Significance of oncogenes and tumor suppressor genes in AML prognosis

Kavianpour, Maria; Ahmadzadeh, Ahmad; Shahrabi, Saeid; Saki, Najmaldin

doi:10.1007/s13277-016-5067-1

Cited by 31 publications

(29 citation statements)

References 131 publications

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“…Tumor suppressor genes have been well documented as cell division regulators that control protein expression. A mutation of these anti-oncogenes may affect cell proliferation, cell cycle and apoptosis, which is then likely to trigger the onset of a specific type of cancer (53). In cancer tissues, abnormal cell growth is mainly caused by the inactivation or lack of tumor suppressor genes (54).…”

Section: Resultsmentioning

confidence: 99%

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Voltage-gated calcium channels: Novel targets for cancer therapy

et al. 2017

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Voltage-gated calcium channels (VGCCs) comprise five subtypes: The L-type; R-type; N-type; P/Q-type; and T-type, which are encoded by α1 subunit genes. Calcium ion channels also have confirmed roles in cellular functions, including mitogenesis, proliferation, differentiation, apoptosis and metastasis. An association between VGCCs, a reduction in proliferation and an increase in apoptosis in prostate cancer cells has also been reported. Therefore, in the present study, the online clinical database Oncomine was used to identify the alterations in the mRNA expression level of VGCCs in 19 cancer subtypes. Overall, VGCC family genes exhibited under-expression in numerous types of cancer, including brain, breast, kidney and lung cancers. Notably, the majority of VGCC family members (CACNA1C, CACNA1D, CACNA1A, CACNA1B, CACNA1E, CACNA1H and CACNA1I) exhibited low expression in brain tumors, with mRNA expression levels in the top 1–9% of downregulated gene rankings. A total of 5 VGCC family members (CACNA1A, CACNA1B, CACNA1E, CACNA1G and CACNA1I) were under-expressed in breast cancer, with a gene ranking in the top 1–10% of the low-expressed genes compared with normal tissue. In kidney and lung cancers, CACNA1S, CACNA1C, CACNA1D, CACNA1A and CACNA1H exhibited low expression, with gene rankings in the top 1–8% of downregulated genes. In conclusion, the present findings may contribute to the development of new cancer treatment approaches by identifying target genes involved in specific types of cancer.

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Section: Resultsmentioning

confidence: 99%

“…Tumor suppressor genes are also a type of cell growth inhibitor and suppress tumor formation genes. Tumor suppressor genes are also under-expressed or downregulated in tumor tissues compared with normal tissue (53). …”

Section: Resultsmentioning

confidence: 99%

Voltage-gated calcium channels: Novel targets for cancer therapy

et al. 2017

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“…In AML, IDH1 and IDH2 mutations are found in about 10%-30% of patients, with a higher frequency in patients with cytogenetically normal AML (CN-AML) [18]. Prognosis of patients harboring mutations in IDH1 and IDH2 is generally poor [7], with an increased probability of relapse [28]. Prognosis could be even worse, with a decreased overall survival (OS), when patients bear other mutations, such as NPM1, FLT3, DNMT3A, ASXL1, RUNX1, and NRAS.…”

Section: Idh1 and Idh2 Mutationsmentioning

confidence: 99%

“…They occur early during the pathogenesis and could collaborate with other mutations to promote different hematological cancers [53]. TET2 mutations are associated with CN-AML or intermediate-risk cytogenetic abnormalities and with increased age, higher WBC and blast counts, low platelet count and FLT3-ITD, NPM1 and ASXL1 mutations, but are mutually exclusive with IDH1 and IDH2 mutations [7,53]. Clearly, different combinations of TET2 and other gene mutations will foresee different outcomes, and the prognostic value of TET2 mutations remain controversial [60].…”

Section: Tet2 Mutationsmentioning

confidence: 99%

“…Though in recent years improvements in therapies led to more favorable prognosis for younger patients, in the elderly the outcome still remains adverse [5]. In most cases AML appears as a de novo disease, but it can also occurs in patients with a previously diagnosed hematological disorder, such as myelodysplastic syndromes (MDSs) or Philadelphia-negative myeloproliferative neoplasms (Ph − MPNs) [6], and in these cases it is usually more resistant to conventional chemotherapy treatments [7]. The pathogenesis of AML shows an excessive proliferation, reduced differentiation and decreased apoptosis of stem cells of myeloid lineage [6,8].…”

Section: Introductionmentioning

confidence: 99%

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Landscape of Tumor Suppressor Mutations in Acute Myeloid Leukemia

Panuzzo

Signorino

Calabrese

et al. 2020

JCM

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Acute myeloid leukemia is mainly characterized by a complex and dynamic genomic instability. Next-generation sequencing has significantly improved the ability of diagnostic research to molecularly characterize and stratify patients. This detailed outcome allowed the discovery of new therapeutic targets and predictive biomarkers, which led to develop novel compounds (e.g., IDH 1 and 2 inhibitors), nowadays commonly used for the treatment of adult relapsed or refractory AML. In this review we summarize the most relevant mutations affecting tumor suppressor genes that contribute to the onset and progression of AML pathology. Epigenetic modifications (TET2, IDH1 and IDH2, DNMT3A, ASXL1, WT1, EZH2), DNA repair dysregulation (TP53, NPM1), cell cycle inhibition and deficiency in differentiation (NPM1, CEBPA, TP53 and GATA2) as a consequence of somatic mutations come out as key elements in acute myeloid leukemia and may contribute to relapse and resistance to therapies. Moreover, spliceosomal machinery mutations identified in the last years, even if in a small cohort of acute myeloid leukemia patients, suggested a new opportunity to exploit therapeutically. Targeting these cellular markers will be the main challenge in the near future in an attempt to eradicate leukemia stem cells.

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Oncogenes and tumor suppressor genes: functions and roles in cancers

Dakal,

Dhabhai,

Pant

et al. 2024

MedComm

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Cancer, being the most formidable ailment, has had a profound impact on the human health. The disease is primarily associated with genetic mutations that impact oncogenes and tumor suppressor genes (TSGs). Recently, growing evidence have shown that X‐linked TSGs have specific role in cancer progression and metastasis as well. Interestingly, our genome harbors around substantial portion of genes that function as tumor suppressors, and the X chromosome alone harbors a considerable number of TSGs. The scenario becomes even more compelling as X‐linked TSGs are adaptive to key epigenetic processes such as X chromosome inactivation. Therefore, delineating the new paradigm related to X‐linked TSGs, for instance, their crosstalk with autosome and involvement in cancer initiation, progression, and metastasis becomes utmost importance. Considering this, herein, we present a comprehensive discussion of X‐linked TSG dysregulation in various cancers as a consequence of genetic variations and epigenetic alterations. In addition, the dynamic role of X‐linked TSGs in sex chromosome–autosome crosstalk in cancer genome remodeling is being explored thoroughly. Besides, the functional roles of ncRNAs, role of X‐linked TSG in immunomodulation and in gender‐based cancer disparities has also been highlighted. Overall, the focal idea of the present article is to recapitulate the findings on X‐linked TSG regulation in the cancer landscape and to redefine their role toward improving cancer treatment strategies.

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Significance of oncogenes and tumor suppressor genes in AML prognosis

Cited by 31 publications

References 131 publications

Voltage-gated calcium channels: Novel targets for cancer therapy

Voltage-gated calcium channels: Novel targets for cancer therapy

Landscape of Tumor Suppressor Mutations in Acute Myeloid Leukemia

Oncogenes and tumor suppressor genes: functions and roles in cancers

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