Iranian Journal of Blood and Cancer
Volume:16 Issue: 3, Sep 2024

Cystic fibrosis (CF) represents a prevalent autosomal recessive condition that predominantly impacts the respiratory and gastrointestinal systems. Abdominal pain in patients with cystic fibrosis is commonly linked to conditions including distal intestinal obstruction syndrome, pancreatitis, or hepatic disease. This case report presents a rare etiology of abdominal pain, specifically mesenteric vein thrombosis (MVT) attributed to hereditary thrombophilia, observed in a pediatric patient diagnosed with cystic fibrosis (CF).

A 3-year-old female patient with a confirmed diagnosis of cystic fibrosis, established through a sweat chloride test, exhibited significant right lower quadrant (RLQ) abdominal pain. The initial diagnostic evaluation, comprising an abdominal series, laboratory assessments, and abdominal ultrasound, ruled out prevalent etiologies including DIOS, pancreatitis, and appendicitis. The presence of persistent pain necessitated additional diagnostic evaluation through a contrast-enhanced CT scan, which subsequently identified mesenteric vein thrombosis. The analysis of genetic testing revealed a homozygous mutation in the MTHFR C677T gene, which is suggestive of hereditary thrombophilia. These findings were corroborated through Sanger sequencing methodologies.

This case highlights the importance of evaluating uncommon conditions such as mesenteric vein thrombosis in pediatric patients with cystic fibrosis who exhibit atypical abdominal pain. An extensive diagnostic strategy, incorporating genetic analysis, is crucial for the prompt identification and focused intervention necessary to avert significant complications. Abdominal pain is a significant clinical symptom that may be associated with various underlying conditions, including cystic fibrosis, venous thrombosis, and mesenteric ischemia. Each of these conditions presents unique challenges in diagnosis and management, necessitating a comprehensive understanding of their pathophysiology and clinical implications.

Cystic fibrosis (CF) is an inheriting disorder that has a strong impact on the pulmonary systems of individuals, as a result, hypoxia might be presented among patients who have CF. In addition, hypoxia is a pathological condition that might be present among patients with sickle cell trait (SCT). However, the simultaneous presentation of both SCT and CF in a patient is rare.

A 7-year-old boy came to the hospital with a chief complaint of cyanosis and cough. In his physical examination, he has low SpO2. His fiber-optic bronchoscopy depicted purulent secretion in the main bronchus. As well, his sweet chloride test was above 80 mmol/L. Thus, by the impression of CF exacerbation, he got HARD treatment and antibiotics. Additionally, during hospitalization, SCT as another impression was diagnosed for him.

Although the co-existence of CF and SCT is rare among patients. The physicians must consider both CF and SCT when a child comes to the emergency room with hypoxia.

Systemic Lupus Erythematosus (SLE) is one of these conditions that presents difficult hurdles since it is a multi-systemic autoimmune condition with a wide range of implications, including an increased risk of cancer among affected people. According to recent evidence, it has been revealed that the lymphoma rate in patients with SLE can be 4 to 7 times higher than that of the general population. This increased risk is to be emphasized through stringent and attentive screening and management as the mechanism of this risk is still under research. Therefore, this section discusses a case study and literature regarding SLE and lymphoma better to comprehend the intricate correlation between the two conditions. Here, we present the case of a 53-year-old male who was just diagnosed with SLE and also suffering from abdominal pain and distention, in which the diagnosis of lymphoma is made via serial investigations. This case, therefore, gives us a lesson on the fact that Lymphoma should be considered as one of the differential diagnoses in SLE patients presenting with abdominal complaints. With the ever-changing knowledge about the basic mechanisms of SLE and appropriate screening techniques, our attention to cancer risk in SLE patients should be increased to achieve better clinical outcomes.

Patients with acute leukemia (AL) are at an increased risk of infection, particularly in acute or critical situations, where timely identification of the cause of infection is crucial. While traditional methods such as microbial cultures remain the gold standard, they require 24–48 hours for results. In recent years, novel biomarkers like neutrophil CD64 expression have been widely investigated as indicators of infection. However, the diagnostic utility of CD64 within the clinical context of AL patients, especially those who are neutropenic and undergoing treatment, has not been extensively studied. Therefore, this study aimed to assess the diagnostic potential of neutrophil CD64 expression in monitoring the progression of infection and evaluating antibiotic therapy in AL patients complicated by infection.

Forty AL patients (20 in the infection group and 20 in the non-infection group), along with 40 healthy controls, were recruited. Data on the percentage of neutrophil CD64+ (%CD64+), CD64 index, C-reactive protein (CRP), white blood cell (WBC) count, and absolute neutrophil count (ANC) were collected.

Patients with infection exhibited higher %CD64+, CD64 index, and CRP levels compared to those without infection (p<0.001). The sensitivity of both %CD64+ and the CD64 index in diagnosing infection was 90%, while their specificities were 83.3% and 86.7%, respectively. Furthermore, in the infection group, both %CD64+ and the CD64 index were significantly down-regulated after effective antibiotic therapy (p<0.001).

CD64 shows significant promise in enhancing diagnostic precision and in assessing the effectiveness of antibiotic therapy in AL patients.

 One of the most common types of leukemia is acute myeloid leukemia (AML). Intrinsic and extrinsic factors may lead to AML. Insulin-like growth factor (IGF) is a mitogenic intermediate from the liver that regulates growth and proliferation in response to GH. In this study, we examined the expression of IGF family genes in bone marrow of AML patients (M3 and Non-M3) and compared them with normal samples.

Forty bone marrow samples from recently diagnosed AML patients along with 15 samples from subjects without hematological malignancies were collected. For molecular tests, RNA extraction and cDNA synthesis were performed. Finally, IGF1, IGF2, IGFBP3, IGF1R, and IGF2R gene expression were examined by Real-Time PCR.

IGF1, IGF1R, and IGFBP3 gene expression were significantly increased in patients with AML. In contrast, IGF2 and IGF2R genes did not show significant expression changes between the two groups.

The expression in this gene family soared in AML patients' bone marrow, compared to normal subjects. This can be caused by malignant cells in the bone marrow. These malignant cells express proteins that increase the number of malignant cells. Moreover, they can be considered as diagnostic biomarkers or therapeutic targets with further research.

Aberrant DNA methylation is a key epigenetic alteration observed in multiple cancers. Acute myeloid leukemia (AML), a prominent form of hematopoietic cancer, is characterized by abnormal proliferation and differentiation of myeloid progenitor cells. This study focuses on examining the methylation status of the CpG islands in the DNMT1 and CDX2 promoter regions and exploring their correlation with prognostic hematological laboratory parameters across three phases of AML: newly diagnosed, undergoing treatment, and in remission.

This follow-up case-control study recruited 11 new cases of confirmed AML admitted to Shariati Hospital in Tehran. All patients received AML treatment according to FDA protocol. The samples (peripheral blood) were collected before medication (new case phase), during medication (under treatment phase), and in the remission phase. Then, genomic DNA was extracted and treated with the bisulfite treatment method. Then, methylation-specific PCR (MSP) was conducted to amplify treated DNAs using two methylated and unmethylated primers related to their promoters' DNMT1 and CDX2 CpG- islands. All statistical analysis was performed using SPSS v.25.

The results of the methylation pattern of DNMT1 gene promoter CpG islands in the present study show that the hemimethylated pattern of the DNMT1 gene promoter is predominant in control (100%), new case phase (90.9%), under treatment phase (72.7%), and remission phase (100%). In the case of the CDX2 gene, the unmethylated pattern is predominant in control (57.14%), new case phase (72.7%), under-treatment phase (90.9%), and remission phase (81.8%). These differences were not statistically significant. No methylated pattern was observed in the control group, and different phases of AML were used for DNMT1 and CDX2. Also, the methylation status of DNMT1 and CDX2 were not correlated with prognostic hematological laboratory parameters.

The methylation patterns of CDX2 and DNMT1 are not different in healthy individuals and AML patients, as well as in different phases of AML. Also, the methylation patterns of CDX2 and DNMT1 cannot help determine the prognosis of AML patients through changes in hematological laboratory parameters.

Hemolytic illness an interaction with Vicia fava, also referred to as fava beans, results in favism. This contact can happen in a few different ways: eating raw, cooked, or dried beans; walking through fields where V. fava is grown and possibly breathing in pollen; and introducing fava beans to a breastfed baby through their mother's milk. In populations, the illness is common. For example, it's typical to walk through fields that have been planted with fava in the northern Iranian provinces of Mazandaran and Guilan. This is a problem in areas where thalassemia is common since patients there frequently need blood transfusions. Although favism has a considerable economic impact, there is a limited number of particular statistics on this matter. This paper explores the implications of recent findings on favism and G6PD for the future.

The COVID-19 pandemic, triggered by the SARS-CoV-2 virus, has posed significant global health challenges, notably affecting individuals with pre-existing conditions like cancer. This review aims to provide an overview of current evidence regarding the bidirectional relationship between COVID-19 and cancer, focusing on potential mechanisms driving this association.

Search Strategy:

 A systematic search of the PubMed, Scopus, and Web of Science databases was conducted to identify studies published between January 2020 and March 2024. Articles were selected based on their relevance to the topic and adherence to rigorous methodological standards.

Research indicates a complex interaction between COVID-19 and cancer, with clinical data highlighting variations in cancer diagnosis, prognosis, and treatment efficacy during SARS-CoV-2 infection. Mechanistic studies suggest that immune system dysregulation, chronic inflammation, and possible viral-induced cellular changes may contribute to cancer progression. Additionally, the pandemic has disrupted cancer care, causing delays in diagnosis and treatment, exacerbating existing healthcare disparities, and negatively affecting patient outcomes.

SARS-CoV-2 impacts cancer progression through a combination of direct and indirect mechanisms. Future studies should focus on identifying vulnerable cancer patient populations, clarifying molecular pathways connecting COVID-19 and cancer progression, and developing tailored therapeutic approaches to mitigate these risks.

Colorectal Cancer (CRC) is the third most common cancer around the world. Among the various factors associated with the development of CRC, bacterial infection and related toxins are considered the most critical risk factors. Several virulence genes, including fimC, cnf1, vat1, hlyD, clbB, clbN, feoA, feoB, fyuA, iroN, ireA, iutA, KpsMT (k1), KpsMTII, and KpsMTIII, have been found to have a more significant influence on the pathogenicity of the bacteria. This research aimed to assess the possible position performed through a few virulence genes in E. coli isolated from the intestinal tissues' biopsies of patients with colorectal cancer. Using microbial and biochemical methods, this study isolated 82 samples of E. coli from all of the 170 biopsies obtained from patients suffering from CRC, inflammatory bowel disease, and normal individuals. Then, the frequency of 15 virulence genes was assessed by applying PCR. The obtained results indicated that two types of bacterial genes as following are more likely to be involved in CRC development: clbB and clbN genes, which are associated with the colibactin polyketide synthesis system, as well as KpsMTIII gene, which is involved in polysaccharide capsule synthesis. In precis, these consequences suggest that the superiority of E. coli containing clbB, clbN, and KpsMTIII plays an extensive role in the inflammation and, therefore, the occurrence of CRC.

The importance of the gut microbiota in human health and disease has been known for a long time. Current investigations involving preclinical and clinical studies have presented numerous lines of evidence indicating that gut microbiota can influence the effectiveness of cancer immunotherapies, particularly immune checkpoint inhibitors (ICIs). The gut microbiota can alter the immune response in the tumor microenvironment (TME) by engaging with innate and adaptive immune cells. Notably, one of the primary methods by which the gut microbiota modulates antitumor immunity is through the production of metabolites, which are small molecules capable of traveling from the gut to other parts of the body and influencing local and systemic antitumor immune responses. This exploration of mechanisms has yielded valuable insights for developing microbiota-based therapeutic strategies such as fecal microbiota transplantation (FMT), probiotics, engineered microbiomes, and specific microbial metabolites. In this review, we explored several possible interventions that could enhance the efficacy of ICIs, thereby potentially restoring or augmenting patient responses to these therapeutic agents.