymphoma. HLA-typing demonstrated that she was homozygous for HLA-DQ8, which is associated with higher risk for celiac disease, more severe gluten sensitivity, and diabetes susceptibility. She responded well to chemotherapy and has been in remission for over 4 years. She remains on a gluten-free diet. This is the first case reporting the association of coeliac disease, type I diabetes, and anaplastic large-cell lymphoma in childhood. The case highlights the malignancy risk in a genetically predisposed individual, and the possible role of a perpetuated immunologic response by prolonged gluten exposure.

scholarly journals ALK-Negative Anaplastic Large Cell Lymphoma Presenting as Disseminated Intravascular Coagulation and Hemophagocytic Lymphohistiocytosis: A Potentially Fatal Presentation

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Uroosa Ibrahim ◽  
Amina Saqib ◽  
Maryam Rehan ◽  
Jean Paul Atallah
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Anaplastic Large Cell Lymphoma ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Lymph Node Biopsy ◽  
Intravascular Coagulation ◽  
Primary Disorder ◽  
Life Threatening ◽  
Large Cell Lymphoma

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening disorder that can be familial in etiology or a result of infections, malignancy, and autoimmune or inflammatory disorders. Disseminated intravascular coagulation (DIC) is common in patients admitted to intensive care units and can confound and delay the diagnosis of HLH. We present a case of a 69-year-old female who presented with dyspnea and malaise. Her condition declined rapidly with laboratory parameters consistent with DIC. In addition, she had a ferritin of 32,522 ng/mL, low haptoglobin, and elevated LDH, and bone marrow biopsy showed hemophagocytic lymphohistiocytes. She was started on HLH-directed therapy, and later, a diagnosis of ALK-negative anaplastic large cell lymphoma was made on an excisional inguinal lymph node biopsy specimen. Our case emphasizes the importance of prompt recognition, diagnosis, and treatment of HLH while workup for a primary disorder is still being pursued.

scholarly journals IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells

Blood ◽  
2009 ◽  
Vol 114 (2) ◽  
pp. 360-370 ◽  
Author(s):  
Ping Shi ◽  
Raymond Lai ◽  
Quan Lin ◽  
Abid S. Iqbal ◽  
Leah C. Young ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Kinase ◽  
Malignant Lymphoma ◽  
Cell Lines ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Type I ◽  
Large Cell Lymphoma

Abstract Type I insulin-like growth factor receptor (IGF-IR) tyrosine kinase plays important roles in the pathogenesis of several malignancies. Although it promotes the growth of stimulated hematopoietic cells, a direct role of IGF-IR in malignant lymphoma has not been identified. Anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma (ALK+ ALCL) is a unique type of T-cell lymphoma. Approximately 85% of ALK+ ALCL cases harbor the translocation t(2;5)(p23;q35), which generates the chimeric oncogene NPM-ALK. In the present study, we explored a possible role of IGF-IR in ALK+ ALCL. Our results demonstrate that IGF-IR and IGF-I are widely expressed in ALK+ ALCL cell lines and primary tumors. Importantly, we identified novel reciprocal functional interactions between IGF-IR and NPM-ALK. Antagonism of IGF-IR decreased the viability, induced apoptosis and cell-cycle arrest, and decreased proliferation and colony formation of ALK+ ALCL cell lines. These effects could be explained by alterations of cell survival regulatory proteins downstream of IGF-IR signaling. Our findings improve current understanding of the biology of IGF-IR and NPM-ALK and have significant therapeutic implications as they identify IGF-IR signaling as a potential therapeutic target in ALK+ ALCL and possibly other types of malignant lymphoma.

scholarly journals Breast implant-associated anaplastic large cell lymphoma in an Asian patient: The first case report from Thailand

2020 ◽  
Vol 47 (5) ◽  
pp. 478-482
Author(s):  
Peera Thienpaitoon ◽  
Wareeporn Disphanurat ◽  
Naree Warnnissorn
Keyword(s):  
Case Report ◽  
Anaplastic Large Cell Lymphoma ◽  
Breast Augmentation ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
The United States ◽  
True Incidence ◽  
First Case ◽  
Large Cell Lymphoma

Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) has received increasing interest among plastic surgeons as a long-term complication of breast augmentation. Although the prognosis is usually good, mortality is a possible outcome. Most of the cases reported in the past two decades have been from the United States, Europe, and Australia, whereas cases of BIA-ALCL in Asia remain rare. Herein, we describe the first known case of BIA-ALCL in Thailand, in which a 32-year-old woman developed BIA-ALCL 3 years after breast augmentation using textured implants. The patient underwent bilateral removal of the implants and ipsilateral total capsulectomy. This case report—the first of its kind from Thailand—should increase awareness of BIA-ALCL among plastic surgeons in Asia. The true incidence of BIA-ALCL in Asia may be underreported.

scholarly journals Breast implant-associated anaplastic large-cell lymphoma: first case detected in a Japanese breast cancer patient

Breast Cancer ◽  
2020 ◽  
Vol 27 (3) ◽  
pp. 499-504
Author(s):  
Yoko Ohishi ◽  
Aki Mitsuda ◽  
Kozue Ejima ◽  
Hidetomo Morizono ◽  
Tomoyuki Yano ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patient ◽  
Breast Cancer Patient ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
First Case ◽  
Large Cell Lymphoma

scholarly journals Molecular characterization of CD30+ anaplastic large-cell lymphoma: high frequency of c-myc proto-oncogene activation

Blood ◽  
1994 ◽  
Vol 83 (12) ◽  
pp. 3581-3590 ◽  
Author(s):  
G Inghirami ◽  
L Macri ◽  
E Cesarman ◽  
A Chadburn ◽  
J Zhong ◽  
...  
Keyword(s):  
Anaplastic Large Cell Lymphoma ◽  
Somatic Mutations ◽  
Cell Lymphoma ◽  
P53 Gene ◽  
Large Cell ◽  
The Other ◽  
Type I ◽  
Pathogenetic Mechanisms ◽  
Other Hand ◽  
Large Cell Lymphoma

Anaplastic large-cell lymphoma (ALCL) represents a morphologically distinct type of non-Hodgkin's lymphoma (NHL) characterized phenotypically by the expression of the CD30 antigen, a new member of the nerve growth factor gene family. The lymphoid origin of ALCL has been documented using immunohistochemical and molecular genetic analyses. However, very little is known so far regarding the precise pathogenetic mechanisms involved in its development and progression. Therefore, we investigated bcl-2, p53, and retinoblastoma gene (Rb) expression immunohistochemically; the occurrence of bcl-2, c-myc, and Rb gene rearrangements using Southern blotting; and the presence of ras and p53 gene somatic mutations by single-strand conformation polymorphism assay in a panel of 18 well-characterized ALCLs. In addition, the presence of Epstein-Barr (EBV) and human T-cell lymphotropic virus type I (HTLV-I) genomes were investigated using polymerase chain reaction. We identified abnormal c-myc gene products in 6 of 18 cases (33%) of ALCL. On the other hand, the bcl-2 and Rb genes were not rearranged and K-, N-, and H-ras gene somatic mutations were not found. Significant levels of p53 protein expression were found in more than 60% of ALCLs, but only a single ALCL carried a p53 gene mutation (exon 5). Only 3 ALCL cases, all occurring in human immunodeficiency virus-infected patients, were positive for EBV genomes. On the other hand, contrary to previous findings, no HTLV-I products could be identified. Despite the fact that the c-myc proto- oncogene appears to be frequently altered in ALCL, no pathognomonic abnormality could be identified and therefore additional studies and new strategies should be designed to identify the pathogenetic mechanisms involved in the development of ALCL.

Diagnosing a Rare Cutaneous Presentation of Anaplastic Large Cell Lymphoma

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Barr D ◽  
◽  
Maslov D ◽  
Goel R ◽  
Field H ◽  
...  
Keyword(s):  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Lymph Node Biopsy ◽  
Cutaneous Lesions ◽  
Anaplastic Lymphoma ◽  
Uncommon Presentation ◽  
Counter Medication ◽  
Large Cell Lymphoma ◽  
Multifocal Disease

Anaplastic Large Cell Lymphoma (ALCL) is a rare aggressive neoplasm. Rapid and progressive lymphadenopathy is common. Due to its aggressive nature, two-thirds of initial presentations are in stage III or IV. Multifocal disease that is primarily cutaneous is rare and extracutaneous spread of the cancer occurs in up to 13 percent of cases. In this case, a patient with systemic ALCL went undiagnosed for two months across three hospitalizations. A 33-year old male presented with multiple cutaneous lesions that had erupted bilaterally on his lower extremities and a fever which was unresponsive to over the counter medication. The patient required three hospitalizations and extensive work up before a diagnosis of Anaplastic Lymphoma Kinase (ALK) -negative CD30+ T-cell lymphoma was made by skin and lymph node biopsy. Diagnosis was delayed due to this patient’s uncommon presentation, the broad list of differential diagnoses, inaccuracies in biopsy, and communication delays from multiple hospital visits. This patient had aggressive ALCL and passed away during the first week of chemotherapy treatment. When there is a concern for malignancy, properly performed biopsies are important to collect from appropriate sites with non-necrotic tissue. Additionally, this case demonstrates the consequences of inadequate communication during handoff between transfer centers. It is important to have a broad differential diagnosis as well as prompt investigation and constant communication between all providers involved when a patient presents with abnormal and aggressively progressing symptoms.

scholarly journals Molecular characterization of CD30+ anaplastic large-cell lymphoma: high frequency of c-myc proto-oncogene activation

Blood ◽  
1994 ◽  
Vol 83 (12) ◽  
pp. 3581-3590 ◽  
Author(s):  
G Inghirami ◽  
L Macri ◽  
E Cesarman ◽  
A Chadburn ◽  
J Zhong ◽  
...  
Keyword(s):  
Anaplastic Large Cell Lymphoma ◽  
Somatic Mutations ◽  
Cell Lymphoma ◽  
P53 Gene ◽  
Large Cell ◽  
The Other ◽  
Type I ◽  
Pathogenetic Mechanisms ◽  
Other Hand ◽  
Large Cell Lymphoma

Abstract Anaplastic large-cell lymphoma (ALCL) represents a morphologically distinct type of non-Hodgkin's lymphoma (NHL) characterized phenotypically by the expression of the CD30 antigen, a new member of the nerve growth factor gene family. The lymphoid origin of ALCL has been documented using immunohistochemical and molecular genetic analyses. However, very little is known so far regarding the precise pathogenetic mechanisms involved in its development and progression. Therefore, we investigated bcl-2, p53, and retinoblastoma gene (Rb) expression immunohistochemically; the occurrence of bcl-2, c-myc, and Rb gene rearrangements using Southern blotting; and the presence of ras and p53 gene somatic mutations by single-strand conformation polymorphism assay in a panel of 18 well-characterized ALCLs. In addition, the presence of Epstein-Barr (EBV) and human T-cell lymphotropic virus type I (HTLV-I) genomes were investigated using polymerase chain reaction. We identified abnormal c-myc gene products in 6 of 18 cases (33%) of ALCL. On the other hand, the bcl-2 and Rb genes were not rearranged and K-, N-, and H-ras gene somatic mutations were not found. Significant levels of p53 protein expression were found in more than 60% of ALCLs, but only a single ALCL carried a p53 gene mutation (exon 5). Only 3 ALCL cases, all occurring in human immunodeficiency virus-infected patients, were positive for EBV genomes. On the other hand, contrary to previous findings, no HTLV-I products could be identified. Despite the fact that the c-myc proto- oncogene appears to be frequently altered in ALCL, no pathognomonic abnormality could be identified and therefore additional studies and new strategies should be designed to identify the pathogenetic mechanisms involved in the development of ALCL.

scholarly journals Breast erythema and nodular skin metastasis as the first manifestation of breast implant-associated anaplastic large cell lymphoma

Rare Tumors ◽  
2021 ◽  
Vol 13 ◽  
pp. 203636132110284
Author(s):  
Noellie Ducastel ◽  
Ioana-Mariana Cimpean ◽  
Ivan Theate ◽  
Olivier Vanhooteghem
Keyword(s):  
T Lymphocyte ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Breast Implants ◽  
Large Cell ◽  
First Case ◽  
Nodular Lesions ◽  
Large Cell Lymphoma ◽  
The Right

Anaplastic large cell lymphoma (BIA-ALCL) associated with rough textured breast implants was first reported in 1997. It is a non-Hodgkin’s lymphoma originating from a T lymphocyte which occurs on average 10.9 years after placement of the breast implant. BIA-ALCL mainly manifests as a periprosthetic seroma or a mass adjacent to the implant. To our knowledge, we describe the first case of BIA-ALCL with initial presentation by indurate erythematous plates located in both breasts and the progressive appearance of several asymptomatic metastatic nodular lesions that have been appearing on the right arm some weeks later.

scholarly journals Analysis of the Molecular Signature of the Breast Implant-Associated Anaplastic Large Cell Lymphoma in an Asian Patient

2020 ◽  
Author(s):  
Il-Kug Kim ◽  
Ki Yong Hong ◽  
Choong-kun Lee ◽  
Bong Gyu Choi ◽  
Hyunjong Shin ◽  
...  
Keyword(s):  
T Cells ◽  
Anaplastic Large Cell Lymphoma ◽  
Molecular Mechanisms ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Breast Implants ◽  
Large Cell ◽  
Genetic Characteristics ◽  
First Case ◽  
Large Cell Lymphoma

Abstract Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL)—a new category of anaplastic large cell lymphoma associated with textured breast implants—has a distinct variation in incidence and is especially rare in Asia. We report the first case of BIA-ALCL in Korea and present its histological and genetic characteristics. A 44-year-old female patient presented with a typical clinical course and symptoms, including breast augmentation with textured breast implants, late-onset peri-implant effusion, and CD30 +ALK − histology, followed by bilateral implant removal and total capsulectomy. For histological analysis, we performed immunohistochemistry of the bilateral breast capsules. For transcriptome analysis, we identified highly upregulated gene sets using RNA-seq and characterized the lymphoma immune cell components. In the lymphoma-associated capsule, CD30 + cells infiltrated not only the lymphoma lesion but also the peritumoral lesion. The morphologies of the myofibroblasts and vessels in the peritumoral lesion were similar to those in the tumoral lesion. We observed strong activation of the JAK/STAT3 pathway and expression of programmed death ligand-1 (PD-L1) in the lymphoma. Unlike the molecular profiles of BIA-ALCL samples from Caucasian patients—all of which contained activated CD4 + T cells—the Asian patient’s profile was characterized by more abundant CD8 + T cells. This study contributes to a better understanding of the pathogenesis and molecular mechanisms of BIA-ALCL in Asian patients that will ultimately facilitate the development of clinical therapies.

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