This review aims to provide comprehensive and practical information on the once-nearly-forgotten but now resurgent roles and trends of autologous transplantation in leukemias. We seek to categorize when it is necessary as a first-line treatment (plasma cell leukemia) and to identify well-defined patient subgroups (such as certain types with intermediate prognosis in AML, APL second remission, etc.) in which autologous transplantation might be comparably or even slightly more effective than allogeneic transplantation, not only in frail patients. In some leukemias, such as CLL, autologous transplantation still does not play a role. Attempts to achieve anti-leukaemic effects in autologous settings have proven largely ineffective, but new approaches might be promising. Newer cell therapies (such as CAR-T) are significantly more effective, and the same applies to in vitro graft purging. However, this area has been investigated relatively recently in an innovative manner, using specific graft pretreatments that may also stimulate anti-leukemic immune responses in autologous cases.

Background: This review aims to provide a comprehensive and practical overview of the evolving role of autologous transplantation in leukaemias, a strategy that was once largely abandoned but has recently regained interest in selected clinical settings. Methods: We reviewed the historical development of autologous transplantation in acute leukaemias, including the early period during which autologous transplantation was considered inferior to allogeneic approaches because of limited graft purification techniques and the inability to induce effective graft-versus-leukaemia (GVL)-like immune responses. We further summarise more recent experimental strategies aimed at improving stem cell purification and enhancing anti-leukaemic immune activity in autologous settings. In addition, we discuss how advances in measurable residual disease (MRD) assessment and molecular risk stratification have contributed to the renewed interest in autologous transplantation in selected subgroups of leukaemia patients. Results: This review identifies clinical situations in which autologous transplantation remains an important therapeutic option, including plasma cell leukaemia, where it continues to represent a standard first-line approach. We also discuss well-defined patient subgroups, particularly selected AML subtypes with intermediate-risk molecular profiles and acute promyelocytic leukaemia (APL) in second remission, in which outcomes following autologous transplantation may be comparable to, or occasionally superior to, those achieved with allogeneic transplantation. In contrast, autologous transplantation currently plays only a limited role in diseases such as chronic lymphocytic leukaemia (CLL) and chronic myeloid leukaemia (CML). Although attempts to induce potent anti-leukaemic immune effects in autologous settings have so far shown limited clinical efficacy, several emerging strategies appear promising and may further expand the role of autologous transplantation, particularly in elderly or frail patients. Discussion: Overall, current molecular and MRD-based risk stratification strategies, together with emerging immunological and graft-manipulation approaches, may redefine the role of autologous transplantation as a personalised therapeutic option in selected subgroups of leukaemia patients.

Immune checkpoint inhibitor-induced immune thrombocytopenia (ICI-ITP) is a rare but severe adverse event that may lead to bleeding complications and may require therapeutic changes or interventions. The clinical condition and interventions are highly complex; there are certainly tumour-type and combination-therapy differences, as well as individual ICI-agent factors that modify the risk of thrombocytopenia. ICI-ITP shares some common features, even though its pathogenesis differs markedly from that of traditional ITP. However, ICI-ITP is a clinically important complication; a deeper analysis of factors related to ICI–platelet interactions is also necessary. White blood cell–lymphocyte and platelet count ratios may have prognostic value in predicting the development of a low platelet count. Platelet counts themselves might influence the effectiveness of ICI-type anticancer interventions by facilitating T-cell-induced neoexpression of PD-1 on platelet surfaces. Baseline platelet counts and immunoglobulin levels may also modify treatment outcomes. Platelet activation can also promote immune-related adverse events. ICI-induced ITP-like syndrome’s prognostic factors are not only experimental facts but also clinically important. The connections among platelet counts, activation, immunoglobulins, and cell ratios are likely important factors influencing ICI-induced ITP risk reduction and the improvement of tumour-directed immune response by tailoring ICI selection to tumour type and specific baseline cellular characteristics.

Sickle cell disease homozygotes are the most exposed to mainly vaso-occlusive, infective hazards and complications, compared to other hemoglobinopathies. The expected lifespan is about 20 years shorter in sickle cell disease affected Afro-Americans comparing to others of the same population but not affected by the disease. The well-known hematological manifestations are early cerebrovascular and cardiovascular events, vaso-occlusive crises, hypo-asplenia, multiple infections, miscarriage, etc. The medical care is extremely complex, needs multidisciplinary approach therefore expertized centers are needed. The highest incidence of the disease in Sub-Saharan Africa and in the USA, but it might appear in any other countries. A comprehensive care including recent innovative therapies (e.g. gene modification) have promising results to prolong survival and better life quality. Orv Hetil. 2025; 166(39): 1531–1537.

A sarlósejtes anaemia homozigóta formában súlyos betegség, amely az élettartamot az afroamerikai populációban évtizedekkel ezelőtt még jelentősen megrövidítette. Ez a haemoglobinopathia jár az ismert hematológiai eltérések közül a legtöbb, vascularis talajon kialakuló idegrendszeri, cardiovascularis, pulmonalis, renalis, infektív és mozgásszervi szövődménnyel, ezért összehangolt és integrált szoros együttműködést kíván a hematológus, a belgyógyász, a kardiológus, az ideggyógyász, a szemész, a szülész és a gyermekgyógyász részéről. A multidiszciplináris megközelítés és a génmódosító kezelések az utóbbi időben javították a túlélést és az életminőséget. Afrika és az Amerikai Egyesült Államok mellett számos eltérő fejlettségű országban is sok, sarlósejtes anaemiában szenvedő beteggel lehet találkozni. A hazánkban tanuló vagy munkát vállaló személyek között is találkozhatunk a betegséggel, ezért indokolt a legújabb eredmények áttekintése. Orv Hetil. 2025; 166(39): 1531–1537.

Aims:The aim is to focus on the risk of transfusion-transmitted diseases, which are emerging in highly vulnerable conditions, especially in hazardous disorders such as sickle cell disease, certain clinical situations, and transplantations. Transplant settings demand even greater vigilance in donor selection, blood preparation, and pathogen screening. They may also involve new lifestyle considerations for the safe selection of organ or stem cell donors—a deeper consideration is mandatory regarding the hepatitis E virus and vidarabine resistance in these high-risk patient groups.Clinical settings: This brief review highlights a high-risk group for bloodborne infections, their transfusion needs, and the criteria for transfusion. The most significant topic is arguably a complex and severe haemoglobinopathy, sickle cell disease (SCD), which requires repeated and frequent transfusions for critically essential reasons, particularly because sickling prevention, splenic function, and immune defence are often impaired. Some pathogens, such as parvovirus B19, pose particular risks in SCD.Bone marrow and solid organ transplantation as potential transmission routes during and after the procedure will also be examined, emphasising more recent data across various transplant scenarios.

Background: Due to the different genetic properties of malignant neoplasms and their tendency to cause the formation of blood clots, the risk of these complications is much higher than in the general population. There is even a higher risk of blood clots forming during chemotherapy or hormone therapy for cancer. Aim: This paper will summarise publications to gain a better understanding of the risks of blood clots associated with checkpoint inhibitors and CAR-T cell therapy of cancer. The review will also address potential problems and guide how to address them. Even when used on their own, checkpoint inhibitors can cause blood clots, albeit at a lower rate than chemotherapy; however, this assumption has not been definitively proven, as ICI-type agents are rarely given to cancer patients as monotherapy (or if given, these cancers baseline thrombogenicity is less active sui generis). The incidence of these problems varies depending on the type of disease, patient characteristics and somewhat on immunotherapeutic drug selection itself. It is important to inform doctors who prescribe these treatments of this fact and try to provide ideas which may help make good individual decisions. The anticoagulant prophylaxis is probably indicated in many such cases, even with monotherapy in cancer. However, still on a somewhat individual basis, as prospective, multicentre, double blind trials are not available, recommendations are based on some rather anecdotal, or retrospective data in respect of disease type, treatment and patient characteristics and the selection of an optimal anticoagulant prophylactic approach.

Despite the availability of many novel therapies for multiple myeloma, it remains an incurable disease with relapse fated in almost all patients. In the era of modern agents, second autologous stem cell transplantation still holds its role in patients relapsing after first-line autologous transplant. The authors reviewed a single-center experience with a second auto-SCT for relapsed multiple myeloma. Thirty patients had received a salvage auto-SCT at the institution. The median follow-up after diagnosis was 86 months, and the median time between transplants was 59.1 months. Response before second ASCT was the following: CR – 11 cases, VGPR – 9 cases, PR – 10 cases. Most patients received reduced dose (140 mg/m2) of melphalan as a conditioning regimen for the second auto-SCT. Treatment-related mortality was 3%. With a median follow-up time of 34 months after the second transplant, median progression-free survival was 24 months. The median PFS in the patients achieving CR or VGPR at day 100 after the second transplantation was 32 months. By 15 months, all patients achieved only partial remission progressed, with a median PFS of 8.5 months. During the follow-up period, no MDS or AML developed, and the frequency of second malignancy was also low, 3%. In conclusion, second autologous stem cell transplantation is a well-tolerated and effective treatment option for relapsed multiple myeloma in selected patients, though with a shorter PFS than in first remission.

Signaling pathways of Retinoblastoma (Rb) protein, Akt-kinase, and Erk-kinase (extracellular signal-regulated kinase) have an important role in the pathogenesis of acute myeloid leukemia. Constitutive activation of these proteins by phosphorylation contributes to cell survival by regulation of cell cycle, proliferation and proapoptotic signaling processes. According to previous data phosphorylated forms of these proteins represent a worse outcome for cancer patients. We investigated the presence of phosphorylated Rb (P-Rb), Akt (P-Akt) and Erk (P-Erk) proteins by Western blot technique using phospho-specific antibodies in bone marrow or peripheral blood samples of 69 AML patients, 36 patients with myelodysplastic syndrome (MDS) and 10 healthy volunteers. Expression level of PTEN (Phosphatase and tensin homolog) and PHLPP (PH domain and leucine-rich repeat Protein Phosphatase) phosphatases, the negative regulators of Akt kinase pathway were also examined. We tested the effect of these proteins on survival and on the correlation with known prognostic features in AML. We found 46.3% of AML patients had detectable P-Rb, 34.7% had P-Akt and 28.9% had P-Erk protein. 66.1% of patients expressing PTEN, 38.9% PHLPP, 37.2% both PTEN and PHLPP and 32.2% neither PTEN nor PHLPP phosphatases. Compared to nucleophosmin mutation (NPMc) negative samples P-Erk was significantly less in nucleophosmin mutated patients, P-Rb was significantly less in patients’ group with more than 30 G/L peripheral leukocyte count by diagnosis. PHLPP was significantly present in FAB type M5. The expression of P-Rb represented significant better overall survival (OS), while P-Akt represented significantly worse event-free survival (EFS) in unfavorable cytogenetics patients. The presence of both PHLPP and PTEN phosphatases contributes to better OS and EFS, although the differences were not statistically significant. We confirmed significant positive correlation between P-Akt and PHLPP. Assessing the phosphorylation of Rb, Akt and Erk may define a subgroup of AML patients who would benefit especially from new targeted treatment options complemented the standard chemotherapy, and it may contribute to monitoring remission, relapse or progression of AML.

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma. The disease is very heterogeneous, with distinct genetic alterations in subtypes. The WHO 2022 5th edition classification identifies several minor groups of large B-cell lymphoma where the pathogenetic role of viruses (like EBV and HHV-8) is identified. Still, most cases fall into the group of DLBCL not otherwise specified (NOS). No review focuses only on this specific lymphoma type in the literature. The pathogenesis of this entity is still not fully understood, but several viruses and bacteria may have a role in the development of the disease. The authors review critical pathogenetic events in the development of DLBCL (NOS) and summarize the data available on several pathogenetic viruses and bacteria that have a proven or may have a potential role in the development of this lymphoma type. The possible role of B-cell receptor signaling in the microenvironment is also discussed. The causative role of the Epstein–Barr virus (EBV), human herpesvirus-8 (HHV-8), Hepatitis C virus (HCV), human immunodeficiency virus (HIV), Hepatitis B virus (HBV), and other viruses are explored. Bacterial infections, such as Helicobacter pylori, Campylobacter jejuni, Chlamydia psittaci, Borrelia burgdorferi, and other bacteria, are also reviewed.

Objective: The Hungarian National Registry for Philadelphia chromosome negative myeloproliferative neoplasms was used to analyse the thromboembolic events (TE) of Hungarian patients with polycythemia vera (PV).Methods: Data from 351 JAK2 V617F-positive patients diagnosed with PV were collected online from 15 haematology centres reporting clinical characteristics, therapeutic interventions and thromboembolic events. TE events were evaluated before and after diagnosis based upon the Landolfi and Tefferi risk assessment scales.Results: TE were reported on 102 patients before diagnosis and 100 during the follow-up period. Comparing to the frequency of major arterial events before PV diagnosis, we can notice a decreasing tendency after diagnosis: from 12.3% to 2.6% (p < .00003). There was no significant change in the rate of major venous events (from 5.1% to 8.5%; p = .1134) or minor arterial events (from 11.7% to 17.4%; p = .073). Bleeding events were recorded in 5.7% of patients. Despite treatment with HU + ASA, 44 patients (43.1%) with prior TE had recurrent thromboembolic complications. The particular analysis of our data revealed a new TE scoring system based on: age, gender, previous TE and iron deficiency at the time of diagnosis.Conclusions: Our registry enables characterisation of patients with PV. The high level of recurrent TE events highlights the need for more effective and risk-adapted therapy.

A terhességi vagy gesztációs thrombocytopenia gyakori eltérés, többnyire nem igényel beavatkozást, társulhat cholestasisszal (laboratóriumi jelekkel és viszketéssel), ismételt terhességnél pedig többnyire újra, hamarabb vagy jelentősebb mértékben lép fel, és a thrombocytopenia általában nem igényel a gondos követésen túl külön beavatkozást. A gesztációs thrombocytopenia a terhesség első felében csekély mértékű, a harmadik trimeszter végére jelentősebb, de az esetek több mint 95%-ában nem éri el a 100 G L −1 alatti értéket. Ha a thrombocytaszám 100 G L −1 alatti, vagy egyéb társuló tünetek indokolják, fontos a differenciáldiagnosztika, amelynek során több, komoly intervenciót igénylő eltérést számításba jöhet, mint a toxaemia-praeccalampsia (HELLP szindróma), akut terhességi zsírmáj, de novo immun thrombocytopeniás purpura vagy relapszus, antifoszfolipid szindróma, congenitalis vagy akut thrombotikus mikroangiopathia, disszeminált intravaszkuláris koaguláció. Ezek többnyire jellegzetes időpontban lépnek fel és sajátos klinikai tünetekkel társulnak, a diagnózisnak megfelelően kezelendők. A súlyossá váló gesztációs thrombocytopenia, azaz ha társuló tünetek nélkül a harmadik trimeszterben 100 G L −1 alatti thrombocytaszám jelenik meg, összetett kérdés, etiológiai vizsgálatok indokoltak, a terápia gyakran empirikus, de az esetek túlnyomó többsége jól befolyásolható, azonban oki kapcsolat főként az immun thrombocytopeniás purpura és thrombotikus mikroangiopathia tekintetében különösen izgalmas kérdés.

Transfusion medicine is traditionally a strong/fundamental part of clinical practice, saving hundreds of millions of lives. However, blood-borne or transmitted infections are a well-known and feared possibility, a risk we relentlessly mitigate. Pathogens are continuously and rather quickly changing, so during the last decade, many, sometimes exotic, new pathogens and diseases were recorded and analyzed, and some of them were proved to be transmitted with transfusions. Blood or blood component transfusions are carried out after cautious preparative screening and inactivation maneuvers, but in some instances, newly recognized agents might escape from standard screening and inactivation procedures. Here, we try to focus on some of these proven or potentially pathogenic transfusion-transmitted agents, especially in immunocompromised patients or bone marrow transplantation settings. These pathogens are sometimes new challenges for preparative procedures, and there is a need for more recent, occasionally advanced, screening and inactivation methods to recognize and eliminate the threat a new or well-known pathogen can pose. Pathogen transmission is probably even more critical in hemophiliacs or bone marrow transplant recipients, who receive plasma-derived factor preparations or blood component transfusions regularly and in large quantities, sometimes in severely immunosuppressed conditions. Moreover, it may not be emphasized enough that transfusions and plasma-derived product administrations are essential to medical care. Therefore, blood-borne transmission needs continued alertness and efforts to attain optimal benefits with minimized hazards.

Treating relapsed and refractory diffuse large B-cell lymphoma is still challenging for clinicians, but the available CAR-T and bispecific antibodies have revolutionized therapy. Autologous stem cell transplantation was the most effective treatment modality previously. The authors reported data from a single center over ten years. The retrospective study included 116 patients, with 53 relapsed cases, 39 primary refractory cases, 19 who had CNS involvement, and 5 who had received primary consolidation transplants. The median duration of follow-up was 46 months. The median event-free survival was 75 months, and the median overall survival was 105 months for all cases. Five-year overall survival was 59%, and event-free survival was 54%. Pretreatment prognostic factors at diagnosis had no effect on the outcome of transplantation. The authors found no difference between survival in relapsed or refractory cases, and the number of salvage lines or the germinal center/activated B-cell type also did not influence the results. Complete metabolic response before transplantation confirmed by 18FDG PET/CT strongly affected survival. The pre-transplant creatinine and CRP levels significantly influenced the long-term outcome. The number of stem cells infused did not affect survival, but engraftment within nine days did result in a longer survival. These data support the finding that the response to salvage therapy did facilitate the identification of a better prognostic group who may still benefit from autologous transplantation.

The scenario of immune pathomechanism-based first- and second-line therapies of immune thrombocytopenia (i.e., immunosuppression, splenectomy) substantially changed approximately more than 20 years ago, giving place and important role for thrombopoietin analogs in steroid refractory cases, positioning splenectomy as third-line intervention. Although this approach became dominant and powerful, refractory cases urged the search for further medications. More recently, the traditional immunological approach received more attention again, and new targets were determined: (1) shortening selectively IgG life span and clearance, (2) modifying complement system in an effort to reduce antibody binding to platelet surface, (3) cell signaling pathway modification efforts to reduce antiplatelet phagocytic events, mainly spleen tyrosine kinase and Bruton tyrosine kinase inhibitory compounds. These new agents seem to be capable alone and probably in different combinations and sequence of increasing platelet count even in thrombopoietin analog refractory adult chronic thrombocytopenic purpura cases. These promising approaches probably will bring new treatment schedules in the adult chronic thrombocytopenic purpura field quite soon, and the scenario moves back to the refreshed immunological basis rewriting many elements of the therapeutic algorithm of thrombocytopenic purpura.

Több mint 20 éve következett be a második szemléletváltás a krónikus felnőttkori idiopathiás thrombocytopeniás purpura (immunthrombocytopenia) kezelésében, amikor felismerték az amúgy megakaryocytás, de a fokozott thrombocytapusztulást mégsem eléggé ellensúlyozó csontvelői thrombocytaképzés serkentésének fontosságát. A thrombopoetinanalógok beléptek a klinikai alkalmazásba, gyorsan átírták az algoritmust, a splenectomia mára a harmadik vonalba került. Ezen paradigmaváltást az egyik szerző 20 éve ebben a folyóiratban is ismertette. Időközben sok tapasztalat gyűlt össze a thrombopoetinanalógok alkalmazásával, nagy előnyeivel, de azzal is, hogy még ezek sem oldanak meg minden terápiás gondot. Ez az útkeresés visszakanyarodott az eredeti antitestindukált immunthrombocytopenia irányba, azaz az immunmoduláns közelítésmódra. Ebben 3 fő irányzat látszik olyan mértékben ígéretesnek, hogy a közeljövőben be fognak épülni a klinikai gyakorlatban a szteroid/TPO-analóg refrakter vagy más, nehezebb idiopathiás thrombocytopeniás purpura esetek ellátási rendjébe. Ezen irányok: (1) szelektív IgG-anyagcsere (clearance)-gyorsítók, (2) komplementmódosítás a thrombocytafelszíni immunglobulin-kötődés csökkentésére, (3) ezen immunfolyamat jelátviteli útjának megváltoztatása tirozin-kináz- (elsősorban lép-tirozin-kináz- és Bruton-tirozin-kináz-) gátlással. Ezen elemek egymagukban, együtt, illetve a jelen modalitásokhoz kapcsolódóan átrajzolhatják az idiopathiás thrombocytopeniás purpura kezelési algoritmusait a közeljövőben, amire ez a közlemény kívánja felhívni a figyelmet. Orv Hetil. 2022; 163(38): 1514–1519.

Autologous hematopoietic stem cell transplantation (HSCT) is often complicated by hemostatic and thrombotic events associated with endothelial cell injury. Thrombotic complications are affected by a disturbed balance between platelets, circulating von Willebrand factor (VWF), and its specific protease, ADAMTS13. HSCT-associated endothelial dysfunction, impaired hemostasis, and inflammation are interrelated processes, and research on the complex interplay of conditioning regimens from engraftment to bone marrow regeneration remains intensive. This prospective observational study comparing lymphoma and multiple myeloma (MM) patients who underwent autologous HSCT explored how platelet count, VWF level, ADAMTS13 activity, and C-reactive protein (CRP) level as potential markers (1) vary in response to therapy, (2) differ between the 2 groups, and (3) correlate with the remission state at 100 days after HSCT. We correlated the quantitative changes in platelet count and levels of VWF, ADAMTS13, and CRP with one another during HSCT and in the remission state in 45 patients with lymphoma and 59 patients with MM who underwent autologous HSCT between 2010 and 2013 at the University of Debrecen. Samples were collected at the start of conditioning chemotherapy, on the day of stem cell transplantation, and at 5, 11, and 100 days following HSCT. CRP levels peaked when platelet counts dropped to a minimum, and these changes were much more pronounced in the lymphoma group. VWF level was the highest, with lower ADAMTS13 activity, at platelet engraftment in both patient groups equally. Diagnostic evidence indicative of thrombotic complications was not found. In the lymphoma group, VWF level prior to conditioning had statistically significant correlations with platelet count, CRP level, and hemoglobin concentration at the time of bone marrow regeneration (P < .001) and during the remission state (P = .034). In the MM group, platelet count before conditioning was correlated with platelet count (P < .001) and white blood cell count (P = .012) at the time of bone marrow regeneration. The statistically significant correlation of the markers at the time of bone marrow regeneration with the preconditioning VWF levels in lymphoma and with the preconditioning platelet counts in MM might indicate the clinical significance of the bone marrow niches of arterioles and megakaryocytes, respectively, where the stem cells are located and regulated. Because preconditioning VWF levels are associated with remission after HSCT in lymphoma patients, VWF should be screened before conditioning, along with the markers used in HSCT protocols, to optimize personalized treatment and reduce therapeutic risks.(c) 2022 The American Society for Transplantation and Cellular Therapy. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Összefoglaló. Az áttekintő közlemény foglalkozik a legfontosabb olyan helyzetekkel, amely a koronavírus-betegség (COVID–19) pandémia idején a kemo- és biológiai terápiás irányelvek változását érinti leukémiában, lymphomákban, csontvelő-transzplantációs helyzetekben. Külön figyelmet kell fordítani és eltérő teendőket kell megfogalmazni a kezelési fázisok, például indukció, konszolidáció, fenntartó és egyéb kezelésmódok tekintetében. Nagy figyelmet érdemelnek a nemzetközi ajánlások, de egyben finom értékelést is kívánnak bizonyos gyógyszerek esetében, például monoklonális antitestek, szteroidok, innovatívabb akut leukémiás szerek, kolóniastimuláló faktorok, JAK2-gátlók, interferonok, tirozin-kináz-gátlók stb. esetében. Foglalkozunk a nemzetközi csontvelő-transzplantációval kapcsolatos ajánlásokkal. Mindent nagyban befolyásol az aktuális COVID-pandémiás helyzet. Természetesen foglalkozunk a vakcináció kérdéseivel is onkohematológiai kórképekben. A COVID és az onkohematológia viszonyrendszere a gyakorlati cselekvések terén még mindig tanuló fázisban van, meg kell találni az összhangot a pandémia és a klinikai gyakorlat összehangolása tekintetében. A gyorsan változó COVID-helyzet megkívánja, hogy ismereteinket és cselekvéseinket napi szinten frissen tartsuk, a szokásosnál többet támaszkodjunk a tapasztalatokra, s figyeljünk oda a standard publikációk mellett a hitelesnek vélt, s a helyzet miatt elengedhetetlenül szükséges, gyorsan kommunikált állásfoglalásokra is. Summary. A brief analysis of international recommendations and applicable clinical decisions are summarized regarding the clinical care of oncohaematological patients in the era of COVID-19 pandemic. General precautionary measures are extremely important. Special attention is paid to different groups of patients (i.e. leukaemias, lymphomas, transplant situations), along with analysing different treatment phases, e.g. watch and wait, induction, consolidation, maintenance, etc. Some recommendations are really remarkable with some drugs and protocols, however they do need fine tuning and careful individual decisions, e.g. monoclonal antibodies, steroids, some innovative agents in acute myeloid leukaemia, colony stimulation, ATRA based therapies, some 2nd line tyrosine kinase inhibitors in chronic myeloid leukaemia, etc. Some aspects of international COVID-19 specific transplantational guidelines are also covered. Vaccination recommendations and experience are also in the focus. It may not be stressed enough, that we are still in the learning phase of harmonization of COVID-19 pandemic and oncohaematology care, this is still a moving target, depending a lot on actual pandemic situation and periods. Considering ever changing COVID situation one should follow peer reviewed publications as before, but of course frequently review new COVID statements, in an effort to preserve, maintain efficiency of endangered oncohaematological care.

Chronic myeloid leukemia is still the most characteristic entity of the chronic myeloproliferative diseases. The tumor promoter role of able-dependent tyrosine kinase activation, which is enhanced by bcr/abl rearrangement (due the classical translocation of Philadelphia chromosomal abnormality) has been quite well clarified. The better understanding of the role of altered cell signalling pathways in the pathogenesis of chronic myeloid leukaemia opened new areas for extensive and fruitful pharmacological research. The first, non-myelosuppressive agent, which was able to reduce the number of Philadelphia positive clonal cells was the interferon group, which drug could substantially prolong the chronic phase and mortality of chronic myeloid leukaemia. Imatinib mesylate, a tyrosine-kinase inhibitor seems to be able to produce clinical and major cytogenetic response in more than 80% of patients. Imatinib is also a powerful agent in the accelerated or blastic phased of chronic myeloid leukaemia. With the advent of these new drugs the therapeutic algorithm of chronic myeloid leukaemia and allogenous bone marrow transplantation seems to be reconsidered, too.

Increased red blood cell count may result from primary erythrocytosis (polycythemia vera), but it is often due to secondary causes with increased erythropoietin levels. Secondary erythrocytosis may also be congenital due to different gene mutations of hemoglobin, hemoglobin stabilization proteins, EPO receptors, or oxygen sensing pathways. Von Hippel- Lindau gene mutation causes altered tissue oxygen sensation in VHL disease, usually with normal hemoglobin. Germline VHL mutations associate with classical VHL disease and represent genetic susceptibility for pheochromocytoma. VHL polymorphisms are mostly considered an innocent phenomenon. Still, some data indicate that these polymorphisms are not always harmless and can occur with prostate, renal, and colon cancer or even with isolated erythrocytosis. Seventy-eight patients referred to our department with elevated hemoglobin were screened for VHL mutations. There were no classical somatic VHL mutations. However, we found heterozygous (GA) or homozygous (AA) rs779805 VHL c.-195G>A polymorphism accompanied by erythrocytosis. These patients are Jak-2 negative, with normal or elevated EPO levels, sometimes with family accumulations and often phlebotomy needs, and in some cases with malignancies in the family. No other cause of erythrocytosis was found. We use phlebotomy regularly, and for those with cardiovascular risk factors, we recommend aspirin.