Teenager with persistent facial edema and induration.

INTRODUCTION: Acute lymphoblastic leukemia (ALL) is the most common oncological disease in the pediatric population; however, skin infiltration occurs only in 1-3% of the patients and almost always manifests after the diagnosis is made. CLINICAL CASE: A male teenage patient who presented with facial edema and infiltration, associated with systemic symptoms such as asthenia and adynamia. On physical examination, the patient presented facial edema and indurated plaques, as well as cervical, inguinal, and axillary adenopathy. Complete blood count showed pancytopenia and a chest X-ray revealed a mediastinal mass. Due to a high suspicion of malignancy a bone marrow and skin biopsy was taken, both with pre-B ALL. Chemotherapy was started and the patient is now in maintenance phase. CONCLUSIONS: Leukemia cutis manifestations are heterogenous, from a small papule to a big nodule. It is more common in patients with acute myeloid leukemia and it is rare in patients with pre-B ALL, specially in the pediatric population. The diagnosis should be done with a biopsy and the treatment is with systemic chemotherapy. The diagnosis should always be considered in patients with unexplained edematous or indurated lesions, especially in the context of systemic symptoms.

INTRODUCCIÓN: La leucemia linfoblástica aguda es la enfermedad oncológica más común en la edad pediátrica; sin embargo, la infiltración a la piel solo ocurre en el 1-3% de los pacientes y se manifiesta habitualmente posterior al diagnóstico de leucemia. CASO CLÍNICO: Adolescente varón que acude a urgencias de nuestra unidad por presentar edema facial persistente, junto con astenia y adinamia. En la exploración física presenta edema facial con placas difusas induradas y adenopatía cervical, inguinal y axilar. Se decide realizar una biometría hemática, que muestra pancitopenia, y una radiografía de tórax, que revela una masa mediastinal. Por sospecha de malignidad se decide realizar una biopsia de médula ósea y de piel, dando como resultado leucemia linfoblástica pre-B en ambas. Se inició quimioterapia y actualmente se encuentra en fase de mantenimiento. CONCLUSIONES: Las manifestaciones clínicas de leucemia cutis son heterogéneas, desde una pápula pequeña hasta lesiones nodulares de diferentes tamaños. Lo más común es verlas en pacientes con leucemia mieloide aguda, y es muy raro en pacientes con leucemia linfoblástica aguda pre-B, especialmente en la edad pediátrica. El diagnóstico se realiza con una biopsia de piel y el tratamiento es con quimioterapia sistémica. Es importante tener en mente este diagnóstico en pacientes con síntomas sistémicos de leucemia.

Autophagy and inflammasome activation are associated with poor response to FLT3 inhibitors in patients with FLT3-ITD acute myeloid leukemia.

Beyond its clinical diversity and severity, acute myeloid leukemia (AML) is known for its complex molecular background and for rewiring biological processes to aid disease onset and maintenance. FLT3 mutations are among the most recurring molecular entities that cooperatively drive AML, and their inhibition is a critical molecularly oriented therapeutic strategy. Despite being a promising avenue, it still faces challenges such as intrinsic and acquired drug resistance, which led us to investigate whether and how autophagy and inflammasome interact and whether this interaction could be leveraged to enhance FLT3 inhibition as a therapeutic strategy. We observed a strong and positive correlation between the expression of key genes associated with autophagy and the inflammasome. Gene set enrichment analysis of the FLT3-ITD samples and their ex vivo response to five different FLT3 inhibitors revealed a common molecular signature compatible with autophagy and inflammasome activation across all poor responders. Inflammasome activation was also shown to strongly increase the likelihood of a poor ex vivo response to the FLT3 inhibitors quizartinib and sorafenib. These findings reveal a distinct molecular pattern within FLT3-ITD AML samples that underscores the necessity for further exploration into how approaching these supportive parallel yet altered pathways could improve therapeutic strategies.

In silico and in vitro study of FLT3 inhibitors and their application in acute myeloid leukemia.

Acute myeloid leukemia (AML) is the most common hematological cancer in the adult population worldwide. Approximately 35% of patients with AML present internal tandem duplication (ITD) mutations in the FMS­like tyrosine kinase 3 (FLT3) receptor associated with poor prognosis, and thus, this receptor is a relevant target for potential therapeutics. Tyrosine kinase inhibitors (TKIs) are used to treat AML; however, their molecular interactions and effects on leukemic cells are poorly understood. The present study aimed to gain insights into the molecular interactions and affinity forces of four TKI drugs (sorafenib, midostaurin, gilteritinib and quizartinib) with the wild­type (WT)­FLT3 and ITD­mutated (ITD­FLT3) structural models of FLT3, in its inactive aspartic acid­phenylalanine­glycine motif (DFG­out) and active aspartic acid­phenylalanine­glycine motif (DFG­in) conformations. Furthermore, the present study evaluated the effects of the second­generation TKIs gilteritinib and quizartinib on cancer cell viability, apoptosis and proliferation in the MV4­11 (ITD­FLT3) and HL60 (WT­FLT3) AML cell lines. Peripheral blood mononuclear cells (PBMCs) from a healthy volunteer were included as an FLT3­negative group. Molecular docking analysis indicated higher affinities of second­generation TKIs for WT­FLT3/DFG­out and WT­FLT3/DFG­in compared with those of the first­generation TKIs. However, the ITD mutation changed the affinity of all TKIs. The in vitro data supported the in silico predictions: MV4­11 cells presented high selective sensibility to gilteritinib and quizartinib compared with the HL60 cells, whereas the drugs had no effect on PBMCs. Thus, the current study presented novel information about molecular interactions between the FLT3 receptors (WT or ITD­mutated) and some of their inhibitors. It also paves the way for the search for novel inhibitory molecules with potential use against AML.

Gut Microbiota Disruption in Hematologic Cancer Therapy: Molecular Insights and Implications for Treatment Efficacy.

Hematologic malignancies (HMs), including leukemia, lymphoma, and multiple myeloma, involve the uncontrolled proliferation of abnormal blood cells, posing significant clinical challenges due to their heterogeneity and varied treatment responses. Despite recent advancements in therapies that have improved survival rates, particularly in chronic lymphocytic leukemia and acute lymphoblastic leukemia, treatments like chemotherapy and stem cell transplantation often disrupt gut microbiota, which can negatively impact treatment outcomes and increase infection risks. This review explores the complex, bidirectional interactions between gut microbiota and cancer treatments in patients with HMs. Gut microbiota can influence drug metabolism through mechanisms such as the production of enzymes like bacterial ß-glucuronidases, which can alter drug efficacy and toxicity. Moreover, microbial metabolites like short-chain fatty acids can modulate the host immune response, enhancing treatment effectiveness. However, therapy often reduces the diversity of beneficial bacteria, such as Bifidobacterium and Faecalibacterium, while increasing pathogenic bacteria like Enterococcus and Escherichia coli. These findings highlight the critical need to preserve microbiota diversity during treatment. Future research should focus on personalized microbiome-based therapies, including probiotics, prebiotics, and fecal microbiota transplantation, to improve outcomes and quality of life for patients with hematologic malignancies.

Venetoclax with low-dose cytarabine, a forgotten combination in patients with acute myeloid leukemia ineligible for intensive chemotherapy: a systematic review.

BACKGROUND: Based on the VIALE-A and VIALE-C studies, the Food and Drug Administration approved venetoclax in 2020 in combination with azacitidine or low-dose cytarabine for the treatment of patients with acute myeloid leukemia ineligible for intensive chemotherapy. After the publication of these studies, venetoclax/azacitidine was assumed to be superior to venetoclax/low-dose cytarabine; however, these studies were not designed to demonstrate superiority between these combinations. Therefore, we conducted a systematic review to describe overall survival, complete remission rate, and composite complete remission rate to assess response of these two regimens in patients with newly diagnosed acute myeloid leukemia who are ineligible for intensive chemotherapy. MATERIALS AND METHODS: The PubMed and Web of Science databases were searched for retrospective studies and complete remission, composite complete remission, and overall survival rates were recorded. RESULTS: Only 11 of the 815 publications identified were eligible to be included n this review, ten studies evaluated the venetoclax/azacitidine combination and one study evaluated the venetoclax/low-dose cytarabine combination. The median overall survival for venetoclax/azacitidine was 10.75 months, whereas for venetoclax/low-dose cytarabine the median overall survival had not been reached at the time of publication. Composite complete remission was 63.3 % for venetoclax/azacitidine and 90 % for venetoclax/low-dose cytarabine. Adverse events were similar for both combinations. CONCLUSIONS: A limited number of studies investigating the venetoclax/low-dose cytarabine combination exist. Based on the available data, the superiority of venetoclax/azacitidine over venetoclax/low-dose cytarabine cannot be assumed for all acute myeloid leukemia patients who are ineligible for intensive chemotherapy. Venetoclax/low-dose cytarabine can still be considered as an option for the drug combinations currently under investigation.

Exploring cell-derived extracellular vesicles in peripheral blood and bone marrow of B-cell acute lymphoblastic leukemia pediatric patients: proof-of-concept study.

Extracellular vesicles (EVs) are heterogeneous, phospholipid membrane enclosed particles that are secreted by healthy and cancerous cells. EVs are present in diverse biological fluids and have been associated with the severity of diseases, which indicates their potential as biomarkers for diagnosis, prognosis and as therapeutic targets. This study investigated the phenotypic characteristics of EVs derived from peripheral blood (PB) and bone marrow (BM) in pediatric patients with B-cell acute lymphoblastic leukemia (B-ALL) during different treatment stages. PB and BM plasma were collected from 20 B-ALL patients at three time points during induction therapy, referred to as: diagnosis baseline (D0), day 15 of induction therapy (D15) and the end of the induction therapy (D35). In addition, PB samples were collected from 10 healthy children at a single time point. The EVs were measured using CytoFLEX S flow cytometer. Calibration beads were employed to ensure accurate size analysis. The following, fluorescent-labeled specific cellular markers were used to label the EVs: Annexin V (phosphatidylserine), CD235a (erythrocyte), CD41a (platelet), CD51 (endothelial cell), CD45 (leukocyte), CD66b (neutrophil), CD14 (monocyte), CD3 (T lymphocyte), CD19, CD34 and CD10 (B lymphoblast/leukemic blast). Our results demonstrate that B-ALL patients had a marked production of EV-CD51/61+, EV-CD10+, EV-CD19+ and EV-CD10+CD19+ (double-positive) with a decrease in EV-CD41a+ on D0. However, the kinetics and signature of production during induction therapy revealed a clear decline in EV-CD10+ and EV-CD19+, with an increase of EV-CD41a+ on D35. Furthermore, B-ALL patients showed a complex biological network, exhibiting distinct profiles on D0 and D35. Interestingly, fold change and ROC curve analysis demonstrated that EV-CD10+CD19+ were associated with B-ALL patients, exhibited excellent clinical performance and standing out as a potential diagnostic biomarker. In conclusion, our data indicate that EVs represent a promising field of investigation in B-ALL, offering the possibility of identifying potential biomarkers and therapeutic targets.

Deciphering genetic and nongenetic factors underlying tumour dormancy: insights from multiomics analysis of two syngeneic MRD models of melanoma and leukemia.

BACKGROUND: Tumour dormancy, a resistance mechanism employed by cancer cells, is a significant challenge in cancer treatment, contributing to minimal residual disease (MRD) and potential relapse. Despite its clinical importance, the mechanisms underlying tumour dormancy and MRD remain unclear. In this study, we employed two syngeneic murine models of myeloid leukemia and melanoma to investigate the genetic, epigenetic, transcriptomic and protein signatures associated with tumour dormancy. We used a multiomics approach to elucidate the molecular mechanisms driving MRD and identify potential therapeutic targets. RESULTS: We conducted an in-depth omics analysis encompassing whole-exome sequencing (WES), copy number variation (CNV) analysis, chromatin immunoprecipitation followed by sequencing (ChIP-seq), transcriptome and proteome investigations. WES analysis revealed a modest overlap of gene mutations between melanoma and leukemia dormancy models, with a significant number of mutated genes found exclusively in dormant cells. These exclusive genetic signatures suggest selective pressure during MRD, potentially conferring resistance to the microenvironment or therapies. CNV, histone marks and transcriptomic gene expression signatures combined with Gene Ontology (GO) enrichment analysis highlighted the potential functional roles of the mutated genes, providing insights into the pathways associated with MRD. In addition, we compared "murine MRD genes" profiles to the corresponding human disease through public datasets and highlighted common features according to disease progression. Proteomic analysis combined with multi-omics genetic investigations, revealed a dysregulated proteins signature in dormant cells with minimal genetic mechanism involvement. Pathway enrichment analysis revealed the metabolic, differentiation and cytoskeletal remodeling processes involved in MRD. Finally, we identified 11 common proteins differentially expressed in dormant cells from both pathologies. CONCLUSIONS: Our study underscores the complexity of tumour dormancy, implicating both genetic and nongenetic factors. By comparing genomic, transcriptomic, proteomic, and epigenomic datasets, our study provides a comprehensive understanding of the molecular landscape of minimal residual disease. These results provide a robust foundation for forthcoming investigations and offer potential avenues for the advancement of targeted MRD therapies in leukemia and melanoma patients, emphasizing the importance of considering both genetic and nongenetic factors in treatment strategies.

Seroprevalence of bovine leukemia virus and association with bovine infectious abortion in Creole breeds from tropical grazing herds in the Colombian Caribbean.

Background and Aim: In the Caribbean region of Colombia, the concomitance of endemic infectious agents is a common problem, and coinfections are possible, increasing the complexity of cattle herds' sanitary, reproductive, and productive problems. This study aimed to estimate the seroprevalence of bovine leukemia virus and its association with bovine infectious abortion in grazing Creole breeds from tropical herds in the Colombian Caribbean. Materials and Methods: For the determination of bovine leukemia virus (BLV), bovine viral diarrhea virus (BVDV), bovine herpes virus-1 (BoHV-1), and Neospora Caninum (NC), the enzyme-linked immunosorbent assay technique was used. Matrix analysis was performed to represent multiple seroprevalence in the same cow. To explore the association between the seroprevalence of BLV and bovine infectious abortion agents, a multivariate logistic regression model was used. Results: The seroprevalence was as follows: BLV 30.78%, BVDV 33.01%, BoHV-1 12.85%, and NC 8.96%. In the multivariate logistic regression model, seroprevalence of BVDV (OR 10.8; 95% CI: 7.5-15.6) and seroprevalence of BoHV-1 (OR 1.8; 95% CI: 1.1-3.0) were associated with the seroprevalence of BLV. Conclusion: Animals infected with BLV are more susceptible to coinfections with BVDV and BoHV-1. Implementing healthy measures against these two immunosuppressive infections could enhance the hygiene of numerous cattle herds. This study was designed as a retrospective cross-sectional study, which limits the ability to confirm that BLV is the primary infection. Further studies to confirm the primary infection of BLV with an active viral coinfection are necessary and the factors associated with these phenomena.

The Nucleolus and Its Interactions with Viral Proteins Required for Successful Infection.

Nuclear bodies are structures in eukaryotic cells that lack a plasma membrane and are considered protein condensates, DNA, or RNA molecules. Known nuclear bodies include the nucleolus, Cajal bodies, and promyelocytic leukemia nuclear bodies. These bodies are involved in the concentration, exclusion, sequestration, assembly, modification, and recycling of specific components involved in the regulation of ribosome biogenesis, RNA transcription, and RNA processing. Additionally, nuclear bodies have been shown to participate in cellular processes such as the regulation of transcription of the cell cycle, mitosis, apoptosis, and the cellular stress response. The dynamics and functions of these bodies depend on the state of the cell. It is now known that both DNA and RNA viruses can direct their proteins to nuclear bodies, causing alterations in their composition, dynamics, and functions. Although many of these mechanisms are still under investigation, it is well known that the interaction between viral and nuclear body proteins is necessary for the success of the viral infection cycle. In this review, we concisely describe the interaction between viral and nuclear body proteins. Furthermore, we focus on the role of the nucleolus in RNA virus infections. Finally, we discuss the possible implications of the interaction of viral proteins on cellular transcription and the formation/degradation of non-coding RNAs.

Preliminary exploration of the expression of acetylcholinesterase in normal human T lymphocytes and leukemic Jurkat T cells.

The classic enzymatic function of acetylcholinesterase (AChE) is the hydrolysis of acetylcholine (ACh) in the neuronal synapse. However, AChE is also present in nonneuronal cells such as lymphocytes. Various studies have proposed the participation of AChE in the development of cancer. The ACHE gene produces three mRNAs (T, H and R). AChE-T encodes amphiphilic monomers, dimers, tetramers (G1 A, G2 A and G4 A) and hydrophilic tetramers (G4 H). AChE-H encodes amphiphilic monomers and dimers (G1 A and G2 A). AChE-R encodes a hydrophilic monomer (G1 H). The present study considered the differences in the mRNA expression (T, H and R) and protein levels of AChE, as well as the molecular forms of AChE, the glycosylation pattern and the enzymatic activity of AChE present in normal T lymphocytes and leukemic Jurkat E6-1 cells. The results revealed that AChE enzymatic activity was higher in normal T lymphocytes than in Jurkat cells. Normal T cells expressed AChE-H transcripts, whereas Jurkat cells expressed AChE-H and AChE-T. The molecular forms identified in normal T cells were G2 A (5.2 S) and G1 A (3.5 S), whereas those in Jurkat cells were G2 A (5.2 S), G1 A (3.5 S) and G4 H (10.6S). AChE in Jurkat cells showed altered posttranslational maturation since a decrease in the incorporation of galactose and sialic acid into its structure was observed. In conclusion, the content and composition of AChE were altered in Jurkat cells compared with those in normal T lymphocytes. The present study opened new avenues for exploring the development of novel therapeutic strategies against T-cell leukemia and for identifying potential molecular targets for the early detection of this type of cancer.

Insights into Asparaginase Allergic Responses: Exploring Pharmacogenetic Influences.

Acute lymphoblastic leukemia represents the most prevalent childhood cancer. Modern chemotherapy has significantly improved outcomes, achieving EFS rates of 80% and OS rates nearing 90% in developed nations, while in developing regions, rates remain below 50%, highlighting disparities, and this difference is due to several factors. Genetic variability plays a role in these drug response disparities, presenting single-nucleotide variations (SNVs). Pharmacogenetic research aims to pinpoint these SNVs early in treatment to predict specific drug responses effectively. This review aims to explore advancements in pharmacogenetics associated with asparaginase (ASNase). ASNase plays a crucial role in the treatment of ALL and is available in three formulations: E. coli, Erwinia, and PEG ASNase. ASNase therapy presents challenges due to adverse effects, like hypersensitivity reactions. Identifying predictive markers for hypersensitivity development beforehand is crucial for optimizing treatments. Several pharmacogenetic studies have investigated the association between SNVs and the risk of hypersensitivity. Key genes include GRIA1, NFATC2, CNTO3, ARHGAP28, MYBBP1A, and HLA. Studies have highlighted associations between SNVs within these genes and hypersensitivity reactions. Notably, most pharmacogenetic investigations of hypersensitivity have focused on patients treated with E. coli, emphasizing the need for broader exploration across different formulations. Future research investigating these variants holds promise for advancing our understanding of ASNase's pharmacogenetics.

Antineoplastic Activity of Sodium Caseinate in a Cytarabine-Resistant Mouse Acute Myeloid Leukemia Cell Line.

BACKGROUND: Acute myeloid leukemia (AML) is a hematological neoplasm of rapid and progressive onset, and is the most common form of leukemia in adults. Chemoresistance to conventional treatments such as cytarabine (Ara-C) and daunorubicin is a main cause of relapse, recurrence, metastasis, and high mortality in AML patients. It is known that sodium caseinate (SC), a salt derived from casein, a milk protein, inhibits growth and induces apoptosis in acute myeloid leukemia cells but not in normal hematopoietic cells. However, it is unknown whether SC retains its antileukemic effect in cytarabine-resistant AML cell lines. OBJECTIVE: To evaluate the antineoplastic effect of SC in cytarabine-resistant leukemia models. METHODS: The SC inhibits the growth and induces apoptosis in parental WEHI-3 AML cells. Here, we generated two cytarabine-resistant sublines, WEHI-CR25 and WEHI-CR50, which exhibit 6- and 16-fold increased resistance to cytarabine, respectively, compared to the parental WEHI-3 cells. Thus, these sublines mimic a chemoresistant model. RESULTS: We demonstrate that WEHI-CR25 and WEHI-CR50 cells retain sensitivity to SC, similar to parental WEHI-3 cells. This sensitivity results in inhibited cell proliferation, induced apoptosis, and increased expression of ENT1 and dCK, molecules involved in the entry and metabolism of Ara-C, while decreasing MDR1 expression. Additionally, we observed that SC prolonged the survival of WEHI-CR50 tumor-bearing mice, despite their resistance to Ara-C. CONCLUSION: This is the first evidence that SC, a milk protein, may inhibit proliferation and induce apoptosis in cytarabine-resistant cells.

Impact of a guaranteed access program to imatinib on the survival of patients with chronic myeloid leukemia.

PURPOSE: This work aimed to evaluate the impact of a guaranteed access program to imatinib on the survival of patients with Chronic Myeloid Leukemia. METHODS: We carried out a retrospective, observational, and analytical study of the database of patients diagnosed with Chronic Myeloid Leukemia of the Instituto Nacional de Cancerología and the Hospital General de México Dr. Eduardo to assess overall survival based on guaranteed access or not to imatinib. RESULTS: With an average follow-up of 99 months, all patients' estimated 20-year overall survival was 72% (95% CI, 76-67). A significant difference was found in the 20-year survival probability in favor of patients with guaranteed access 76% (95% CI, 81-71) vs. 61% (95% CI, 69-52) (p < 0.001), in addition to those in which they had better attachment 81.2% (95% CI, 85-76) vs. 44.9% (95% CI, 52-37) (p < 0.001). CONCLUSION: CML is the most frequent chronic leukemia in Mexico. It mainly affects the economically active population (mean age 40), and the prognosis in our country has improved, emulating developed countries; however, the results depend on access to treatment and proper monitoring.

Intragenic antimicrobial peptide Hs02 toxicity against leukemia cell lines is associated with increased expression of select pyroptotic components.

The anticancer potential of some antimicrobial peptides has been reported. Hs02 is a recently characterized Intragenic Antimicrobial Peptide (IAP), which was able to exhibit potent antimicrobial and anti-inflammatory action. In this study, we evaluate for the first time the antineoplastic potential of the Hs02 IAP using cell lines representing the main types of leukemia as cancer models. Interestingly, this peptide decreased the viability of several leukemic cell lines, without compromising the viability of PBMCs in the same concentration. In the HL-60 line, treatment with Hs02 controlled cell division, leading to cell arrest in the G1 phase of the cell cycle. More importantly, HL-60 cells treated with Hs02 undergo cell death, with the formation of pores in the plasma membrane and the release of LDH. Accordingly, Hs02 treatment stimulated the expression of components involved in pyroptosis, such as NLRP1, CASP-1, GSDME, and IL-1ß. Taken together, our data characterize the antineoplastic potential of Hs02 and open an opportunity for both evaluating the peptide's antineoplastic potential in other cancer models and using this molecule as a template for new peptides with therapeutic potential against cancer.

Proteomic Dynamics of Multidrug Resistance Mechanisms in Lucena 1 Cell Line.

The Lucena 1 cell line, derived from the human chronic myeloid leukemia cell line K562 under selective pressure of vincristine supplementation, exhibits multidrug resistance (MDR). This study aims to explore and elucidate the underlying mechanisms driving MDR in the Lucena 1 cell line. A proteomic analysis comparing K562 and Lucena 1 revealed qualitative differences, with a focus on the ATP-dependent efflux pump, Translocase ABCB1, a key contributor to drug resistance. Tubulin analysis identified two unique isoforms, Tubulin beta 8B and alpha chain-like 3, exclusive to Lucena 1, potentially influencing resistance mechanisms. Additionally, the association of Rap1A and Krit1 in cytoskeletal regulation and the presence of STAT1, linked to the urea cycle and tumor development, offered insights into Lucena 1's distinctive biology. The increased expression of carbonic anhydrase I suggested a role in pH regulation. The discovery of COP9, a tumor suppressor targeting p53, further highlighted the Lucena 1 complex molecular landscape. This study offers new insights into the MDR phenotype and its multifactorial consequences in cellular pathways. Thus, unraveling the mechanisms of MDR holds promise for innovating cancer models and antitumor targeted strategies, since inhibiting the P-glycoprotein (P-gp)/ABCB1 protein is not always an effective approach given the associated treatment toxicity.

Immunocytochemistry of bone marrow aspirates: a tool in the diagnosis of feline leukemia virus infection in cats.

Feline leukemia virus (FeLV) is a highly debilitating cat pathogen due to its ability to cause many pathological changes. Therefore, identifying the virus directly in bone marrow can be a highly relevant diagnostic tool even in the absence of viraemia. The aim of this study was to compare the diagnostic efficiency of immunocytochemistry (ICC) of bone marrow aspirates with enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR). Blood samples were collected from 188 cats and separated into aliquots of whole blood for nested PCR using the U3 LTR region and the gag gene of FeLV-A as reference and serum for detection of the p27 antigen by ELISA. Bone marrow samples from these cats were placed on silanized slides for anti-FeLV ICC using gp70 as primary antibody. A total of 28.2% of the cats tested for FeLV were positive in at least one of the tests, with 26.6% positive by PCR, 18.1% by ICC and 11.2% by ELISA. Cohen's kappa agreement test revealed moderate agreement between ELISA and PCR results and substantial agreement between ICC and ELISA and between ICC and PCR. The results indicated that ICC of bone marrow is an efficient novel diagnostic test for FeLV infection.

Medical Imagery: Cytomegalovirus sialadenitis in a patient with B-cell acute lymphoblastic leukemia.

Cytomegalovirus (CMV) can cause a broad range of diseases, with severity depending on immune status, comorbidities, and age. Initial CMV infection usually occurs in childhood and is typically asymptomatic, leading to lifelong latency. In immunocompromised patients, CMV can affect multiple organs, but salivary gland infections are rare. This study presents a case of a 66-year-old woman with B-cell acute lymphoblastic leukemia who developed swelling and pain in the right preauricular region during pre-transplant consolidation therapy. Despite a recent bone marrow biopsy indicating morphological remission and a flow cytometry analysis detecting only 0.04 % B lymphoblasts, she exhibited these symptoms. A CT scan revealed enlargement, hyperdensity, and enhancement of the right parotid glands, with accompanying subcutaneous edema. A biopsy of the right parotid gland showed a dense interstitial lymphoplasmacytic infiltrate with numerous Cowdry bodies and smaller granular cytoplasmic inclusions, all testing positive for CMV immunohistochemistry. The findings confirm the diagnosis of CMV sialadenitis in an immunocompromised patient. This case underscores the importance of considering CMV infections in similar clinical scenarios, particularly in patients with compromised immune systems.

Clinical and Microbiological Characteristics of Febrile Neutropenia During Induction Chemotherapy in Adults With Acute Leukemia.

BACKGROUND: Few studies regarding infectious causes of febrile neutropenia (FN) in Mexico are available. AIMS: We aimed to describe clinical and microbiological characteristics of FN episodes during induction chemotherapy in adults with acute leukemia. METHODS AND RESULTS: This retrospective cohort from a Mexican tertiary care center included adults with newly diagnosed acute leukemia between January 2014, and December 2018. Clinical and microbiological characteristics were summarized using descriptive statistics. Univariate analyses for associations between clinical characteristics and FN and/or death were made; logistic regression analysis was performed to assess relationships with FN. Kaplan-Meier survival estimates were modeled for antimicrobial prophylaxis and FN. Ninety-five patients were included. Median age was 28 (IQR 20-43), 49 (52%) were males, and 74 (78%) developed FN (74/95). Among these, 98% had an identified source of infection (73/74) and 65% had >1. Common infections were urinary tract infection (24%), bacterial sinusitis (20%), and bacterial pneumonia (19%). Gram-negatives were the most frequently isolated microorganisms (69%), followed by Gram-positives (21%), and fungi (9%). Antimicrobial prophylaxis was inversely associated with FN (aOR = 0.07, CI 0.008-0.060, p = 0.02). Invasive fungal diseases were associated with 30-day mortality (aOR = 9.46, 95% CI 1.66-54.05). CONCLUSION: Infections caused 98% of the FN episodes. Gram-negative bacteria are the most common pathogens.

Delayed manifestation of proliferative retinopathy associated with chronic myeloid leukemia.

Purpose: This report highlights a rare case of delayed manifestation of proliferative retinopathy associated with chronic myeloid leukemia (CML) during remission. Observations: Case report and review of the literature; In this case report, we outline the delayed manifestation and clinical progression of proliferative retinopathy in a 52-year-old male patient with a history of CML diagnosed in 2001. Initially, the patient presented with a white blood cell count (WBC) of 402,200/µl, and the leukocytosis persisted until 2005. Thereafter, the patient remained in remission for over 15 years without any visual complaints until 2022. At that time, the patient sought medical attention due to a ten-day history of left eye visual impairment, leading to the discovery of peripheral neovascularization in both eyes and vitreous hemorrhage in the left eye during fundus examination. The WBC count at the time of presentation to the Emergency Department was 10,460/µl. The patient was treated with fluorescein angiography guided panretinal photocoagulation to the areas of ischemic retina. Subsequent follow-up after eight months demonstrated regression of neovascularization. Conclusions and Importance: Our findings highlight the occurrence of proliferative retinopathy in the context of CML, uniquely manifesting during remission. This case emphasizes the importance of ophthalmological assessments not only at the time of CML diagnosis but also during subsequent follow-ups, recognizing the potential for delayed presentation of ocular complications.