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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the pathogenesis and progression of several cancers. However, the potential effect of MALAT1 in primary gastrointestinal diffuse large B-cell lymphoma (PGI-DLBCL) has not been elucidated. This study aimed to explore the prognostic value of MALAT1 in patients with PGI-DLBCL. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the expression of MALAT1 in 90 patients with PGI-DLBCL. MALAT1 was remarkably upregulated in PGI-DLBCL tissues compared to paired adjacent non-tumor tissues (P < 0.001), and the area under the receiver operating characteristic (ROC) curve (AUC) was 0.838. MALAT1 expression was further increased in the non-germinal center B-cell-like (non-GCB), advanced stage (stages IIE-IV) and International Prognostic Index (IPI) score (3–5) groups (P = 0.01, P < 0.001 and P < 0.001, respectively). Furthermore, Kaplan–Meier analysis showed that elevated MALAT1 expression correlated with inferior overall survival (OS) and progression-free survival in PGI-DLBCL patients (P < 0.001 and P < 0.001, respectively), and our multivariate analysis results suggested that upregulation of MALAT1 and high IPI score (3–5) were two unfavorable prognostic factors for PGI-DLBCL. In conclusion, our results demonstrate that MALAT1 may serve as a novel prognostic biomarker and an ideal therapeutic target for patients with PGI-DLBCL. [ABSTRACT FROM AUTHOR]

Napsin A is widely used in the diagnosis of lung adenocarcinoma and has also been reported to be positive in cases of thyroid carcinomas. We investigated napsin A levels through immunohistochemistry on whole sections of 210 primary thyroid tumors of various subtypes and another 41 metastatic thyroid carcinomas, and compared these with 125 primary and 25 metastatic lung adenocarcinomas. The results showed that napsin A was expressed in 23.8% thyroid tumors and 30.3% papillary thyroid carcinomas. Most cases showed a focal and weak to moderate expression. In comparison, 80.8% primary lung adenocarcinomas expressed napsin A, with mostly diffused and strong expression. For metastatic carcinomas of thyroid and lung origin, napsin A was detected in 39.0% of thyroid carcinomas in contrast to 88.0% in cases of lung adenocarcinomas. Comparisons of additional markers, TTF-1, CK7, thyroglobulin, and Pax-8 in metastatic carcinomas showed the overlapping expression of immunomarkers of TTF-1 and CK7. Thyroglobulin and Pax-8 were useful for distinguishing between metastatic carcinomas; however, Pax-8 may be a superior marker due to its higher sensitivity. The clinicopathological analysis of papillary thyroid carcinomas showed that the expression of napsin A was positively correlated with lymph node metastasis (p = 0.030). Here, we focused on the expression of napsin A in thyroid tumors and compared it with that in lung adenocarcinomas. The expression of napsin A is common in thyroid tumors and the combined expression of napsin A and TTF-1 in a metastatic thyroid carcinoma is a cause for concern due to chances of misdiagnosis as lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

The long-term survival of patients with acute myeloid leukemia (AML) is dismally poor. A permanent cure of AML requires elimination of leukemic stem cells (LSCs), the only cell type capable of initiating and maintaining the leukemic clonal hierarchy. We report a therapeutic approach using an activating monoclonal antibody directed to the adhesion molecule CD44. In vivo administration of this antibody to nonobese diabetic-severe combined immune-deficient mice transplanted with human AML markedly reduced leukemic repopulation. Absence of leukemia in serially transplanted mice demonstrated that AML LSCs are directly targeted. Mechanisms underlying this eradication included interference with transport to stem cell–supportive microenvironmental niches and alteration of AML-LSC fate, identifying CD44 as a key regulator of AML LSCs. The finding that AML LSCs require interaction with a niche to maintain their stem cell properties provides a therapeutic strategy to eliminate quiescent AML LSCs and may be applicable to other types of cancer stem cells. [ABSTRACT FROM AUTHOR]