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HNT-34

Cat.No.: CSC-C0601

Source: acute myeloid leukemia

Morphology: round cells growing singly and in clusters in suspension

Culture Properties: suspension

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Cat.No.
CSC-C0601
Description
Established in 1994 from the peripheral blood of a 47-year-old woman with acute myeloid leukemia (AML FAB M4) secondary to previous myelodysplastic syndromes (MDS), specifically chronic myelomonocytic leukemia (CMML); described to carry the t(3;3)(q21;q26) leading to MECOM (EVI1) overexpression and the Philadelphia chromosome t(9;22) expressing both P190 and P210 BCR-ABL1 chimeric transcripts
Source
acute myeloid leukemia
Recommended Medium
Culture Properties
suspension
Morphology
round cells growing singly and in clusters in suspension
Karyotype
Human flat-moded near-diploid karyotype with 7% polyploidy; 46(44-48)<2n>XX, t(3;3)(q21;q26), t(9;22)(q34;q11), del(17)( ?p12.2p13.1), del(20)(q13.1q13.2); t(3;3) and t(9;22) effect rearrangement of MECOM (EVI1) and BCR-ABL1, respectively; matches publish
Quality Control
Mycoplasma: negative in microbiological culture, PCR assays
Immunology: CD3 -, CD4 +, CD13 +, CD15 +, CD19 -, CD33 +, CD34 +, HLA-DR +
Viruses: PCR: EBV -, HBV -, HCV -, HIV -, HTLV-I/II -, SMRV -
Storage and Shipping
Frozen with 70% medium, 20% FBS, 10% DMSO
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

HNT-34 was established from the peripheral blood of a 45-year-old female patient with acute myeloid leukemia (AML) transformed from chronic myelomonocytic leukemia (CMMoL) with 3q21q26 syndrome. Morphologically, HNT-34 cells are undifferentiated blasts which were negative for myeloperoxidase. HNT-34 cells are positive for CD4, CD13, CD33 and CD34, but negative for CD41a and CD42b. The cells actively proliferated in suspension with a doubling time of 26-27h in the absence of any growth factors. Neither proliferative advantage nor differentiation was observed with the addition of G-CSE GM-CSF, IL-3, TPO, DMSO or PMA.

The establishment of HNT-34 provides a valuable model for studying the biology of myeloid leukemia, exploring the mechanisms of leukemogenesis, and evaluating treatment strategies. At present, the research and application of HNT-34 are mainly focused on studying the efficacy of new anticancer drugs, understanding the mechanisms of drug resistance, and revealing the role of gene mutations in treatment response. HNT-34 has also been used to investigate the impact of the tumor microenvironment on leukemia progression, making it an important tool to advance our understanding of myeloid leukemia and improve clinical outcomes for patients.

NRIP1 Knockdown Affects Proliferation, Viability, and Response to Retinoic Acid in Chromosome 3 Rearranged Acute Myeloid Leukemia Cells

Aberrant expression of Ecotropic Viral Integration Site 1 (EVI1) is a hallmark of acute myeloid leukemia (AML) with inv(3) or t(3;3), which is a disease subtype with especially poor outcome. In studying transcriptomes from AML patients with chromosome 3q rearrangements, we identified a significant upregulation of the Nuclear Receptor Interacting Protein 1 (NRIP1) as well as its adjacent non-coding RNA LOC101927745. NRIP1 knockdown negatively affects the proliferation and survival of 3q-rearranged AML cells and increases their sensitivity to all-trans retinoic acid, suggesting that NRIP1 is relevant for the pathogenesis of inv(3)/t(3;3) AML and could serve as a novel therapeutic target in myeloid malignancies with 3q abnormalities.

The retinoic acid receptor co-factor NRIP1 is uniquely upregulated and represents a therapeutic target in acute myeloid leukemia with chromosome 3q rearrangements.Fig. 1. Knockdown of NRIP1 induces apoptosis and increases sensitivity to all-trans retinoic acid in t(3;3) acute myeloid leukemia cells (Grasedieck, Sarah, et al. 2021).

Differential Nucleolar Stress Response in NPM1-Mutated Versus NPM1 wild-type AML cells

Acute myeloid leukemia (AML) with mutated NPM1 accounts for one-third of newly diagnosed AML. Despite recent advances, treatment of relapsed/refractory NPM1-mutated AML remains challenging, with the majority of patients eventually dying due to disease progression. Dactinomycin is a low-cost chemotherapeutic agent, which has been anecdotally reported to induce remission in NPM1-mutated patients, although its mechanism of action remains unclear. To explore whether NPM1-mutated cells may have lower thresholds for nucleolar stress response than NPM1 wild-type cells, we exposed to dactinomycin OCI-AML3 and IMS-M2 cells as well as OCI-AML2 and HNT-34 cells, all of which have detectable TP53 levels by western blot. We found that low-dose dactinomycin generates more efficient stress response in cells expressing NPM1 mutant compared to wild-type cells, suggesting that NPM1-mutated AML may be more sensitive to nucleolar stress.

Western blot analysis of TP53, NPM1mut, wild-type NPM1 (WT NPM1), P21, and PARP in OCI-AML3, IMS-M2, OCI-AML2, and HNT-34 cells treated with dactinomycin.Fig. 2. NPM1mut facilitates nucleolar stress response to dactinomycin (Gionfriddo, Ilaria, et al. 2021).

What is a karyotype of a tumor cell that can be characterized?

Cancer karyotypes can be distinguished by the level of their complexity, varying from the presence of only one abnormal chromosome in the diploid set of chromosomes up to very complex karyotypes with almost every chromosome structurally rearranged and/or present in abnormal quantity.

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Average Rating: 5.0    |    1 Scientist has reviewed this product

Consistent results

We have received consistent results with this tumor cell product, giving us confidence in our research findings.

10 Mar 2023


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