TACC3 expression as a prognostic factor in aggressive types of adult T‐cell leukemia/lymphoma patients

Abstract

Adult T-cell leukemia/lymphoma (ATLL) is a malignant peripheral T-cell neoplasm associated with human T-cell leukemia virus type-1 (HTLV-1). Approximately 10 to 20 million people are infected with HTLV-1 worldwide, with at least 1 million of these infections occurring in Japan. Approximately 1000 HTLV-1 carriers develop ATLL each year after an incubation period of several decades. 1,2 Based on clinical and laboratory findings, ATLL is classified into four clinical subtypes: acute, lymphoma, chronic, and smoldering. The acute and lymphoma subtypes are regarded as aggressive ATLLs; therefore, patients diagnosed with these subtypes undergo several intensive rounds of chemotherapy and stem cell transplantation. 3,4 Diagnosis at an older age is identified as a poor prognostic factor in

Elevated expression of transforming acidic coiled‐coil‐containing protein 3 (TACC3) reflects aggressiveness of primary central nervous system lymphomas

“…6 Previously, authors also revealed that TACC3 overexpression contributes to the aggressiveness of ATLL. 16 In this study, on PCNSLs, TACC3 expression was not associated with p53 and Ki-67 expression, and clinical factors. In addition, p53 and Ki-67 expression did not affect patient prognosis.…”

“…[1][2][3][4][5] Besides this, microtubule/centrosome defects cause chromosomal instability, and are associated with neoplastic processes. 2,3,[6][7][8][9][10][11][12][13][14][15][16][17] In fact, high expression of TACC3 and poor patient prognosis have been demonstrated in non-small cell lung cancer (NSCLC), esophageal carcinoma, hepatocellular carcinoma, gastric carcinoma, soft tissue sarcomas (STS), osteosarcoma, prostate carcinoma, adult T-cell leukemia/lymphoma (ATLL) and rectal carcinoma. [6][7][8][9][10][11][14][15][16][17] However, Lauffart et al showed in ovarian surface epithelial tumors that TACC3 expression was lost in 67.7% of tumors, and suggested that TACC3 gene mutation, mislocalization or loss might serve as alternative mechanisms of functional inactivation of GATA4/6 and BRCA1, leading to dedifferentiation and malignant transition.…”

“…Deficiency of TACC3 leads to growth retardation and embryonic fatality during embryonic development due to a malfunction of differentiation, and induces dysfunction of p53‐mediated apoptosis 1–5 . Besides this, microtubule/centrosome defects cause chromosomal instability, and are associated with neoplastic processes 2,3,6–17 . In fact, high expression of TACC3 and poor patient prognosis have been demonstrated in non‐small cell lung cancer (NSCLC), esophageal carcinoma, hepatocellular carcinoma, gastric carcinoma, soft tissue sarcomas (STS), osteosarcoma, prostate carcinoma, adult T‐cell leukemia/lymphoma (ATLL) and rectal carcinoma 6–11,14–17 .…”

Expression of telomerase reverse transcriptase in peripheral T‐cell lymphoma

“…PTCL-NOS and ATLL cases were included in our previous studies. [16][17][18][19][20][21] All cases were reviewed by experienced hematopathologists (O. K., M. H.) according to the World Health Organization classification. 22 Clinical information was collected by reviewing the patients' medical charts.…”

Emerging Therapeutic Landscape of Peripheral T-Cell Lymphomas Based on Advances in Biology: Current Status and Future Directions

“…Activating mutations in NOTCH1 occur in approximately 30% of ATLL cases, whereas the expression of FBXW7 mutations occur in 25% of cases [52]. TACC3, vital for microtubule growth during cell division, is an independent prognostic factor for poor OS [53]. The hepatocyte growth factor may activate the c-Met pathway in an autocrine manner and confer aggressiveness to lymphomatous ATLL [54].…”