scholarly journals Patient-Physician Communication in Acute Myeloid Leukemia and Myelodysplastic Syndrome

2021 ◽  
Vol 17 (1) ◽  
pp. 264-270
Author(s):  
Emanuela Morelli ◽  
Olga Mulas ◽  
Giovanni Caocci
Keyword(s):  
Acute Myeloid Leukemia ◽  
Acute Myeloid Leukaemia ◽  
Myelodysplastic Syndrome ◽  
Myeloid Leukaemia ◽  
Myeloid Leukemia ◽  
Patient Communication ◽  
Communication Styles ◽  
Physician Relationship ◽  
The Impact ◽  
Acute Myeloid

Introduction: An effective communication is an integral part of the patient-physician relationship. Lack of a healthy patient-physician relationship leads to a lower level of patient satisfaction, scarce understanding of interventions and poor adherence to treatment regimes. Patients need to be involved in the therapeutic process and the assessment of risks and perspectives of the illness in order to better evaluate their options. Physicians, in turn, must convey and communicate information clearly in order to avoid misunderstandings and consequently poor medical care. The patient-physician relationship in cancer care is extremely delicate due to the complexity of the disease. In cancer diagnosis, the physician must adopt a communicative approach that considers the psychosocial factors, needs and patient’s preferences for information,which in turn all contribute to affect clinical outcomes. Search Strategy and Methods : This review was conducted using the Preferred Reporting Items for Systematic and Meta-analyses (PRISMA) statement. We included studies on the importance of physician-patient communication in Acute Myeloid Leukaemia and Myelodysplastic Syndrome care. We searched PubMed, Web of Sciences, Scopus, Google scholar for studies published from December 1 st , 2020 up to March 1 st , 2021. Using MeSH headings, we search for the terms “Physician and patient communication AND Acute Myeloid leukemia” or “Myelodysplastic syndrome” or “Doctor” or “Clinician”, as well as variations thereof . Purpose of the Review : This review examines the progress in communication research between patient and physician and focuses on the impact of communication styles on patient-physician relationshipin hematologic cancers, including Acute Myeloid Leukaemia and Myelodysplastic Syndromes.

scholarly journals Preferential transcription of the mutated allele in NPM1 mutated acute myeloid leukaemia

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
G. D. Bailey ◽  
L. Doolan ◽  
A. Baskar ◽  
L. C. Smith ◽  
C. H. Seedhouse
Keyword(s):  
Acute Myeloid Leukemia ◽  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Myeloid Leukemia ◽  
Splice Variants ◽  
Wild Type ◽  
Significant Bias ◽  
Acute Myeloid

Abstract Nucleophosmin is commonly both over-expressed and mutated in acute myeloid leukemia (AML). NPM1 mutations are always heterozygous. In addition, NPM1 has a number of different splice variants with the major variant encoded by exons 1–9 and 11–12 (NPM1.1). Further variants include NPM1.2 which lacks exons 8 and 10 and NPM1.3 which comprises exons 1–10 (and so lacks the region of sequence mutated in AML). In this study we quantified the expression of these three variants in 108 AML patient samples with and without NPM1 mutations and also assessed the level of expression from the wild-type and mutant alleles in variants NPM1.1 and NPM1.2. The results show that NPM1.1 is the most commonly expressed variant, however transcripts from wild-type and mutated alleles do not occur at equal levels, with a significant bias toward the mutated allele. Considering the involvement of mutant nucleophosmin in the progression and maintenance of AML, a bias towards mutated transcripts could have a significant impact on disease maintenance.

Roles of TET2 and C-CBL Mutations In the Progression of De Novo Myelodysplastic Syndrome to Acute Myeloid Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4019-4019
Author(s):  
Hsiao-Wen Kao ◽  
Seishi Ogawa ◽  
Masashi Sanada ◽  
Der-Cherng Liang ◽  
Chang-Liang Lai ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myelodysplastic Syndrome ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Mutational Analysis ◽  
Conflicts Of Interest ◽  
Direct Sequencing ◽  
Increased Risk ◽  
The Impact ◽  
Acute Myeloid

Abstract Abstract 4019 Background. The molecular pathogenesis of myelodysplastic syndrome (MDS) and its role in the progression to secondary acute myeloid leukemia (sAML) remain to be further explored. Somatic TET2 and C-CBL mutations have recently been described in myeloid neoplasms including MDS and sAML. Most studies of TET2 or C-CBL mutations were carried out separately either at MDS or at sAML phases. There was also a discrepancy in the results of the impact of TET2 and C-CBL mutations on outcome of MDS patients. Aims. We aimed (1) to correlate the TET2 and C-CBL mutations with clinicohematological features and outcome, and (2) to determine the role of TET2 or C-CBL gene mutations in sAML derived from MDS. Materials and Methods. Bone marrow (BM) samples from 161 MDS patients (3 RCUD, 1 RARS, 36 RCMD, 118 RAEB, 1 MDS5q-, 2 MDS-U) at initial diagnosis were analyzed for both TET2 and C-CBL mutations; 49 of them had matched paired sAML BM samples available for comparative analysis. Mutational analysis was performed by DHPLC and/or direct sequencing of all RT-PCR or DNA-PCR products amplified with different primer pairs covering the whole coding sequences of TET2 and exons 7 to 9 of C-CBL. Results. The frequency of TET2 and C-CBL mutations in 161 MDS patients was 17.9 % and 1.9 %, respectively. Seven patients with polymorphism/germ line mutations or missense mutations outside of BOX 1 or 2 of TET2 gene were excluded. Of the 26 patients with 38 TET2 mutations, 14 had nonsense, 11 missense, 11 frameshift, 1 deletion, and 1 splice site mutations; 12 of them had double mutations. Three patients had C-CBL mutations (Y371S, F418S and G415S) at MDS phase. No patient had coexistence of TET2 and C-CBL mutations. TET2 mutations were significantly associated with increased risk of AML transformation (P= 0.037), whereas C-CBL mutations did not influence the risk of AML transformation (P=0.335). Patients carrying TET2 mutations had a trend of shorter time to sAML compared with those without TET2 mutations (estimated median time to sAML 8.7 months vs 15.0 months, P=0.067). Except for lower platelet count in patients with TET2 mutations (P=0.038), there were no significant differences in clinicohematological features including age, sex, hemoglobin level, white blood cell count, percentage of blasts in BM or peripheral blood, cytogenetics or IPSS (≤1.5 vs ≥2.0) between patients with and without TET2 or C-CBL mutations. No significant differences were found in overall survival with respect to mutation status of TET2 (P= 0.244) or C-CBL (P= 0.646). Of the 49 paired BM samples, 3 patients harboring C-CBL mutations at MDS phase retained the identical mutations and another 3 acquired C-CBL mutations (L370_Y371 ins L, L399V and C416W) during sAML evolution. There was an increased risk of acquiring C-CBL mutations during AML transformation (odds ratio=4.16, P=0.041), whereas TET2 mutation patterns remained unchanged and none acquired or lost TET2 mutations in sAML progression. Conclusions. Our results showed an increased risk of acquiring C-CBL mutations during sAML transformation. TET2 mutations played a role as an initial event in the development of MDS in a subset of patients and were associated with more frequent and rapid sAML evolution. Supported by grants NHRI-EX99-9711SI, NSC97-2314-B-182-011-MY3 and DOH99-TD-C-111-006. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Bridging-to-transplant with azacitidine for myelodysplastic syndrome and acute myeloid leukemia, reduces the incidence of acute graft-versus-host disease

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Koichi Murakami ◽  
Hironori Ueno ◽  
Takashi Okabe ◽  
Toshiya Kagoo ◽  
Saigen Boku ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myelodysplastic Syndrome ◽  
Graft Versus Host Disease ◽  
Myeloid Leukemia ◽  
Host Disease ◽  
Graft Versus Host ◽  
Pre Treatment ◽  
Bridging To Transplant ◽  
The Impact ◽  
Acute Myeloid

Allogeneic stem cell transplantation (allo-SCT) is the only curative option for myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Azacitidine (AZA) has a good toxicity profile compared with intensive chemotherapy and can be considered a pre-transplant regimen in elderly patients and in patients with comorbidities. To investigate the impact of pre-transplant AZA on patient outcome after allo-SCT, we conducted a retrospective analysis of AZA pre-treatment followed by allo-SCT in patients with high-risk MDS and AML. Twenty patients who were divided into two groups according to AZA treatment given prior to allo-SCT (AZA <em>vs</em> non- AZA group, 10 each). Overall survival, event-free survival and incidence of chronic graft-versus-host disease (GVHD) were not significantly different between the two groups. The overall incidence of grade II to IV acute GVHD in the AZA group was significantly lower than that in the non-AZA group (P=0.004). Bridging to transplant with AZA should be considered as an immunomodulator and effective treatment strategy for patients with MDS and AML.

scholarly journals Familiáris myelodysplasiás szindróma és akut myeloid leukaemia klinikai és genetikai háttere

2016 ◽  
Vol 157 (8) ◽  
pp. 283-289
Author(s):  
Péter Attila Király ◽  
Krisztián Kállay ◽  
Dóra Marosvári ◽  
Gábor Benyó ◽  
Anita Szőke ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myelodysplastic Syndrome ◽  
Myeloid Leukaemia ◽  
Myeloid Leukemia ◽  
Genetic Basis ◽  
Increased Risk ◽  
Platelet Disorder ◽  
Telomere Biology ◽  
Familial Platelet Disorder ◽  
Acute Myeloid

Myelodysplastic syndrome and acute myeloid leukaemia are mainly sporadic diseases, however, rare familial cases exist. These disorders are considered rare, but are likely to be more common than currently appreciated, and are characterized by the autosomal dominant mutations of hematopoietic transcription factors. These syndromes have typical phenotypic features and are associated with an increased risk for developing overt malignancy. Currently, four recognized syndromes could be separated: familial acute myeloid leukemia with mutated CEBPA, familial myelodysplastic syndrome/acute myeloid leukemia with mutated GATA2, familial platelet disorder with propensity to myeloid malignancy with RUNX1 mutations, and telomere biology disorders due to mutations of TERC or TERT. Furthermore, there are new, emerging syndromes associated with germline mutations in novel genes including ANKRD26, ETV6, SRP72 or DDX41. This review will discuss the current understanding of the genetic basis and clinical presentation of familial leukemia and myelodysplasia. Orv. Hetil., 2016, 157(8), 283–289.

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