Sea-blue histiocytosis in a patient with acute myeloid leukemia with myelodysplasia-related changes harboring isolated trisomy 9: pathognomonic or a coincidence?

Although isolated trisomy 9, a form of chromosome aneuploidy, is rare in acute myeloid leukemia (AML), up to 30 cases of AML involving isolated trisomy 9 have been reported to date. We report the case of a 77-year-old female with AML, in which trisomy 9 was detected as an isolated aberration. In addition, the patient's bone marrow displayed so-called sea-blue histiocytosis. The accumulation of further cases of isolated trisomy 9-harboring AML involving sea-blue histiocytosis is necessary to determine whether the coexistence of these findings is pathognomonic or a coincidence.

[Bacteremia Due to Edwardsiella tarda Emerging after Chemotherapy for Recurrent Ph-Positive Acute Lymphoblastic Leukemia].

We report the case ofa 76-year-old man who had bacteremia due to Edwardsiella tarda during the course ofchemotherapy, including ponatinib, for the treatment of recurrent Philadelphia-positive acute lymphoblastic leukemia. Treatment with cefepime improved his general condition. The number ofreported cases ofbacteremia due to Edwardsiella tarda is limited. Further accumulation ofcases is necessary to obtain accurate data such as the risk factors of Edwardsiella tarda bacteremia.

An isolated der(1;21)(q10;q10) translocation in a patient with myelodysplastic syndrome: a case report.

Whole-arm translocations are relatively rare among hematological malignancies. There are a few reports on myeloid malignancies harboring der(1;21)(q10;q10). A 65-year-old male was referred to our hospital due to squamous cell carcinoma of the lung. Pembrolizumab monotherapy resulted in progression, and so chemotherapy involving nab-paclitaxel and carboplatin was administered thereafter. The patient developed cytopenia, and his bone marrow exhibited dysplasia. Chromosomal analysis revealed a whole-arm translocation, der(1;21)(q10;q10). Thus, the patient was diagnosed with myelodysplastic syndrome. The der(1;21)(q10;q10) translocation is a rare variant of the der(1;7)(q10;p10) translocation, which is an adverse prognostic factor for myeloid neoplasms. Clarifying the clinical features of myeloid neoplasms in patients with der(1;21)(q10;q10) would facilitate the elucidation of their tumorigenic mechanisms.

[Septic shock due to Citrobacter braakii following high-dose cytosine arabinoside therapy in a patient with acute myeloid leukemia].

Here, we report a case of a 67-year-old man who had septic shock due to Citrobacter braakii infection during the course of chemotherapy with high-dose cytosine arabinoside for acute myeloid leukemia. Treatment with cefepime rapidly improved his condition. The number of reported cases of sepsis due to Citrobacter braakii is limited. Further accumulation of cases is necessary to obtain accurate data such as the risk factors for Citrobacter braakii infections.

Trisomy 6 as the sole stemline abnormality in a patient with acute monocytic leukemia: a case report.

It is rare for trisomy 6 to occur as the sole autosomal anomaly in hematological malignancies, but this finding has been reported to be associated with a hypoplastic bone marrow. We report the case of a 75-year-old male with acute monocytic leukemia, in which trisomy 6 was detected as the sole stemline abnormality. We also summarize the 26 published cases of acute myeloid leukemia involving isolated trisomy 6.

A Rare t(5;11)(q35;q13) Translocation in an Elderly Patient With Acute Myeloid Leukemia With Maturation: A Case Report.

The t(5;11)(q35;q13) reciprocal translocation is a rare chromosomal abnormality that can arise in myeloid neoplasms, mainly in children and younger adults. Here, we report a case of acute myeloid leukemia with maturation, involving an 85-year-old, in which the tumor cells harbored the t(5;11)(q35;q13) chromosomal abnormality. We also address the diagnostic and immunophenotypic characteristics of acute myeloid leukemia involving t(5;11)(q35;q13), along with a review of the literature.

Therapy-related myelodysplastic syndrome: a case study.

We present a case of therapy-related myelodyspastic syndrome in which the t(3;8)(q26;q24) translocation appeared, even though no chromosomal abnormalities were found at the initial diagnosis of acute myeloid leukemia. To the best of our knowledge, there have only been around 20 reported cases of myeloid malignancies involving t(3;8)(q26;q24). We discuss the characteristics of t(3;8)(q26;q24) along with a review of literature.

Inhibition of Stabilin-2 elevates circulating hyaluronic acid levels and prevents tumor metastasis.

Hyaluronic acid (HA) has been implicated in the proliferation and metastasis of tumor cells. However, most previous studies were conducted on extracellular matrix or pericellular HA, and the role of circulating HA in vivo has not been studied. HA is rapidly cleared from the bloodstream. The scavenger receptor Stabilin-2 (Stab2) is considered a major clearance receptor for HA. Here we report a dramatic elevation in circulating HA levels in Stab2-deficient mice without any overt phenotype. Surprisingly, the metastasis of B16F10 melanoma cells to the lungs was markedly suppressed in the Stab2-deficient mice, whereas cell proliferation was not affected. Furthermore, administration of an anti-Stab2 antibody in Stab2(+) mice elevated serum HA levels and prevented the metastasis of melanoma to the lung, and also suppressed spontaneous metastasis of mammary tumor and human breast tumor cells inoculated in the mammary gland. Administration of the antibody or high-dose HA in mice blocked the lodging of melanoma cells to the lungs. Furthermore, HA at high concentrations inhibited the rolling/tethering of B16 cells to lung endothelial cells. These results suggest that blocking Stab2 function prevents tumor metastasis by elevating circulating HA levels. Stab2 may be a potential target in antitumor therapy.

[A case report of conversion therapy for initially unresectable colorectal cancer liver metastases after cetuximab as third-line treatment].

The introduction of monoclonal antibodies into the treatment protocols for metastatic colorectal cancer(mCRC)has significantly improved outcomes. There are some patients with mCRC, initially judged unresectable, who become resectable after chemotherapy. For patients with isolated liver metastases, surgical resection is recommended when feasible. We experienced a case in which an initially unresectable mCRC liver metastases converted into a resectable one after cetuximab monotherapy as third-line treatment. The sample from hepatectomy was a pathologically complete response; no remnants were detected. The management of liver metastases contributes to improvements in the clinical setting. For conducting a multimodal treatment of mCRC, the participation of various specialists such as medical oncologists, colorectal/hepaticsurgeons and diagnostic/therapeutic radiologists is indispensable. Furthermore, it is necessary to construct an evidence-based consensus on potentially resectable CRC liver metastases in each hospital.

Junctional adhesion molecule-A, JAM-A, is a novel cell-surface marker for long-term repopulating hematopoietic stem cells.

Junctional adhesion molecule-A (JAM-A/JAM-1/F11R) is a cell adhesion molecule expressed in epithelial and endothelial cells, and also hematopoietic cells, such as leukocytes, platelets, and erythrocytes. Here, we show that JAM-A is expressed at a high level in the enriched hematopoietic stem cell (HSC) fraction; that is, CD34(+)c-Kit(+) cells in embryonic day 11.5 (E11.5) aorta-gonod-mesonephros (AGM) and E11.5 fetal liver (FL), as well as c-Kit(+)Sca-1(+)Lineage(-) (KSL) cells in E14.5 FL, E18.5FL, and adult bone marrow (BM). Although the percentage of JAM-A(+) cells in those tissues decreases during development, the expression in the HSC fraction is maintained throughout life. Colony-forming assays reveal that multilineage colony-forming activity in JAM-A(+) cells is higher than that in JAM-A(-) cells in the enriched HSC fraction in all of those tissues. Transplantation assays show that long-term reconstituting HSC (LTR-HSC) activity is exclusively in the JAM-A(+) population and is highly enriched in the JAM-A(+) cells sorted directly from whole BM cells by anti-JAM-A antibody alone. Together, these results indicate that JAM-A is expressed on hematopoietic precursors in various hematopoietic tissues and is an excellent marker to isolate LTR-HSCs.