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Brazilian Journal of Microbiology :... Jun 2023Infections caused by uncommon Candida species have dramatically increased in recent decades, mostly among hematological malignancies. This report aims to present a case...
Infections caused by uncommon Candida species have dramatically increased in recent decades, mostly among hematological malignancies. This report aims to present a case of Candida pararugosa bloodstream infection, review previous cases with C. pararugosa infections, and provide a concise review of the clinical background, risk factors, and brief the management of infections. A 3-year-old boy with a history of acute myeloid leukemia was hospitalized in Omid Hospital, Isfahan, Iran. Two consecutive blood cultures were taken from the peripheral vein and port catheter; after that, empirically meropenem was administered. Candida pararugosa were isolated from blood-based on conventional and molecular assays. Furthermore, the antifungal susceptibility profiles of the isolate were determined, which exhibited resistance to fluconazole (8 μg/mL). Antifungal therapy with caspofungin and removing the patient's port led to a significant clinical improvement of the patient's conditions. So far, in the literature review, 10 cases of clinical C. pararugosa isolates were found, of which 5 patients had bloodstream infections. Most patients with C. pararugosa infection presented with specific underlying conditions, such as malignancy, sarcoma, surgery, and adult acute myeloid leukemia. Patients with indwelling catheters run a high risk of acquiring C. pararugosa bloodstream infection. Therefore, special consideration should be given to opportunistic fungal infections in immunocompromised individuals using catheters.
Topics: Male; Adult; Humans; Child, Preschool; Antifungal Agents; Fluconazole; Catheter-Related Infections; Leukemia, Myeloid, Acute; Catheters; Sepsis; Microbial Sensitivity Tests; Drug Resistance, Fungal
PubMed: 37157053
DOI: 10.1007/s42770-023-00985-5 -
Turkish Archives of Pediatrics May 2023
PubMed: 37144271
DOI: 10.5152/TurkArchPediatr.2023.22216 -
Journal of Orthopaedic Case Reports Feb 2023Chloromas are defined as metastatic granulocytic solid tumors of myeloid origin occurring at an extramedullary site. In this case report, we present an uncommon case of...
INTRODUCTION
Chloromas are defined as metastatic granulocytic solid tumors of myeloid origin occurring at an extramedullary site. In this case report, we present an uncommon case of chronic myeloid leukemia (CML) presenting with metastatic sarcoma to the dorsal spine causing acute paraparesis.
CASE REPORT
A 36-year-old male presented in the OPD with complaints of progressive upper back pain and acute paraparesis since a 1 week. The patient is a previously diagnosed case of CML on treatment for the same. MRI of the dorsal spine indicated extradural soft-tissue lesions in D5-D9 extending to the right side of the spinal canal displacing the cord to the left. Considering the acute paraparesis that the patient developed, he was taken for an emergency decompression of the tumor. Microscopy showed infiltration of fibrocartilaginous tissue of polymorphous origin mixed with atypical myeloid precursor cells. Immunohistochemistry reports show atypical cells diffusely expressing myeloperoxidase, focally expressing CD34 and Cd117.
CONCLUSION
Rare case reports like this are the only literature available on remission in CML cases with sarcomas. The acute paraparesis in our patient was prevented from increasing to a paraplegia by surgical means. Immediate decompression of the spinal cord in patients with paraparesis and associated radiotherapy and chemotherapy should be considered in all patients with myeloid sarcomas of CML origin. While examining patients of CML, the possibility of a granulocytic sarcoma should always be kept in mind.
PubMed: 37144072
DOI: 10.13107/jocr.2023.v13.i02.3544 -
Breast Cancer Research : BCR May 2023Breast cancer survivors are living longer due to early detection and advances in treatment and are at increased risk for second primary cancers. Comprehensive evaluation...
BACKGROUND
Breast cancer survivors are living longer due to early detection and advances in treatment and are at increased risk for second primary cancers. Comprehensive evaluation of second cancer risk among patients treated in recent decades is lacking.
METHODS
We identified 16,004 females diagnosed with a first primary stage I-III breast cancer between 1990 and 2016 (followed through 2017) and survived ≥ 1 year at Kaiser Permanente (KP) Colorado, Northwest, and Washington. Second cancer was defined as an invasive primary cancer diagnosed ≥ 12 months after the first primary breast cancer. Second cancer risk was evaluated for all cancers (excluding ipsilateral breast cancer) using standardized incidence ratios (SIRs), and a competing risk approach for cumulative incidence and hazard ratios (HRs) adjusted for KP center, treatment, age, and year of first cancer diagnosis.
RESULTS
Over a median follow-up of 6.2 years, 1,562 women developed second cancer. Breast cancer survivors had a 70% higher risk of any cancer (95%CI = 1.62-1.79) and 45% higher risk of non-breast cancer (95%CI = 1.37-1.54) compared with the general population. SIRs were highest for malignancies of the peritoneum (SIR = 3.44, 95%CI = 1.65-6.33), soft tissue (SIR = 3.32, 95%CI = 2.51-4.30), contralateral breast (SIR = 3.10, 95%CI = 2.82-3.40), and acute myeloid leukemia (SIR = 2.11, 95%CI = 1.18-3.48)/myelodysplastic syndrome (SIR = 3.25, 95%CI = 1.89-5.20). Women also had elevated risks for oral, colon, pancreas, lung, and uterine corpus cancer, melanoma, and non-Hodgkin lymphoma (SIR range = 1.31-1.97). Radiotherapy was associated with increased risk for all second cancers (HR = 1.13, 95%CI = 1.01-1.25) and soft tissue sarcoma (HR = 2.36, 95%CI = 1.17-4.78), chemotherapy with decreased risk for all second cancers (HR = 0.87, 95%CI = 0.78-0.98) and increased myelodysplastic syndrome risk (HR = 3.01, 95%CI = 1.01-8.94), and endocrine therapy with lower contralateral breast cancer risk (HR = 0.48, 95%CI = 0.38-0.60). Approximately 1 in 9 women who survived ≥ 1 year developed second cancer, 1 in 13 developed second non-breast cancer, and 1 in 30 developed contralateral breast cancer by 10 years. Trends in cumulative incidence declined for contralateral breast cancer but not for second non-breast cancers.
CONCLUSIONS
Elevated risks of second cancer among breast cancer survivors treated in recent decades suggests that heightened surveillance is warranted and continued efforts to reduce second cancers are needed.
Topics: Humans; Female; Neoplasms, Second Primary; Breast Neoplasms; Cancer Survivors; Risk Factors; Incidence; Myelodysplastic Syndromes
PubMed: 37138341
DOI: 10.1186/s13058-023-01647-y -
Haematologica Dec 2023
Review
Topics: Humans; Myeloproliferative Disorders; Lymphoma; Eosinophilia; Sarcoma; Oncogene Proteins, Fusion; Janus Kinase 2
PubMed: 37102606
DOI: 10.3324/haematol.2022.282228 -
Frontiers in Immunology 2023Myeloid derived suppressor cells (MDSCs) are a heterogenous population of myeloid cells derived from monocyte and granulocyte precursors. They are pathologically... (Review)
Review
Myeloid derived suppressor cells (MDSCs) are a heterogenous population of myeloid cells derived from monocyte and granulocyte precursors. They are pathologically expanded in conditions of ongoing inflammation where they function to suppress both innate and adaptive immunity. They are subdivided into three distinct subsets: monocytic (M-) MDSC, polymorphonuclear (or neutrophilic) (PMN-) MDSC and early-stage (e-) MDSC that may exhibit differential function in different pathological scenarios. However, in cancer they are associated with inhibition of the anti-tumour immune response and are universally associated with a poor prognosis. Seven human viruses classified as Group I carcinogenic agents are jointly responsible for nearly one fifth of all human cancers. These viruses represent a large diversity of species, including DNA, RNA and retroviridae. They include the human gammaherpesviruses (Epstein Barr virus (EBV) and Kaposi's Sarcoma-Associated Herpesvirus (KSHV), members of the high-risk human papillomaviruses (HPVs), hepatitis B and C (HBV, HCV), Human T cell leukaemia virus (HTLV-1) and Merkel cell polyomavirus (MCPyV). Each of these viruses encode an array of different oncogenes that perturb numerous cellular pathways that ultimately, over time, lead to cancer. A prerequisite for oncogenesis is therefore establishment of chronic infection whereby the virus persists in the host cells without being eradicated by the antiviral immune response. Although some of the viruses can directly modulate the immune response to enable persistence, a growing body of evidence suggests the immune microenvironment is modulated by expansions of MDSCs, driven by viral persistence and oncogenesis. It is likely these MDSCs play a role in loss of immune recognition and function and it is therefore essential to understand their phenotype and function, particularly given the increasing importance of immunotherapy in the modern arsenal of anti-cancer therapies. This review will discuss the role of MDSCs in viral oncogenesis. In particular we will focus upon the mechanisms thought to drive the MDSC expansions, the subsets expanded and their impact upon the immune microenvironment. Importantly we will explore how MDSCs may modulate current immunotherapies and their impact upon the success of future immune-based therapies.
Topics: Humans; Myeloid-Derived Suppressor Cells; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Neoplasms; Carcinogenesis; Viruses; Tumor Microenvironment
PubMed: 37033972
DOI: 10.3389/fimmu.2023.1161848 -
Clinical Case Reports Mar 2023Recognition of cutaneous myeloid sarcoma is important for all dermatologists to avoid further progression to acute myeloid leukemia. Nevertheless, we highlight the...
Recognition of cutaneous myeloid sarcoma is important for all dermatologists to avoid further progression to acute myeloid leukemia. Nevertheless, we highlight the presence of a favorable clinical outcome in some patients with spontaneous regression.
PubMed: 36998328
DOI: 10.1002/ccr3.7154 -
Pathobiology : Journal of... 2023Primary effusion lymphoma (PEL) is a malignant lymphomatous effusion, which by definition is Kaposi sarcoma herpesvirus/human herpesvirus 8-positive. PEL typically...
INTRODUCTION
Primary effusion lymphoma (PEL) is a malignant lymphomatous effusion, which by definition is Kaposi sarcoma herpesvirus/human herpesvirus 8-positive. PEL typically occurs in HIV-infected patients but can also occur in HIV-negative individuals, including in organ transplant recipients. Tyrosine kinase inhibitors (TKIs) are currently the standard of care for patients with chronic myeloid leukemia (CML), BCR::ABL1-positive. Although TKIs are extremely effective in treating CML, they alter T-cell function by inhibiting peripheral T-cell migration and altering T-cell trafficking and have been associated with the development of pleural effusions.
CASE PRESENTATION
We report a case of PEL in a young, relatively immunocompetent patient with no history of organ transplant receiving dasatinib for CML, BCR::ABL1-positive.
DISCUSSION
We hypothesize that the loss of T-cell function secondary to TKI therapy (dasatinib) may have resulted in the unchecked cellular proliferation of Kaposi sarcoma herpesvirus (KSHV)-infected cells, leading to the emergence of a PEL. We recommend cytologic investigation and KSHV testing in patients being treated with dasatinib for CML who present with persistent or recurrent effusions.
Topics: Humans; Dasatinib; Lymphoma, Primary Effusion; Sarcoma, Kaposi; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Herpesvirus 8, Human; HIV Infections
PubMed: 36996787
DOI: 10.1159/000530429 -
Cancers Mar 2023-mutant cancers are frequent, metastatic, lethal, and largely undruggable. While interleukin (IL)-1β and nuclear factor (NF)-κB inhibition hold promise against cancer,...
-mutant cancers are frequent, metastatic, lethal, and largely undruggable. While interleukin (IL)-1β and nuclear factor (NF)-κB inhibition hold promise against cancer, untargeted treatments are not effective. Here, we show that human -mutant cancers are addicted to IL-1β via inflammatory versican signaling to macrophage inhibitor of NF-κB kinase (IKK) β. Human pan-cancer and experimental NF-κB reporter, transcriptome, and proteome screens reveal that -mutant tumors trigger macrophage IKKβ activation and IL-1β release via secretory versican. Tumor-specific versican silencing and macrophage-restricted IKKβ deletion prevents myeloid NF-κB activation and metastasis. Versican and IKKβ are mutually addicted and/or overexpressed in human cancers and possess diagnostic and prognostic power. Non-oncogene /IL-1β addiction is abolished by IL-1β and TLR1/2 inhibition, indicating cardinal and actionable roles for versican and IKKβ in metastasis.
PubMed: 36980752
DOI: 10.3390/cancers15061866 -
Diagnostic Pathology Mar 2023
PubMed: 36978113
DOI: 10.1186/s13000-023-01326-8