We report a 53-year-old man presenting with a sore throat, chest pain, and dysphagia. We diagnosed phlegmonous esophagogastritis. Contrast-enhanced CT revealed diffuse thickening of the esophagus and stomach wall with an intramural low-density area surrounded by peripheral rim enhancement. On postcontrast CT, the cranial side of the abscess was continuous with the pharyngeal submucosa, suggesting the source of the inflammation. Upper gastrointestinal endoscopy demonstrated purulent material draining from esophageal and gastric ulcers. Acute phlegmonous esophagogastritis is a rare disorder characterized by diffuse infiltration of inflammatory cells to the submucosa of the esophagus and stomach. Detecting a connection of esophageal lesion with the pharynx may lead to a better clinical assessment of the disease.

We herein described a female patient in her 60s with metastatic breast cancer who concomitantly developed stage IV follicular lymphoma (FL). Lymph node biopsy revealed FL grade 3A histopathology. Lymphoma cells were positive for CD10, CD20, CD79a, BCL2, and BCL6 and negative for CD3. G-banding and fluorescence in situ hybridization showed a major cytogenetic clone marked with t(14;18)(q32;q21)/IGH::BCL2 and a minor clone with a 3-break translocation, t(3;14;18)(q27;q32;q21), involving BCL6, IGH, and BCL2. We amplified the DNA fragments encompassing the BCL2::IGH and BCL6::IGH junctions by a long-distance polymerase chain reaction and found that the former fragment comprised sequences of the far 3′ major breakpoint region cluster of BCL2 followed by IGHJ6 and those of IGHG1, while the latter fragment comprised sequences of the major translocation cluster of BCL6 and those of IGHG2. In der(3)t(3;14;18), the coding exons of BCL2 and BCL6 aligned in the same transcriptional orientation and the intronic Eμ enhancer of IGH was present between the two genes. We proposed that t(3;14;18) was generated by two-step translocations and BCL2::IGH and BCL6::IGH involved the same IGH allele.

The anaplastic lymphoma kinase gene (ALK) is located at chromosome 2p23 and encodes a transmembrane receptor tyrosine kinase. As a result of chromosomal translocation/inversion, the 3′ sequence of ALK fuses to the 5′ sequence of a partner gene, producing an oncogenic chimeric protein that activates downstream signal transduction pathways. ALK fusion genes are found in diverse tumor types of different lineages, including hematological neoplasms. ALK-positive (ALK+) anaplastic large cell lymphoma (ALCL) is a distinct subtype of peripheral T-cell lymphoma that is characterized by the expression of CD30 and ALK by immunohistochemistry (IHC). Approximately 70 to 80% of ALK+ ALCL cases have t(2;5)(p23;q35)/NPM1::ALK associated with the nuclear/cytoplasmic ALK IHC staining pattern. In the remaining cases, ALK fuses to various partner genes and ALK staining pattens vary with these partners. ALK+ large B-cell lymphoma (LBCL), accounting for <1% of all diffuse large B-cell lymphoma cases, is characterized by an immunoblast/plasmablast-like cytomorphology. ALK+ LBCL cases with t(2;17)(p23;q23)/CLTC::ALK show the cytoplasmic granular pattern of ALK IHC. Acute myeloid leukemia (AML) harboring inv(2)(p23q13)/RANBP2::ALK defines a small subset of AML characterized by monocytic differentiation and monosomy 7. Extramedullary plasmacytoma/multiple myeloma with the ALK fusion gene shares cytomorphological and immunophenotypic features with ALK+ LBCL. ALK+ histiocytosis is an emerging rare histiocytic entity and most cases carry KIF5B::ALK. The antibody-drug conjugate, brentuximab vedotin, which targets cell-surface CD30, is approved for the treatment of ALK+ ALCL as a single agent or in combination with other cytotoxic agents in both the front-line and relapsed/refractory (R/R) settings. R/R ALK+ hematological neoplasms respond well to first- to third-generation ALK tyrosine kinase inhibitors and an optimal treatment strategy including these novel agents is being tested.