scholarly journals MBCL-08. INTEGRATIVE MOLECULAR ANALYSIS OF PATIENT-MATCHED DIAGNOSTIC AND RELAPSED MEDULLOBLASTOMAS

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii389-iii389
Author(s):  
Rahul Kumar ◽  
Maximilian Deng ◽  
Kyle Smith ◽  
Anthony Liu ◽  
Girish Dhall ◽  
...  
Keyword(s):  
Molecular Analysis ◽  
Copy Number ◽  
Driver Mutations ◽  
P Value ◽  
Next Generation ◽  
Driver Genes ◽  
Methylation Array ◽  
Primary Tumors ◽  
Group 4 ◽  
Group 3

Abstract INTRODUCTION The next generation of clinical trials for relapsed medulloblastoma demands a thorough understanding of the clinical behavior of relapsed tumors as well as the molecular relationship to their diagnostic counterparts. METHODS A multi-institutional molecular cohort of patient-matched (n=126 patients) diagnostic MBs and relapses/subsequent malignancies was profiled by DNA methylation array. Entity, subgroup classification, and genome-wide copy-number aberrations were assigned while parallel next-generation (whole-exome or targeted panel) sequencing on the majority of the cohort facilitated inference of somatic driver mutations. RESULTS Comprised of WNT (2%), SHH (41%), Group 3 (18%), Group 4 (39%), primary tumors retained subgroup affiliation at relapse with the notable exception of 10% of cases. The majority (8/13) of discrepant classifications were determined to be secondary glioblastomas. Additionally, rare (n=3) subgroup-switching events of Group 4 primary tumors to Group 3 relapses were identified coincident with MYC/MYCN pathway alterations. Amongst truly relapsing MBs, copy-number analyses suggest somatic clonal divergence between primary MBs and their respective relapses with Group 3 (55% of alterations shared) and Group 4 tumors (63% alterations shared) sharing a larger proportion of cytogenetic alterations compared to SHH tumors (42% alterations shared; Chi-square p-value < 0.001). Subgroup- and gene-specific patterns of conservation and divergence amongst putative driver genes were also observed. CONCLUSION Integrated molecular analysis of relapsed MB discloses potential mechanisms underlying treatment failure and disease recurrence while motivating rational implementation of relapse-specific therapies. The degree of genetic divergence between primary and relapsed MBs varied by subgroup but suggested considerably higher conservation than prior estimates.

scholarly journals Clinical Outcomes and Patient-Matched Molecular Composition of Relapsed Medulloblastoma

2021 ◽  
Vol 39 (7) ◽  
pp. 807-821
Author(s):  
Rahul Kumar ◽  
Kyle S. Smith ◽  
Maximilian Deng ◽  
Colt Terhune ◽  
Giles W. Robinson ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Local Relapse ◽  
Genetic Alterations ◽  
Driver Genes ◽  
Methylation Array ◽  
Molecular Subgroup ◽  
Term Survival ◽  
Molecular Features ◽  
Group 4 ◽  
Group 3

PURPOSE We sought to investigate clinical outcomes of relapsed medulloblastoma and to compare molecular features between patient-matched diagnostic and relapsed tumors. METHODS Children and infants enrolled on either SJMB03 (NCT00085202) or SJYC07 (NCT00602667) trials who experienced medulloblastoma relapse were analyzed for clinical outcomes, including anatomic and temporal patterns of relapse and postrelapse survival. A largely independent, paired molecular cohort was analyzed by DNA methylation array and next-generation sequencing. RESULTS A total of 72 of 329 (22%) SJMB03 and 52 of 79 (66%) SJYC07 patients experienced relapse with significant representation of Group 3 and wingless tumors. Although most patients exhibited some distal disease (79%), 38% of patients with sonic hedgehog tumors experienced isolated local relapse. Time to relapse and postrelapse survival varied by molecular subgroup with longer latencies for patients with Group 4 tumors. Postrelapse radiation therapy among previously nonirradiated SJYC07 patients was associated with long-term survival. Reirradiation was only temporizing for SJMB03 patients. Among 127 patients with patient-matched tumor pairs, 9 (7%) experienced subsequent nonmedulloblastoma CNS malignancies. Subgroup (96%) and subtype (80%) stabilities were largely maintained among the remainder. Rare subgroup divergence was observed from Group 4 to Group 3 tumors, which is coincident with genetic alterations involving MYC, MYCN, and FBXW7. Subgroup-specific patterns of alteration were identified for driver genes and chromosome arms. CONCLUSION Clinical behavior of relapsed medulloblastoma must be contextualized in terms of up-front therapies and molecular classifications. Group 4 tumors exhibit slower biological progression. Utility of radiation at relapse is dependent on patient age and prior treatments. Degree and patterns of molecular conservation at relapse vary by subgroup. Relapse tissue enables verification of molecular targets and identification of occult secondary malignancies.

scholarly journals PATH-54. MULTI-DIMENSIONAL MOLECULAR CHARACTERIZATION OF PATIENT-MATCHED MEDULLOBLASTOMA AT DIAGNOSIS AND RELAPSE

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi155-vi155
Author(s):  
Rahul Kumar ◽  
Maximilian Deng ◽  
Kyle Smith ◽  
Anthony P Y Liu ◽  
Vasilisa Rudneva ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Copy Number ◽  
Molecular Subgroup ◽  
Global Methylation ◽  
Primary Tumors ◽  
Early Therapy ◽  
Group 4 ◽  
Group 3 ◽  
Relapsed Disease

Abstract INTRODUCTION Recurrent medulloblastoma (MB) confers an abysmal prognosis with ~10% 5-year overall survival. Optimal treatment paradigms for relapsed disease are largely unknown. Conservation of molecular subgroup at relapse has been described and divergent clonal evolution implicated, yet multi-dimensional molecular characterization of larger cohorts are warranted to substantiate these findings and to disclose potential mechanisms underlying treatment failure and disease recurrence. METHODS A multi-institutional series of 85 patient-matched, primary MBs and their relapses was profiled by DNA methylation array (Illumina 450K/850K). Entity and molecular subgroup classifications were assigned using random forest tumor classifiers (Molecular Neuropathology v.11b4). Genome-wide copy-number aberrations were also inferred from these data while parallel next-generation (whole-exome or targeted panel) sequencing on the majority of the cohort facilitated inference of somatic driver mutations. RESULTS Comprised of WNT (1%), SHH (41%), Group 3 (22%), Group 4 (35%), primary tumors largely retained subgroup affiliation at relapse with the notable exception of 14% of cases. The majority (8/12) of discrepant classifications were determined to be secondary glioblastomas, while three Group 4 primary tumors relapsed as Group 3. Amongst conserved pairs, copy-number analyses suggest somatic clonal divergence between primary MBs and their respective relapses with an average of 0.8 (range 0–5) primary-specific and 2.0 (range 0–11) relapse-specific cytogenetic alterations. Despite high global methylation correlations between primary/relapse pairs (median 0.95), epigenetic evolution at relapse is suggested by the lower degree of conservation amongst promoter-associated probes (median 0.83, p < 2.2e-16). CONCLUSION Secondary malignancy, particularly glioblastoma, may masquerade as relapsed MB, highlighting the utility of molecular characterization for relapsed disease and necessity for vigilant clinical surveillance. By deciphering the evolution of MB from diagnosis to relapse, a fundamental understanding of disease pathogenesis may be garnered, motivating rational and targeted clinical interventions in early therapy and at the time of relapse.

Does histological assessment accurately distinguish separate primary lung adenocarcinomas from intrapulmonary metastases? A study of paired resected lung nodules in 32 patients using a routine next-generation sequencing panel for driver mutations

2021 ◽  
pp. jclinpath-2021-207421
Author(s):  
Frido K Bruehl ◽  
Erika E Doxtader ◽  
Yu-Wei Cheng ◽  
Daniel H Farkas ◽  
Carol Farver ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Molecular Analysis ◽  
Low Frequency ◽  
Driver Mutations ◽  
Lung Nodules ◽  
Driver Gene ◽  
Next Generation ◽  
Histological Assessment ◽  
Lung Adenocarcinomas ◽  
Generation Sequencing

AimVarious approaches have been reported for distinguishing separate primary lung adenocarcinomas from intrapulmonary metastases in patients with two lung nodules. The aim of this study was to determine whether histological assessment is reliable and accurate in distinguishing separate primary lung adenocarcinomas from intrapulmonary metastases using routine molecular findings as an adjunct.MethodsWe studied resected tumour pairs from 32 patients with lung adenocarcinomas in different lobes. In 15 of 32 tumour pairs, next-generation sequencing (NGS) for common driver mutations was performed on both nodules. The remainder of tumour pairs underwent limited NGS, or EGFR genotyping. Tumour pairs with different drivers (or one driver/one wild-type) were classified as molecularly unrelated, while those with identical low-frequency drivers were classified as related. Three pathologists independently and blinded to the molecular results categorised tumour pairs as related or unrelated based on histological assessment.ResultsOf 32 pairs, 15 were classified as related by histological assessment, and 17 as unrelated. Of 15 classified as related by histology, 6 were classified as related by molecular analysis, 4 were unrelated and 5 were indeterminate. Of 17 classified as unrelated by histology, 14 were classified as unrelated by molecular analysis, none was related and 3 were indeterminate. Histological assessment of relatedness was inaccurate in 4/32 (12.5%) tumour pairs.ConclusionsA small but significant subset of two-nodule adenocarcinoma pairs is inaccurately judged as related by histological assessment, and can be proven to be unrelated by molecular analysis (driver gene mutations), leading to significant downstaging.

scholarly journals Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors

2018 ◽  
Vol 116 (2) ◽  
pp. 619-624 ◽  
Author(s):  
Charles Li ◽  
Elena Bonazzoli ◽  
Stefania Bellone ◽  
Jungmin Choi ◽  
Weilai Dong ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Somatic Mutations ◽  
Driver Mutations ◽  
Cancer Evolution ◽  
Metastatic Tumors ◽  
Driver Genes ◽  
Primary Tumors ◽  
Mutational Landscape ◽  
Recurrent Tumors ◽  
Bet Inhibitors

Ovarian cancer remains the most lethal gynecologic malignancy. We analyzed the mutational landscape of 64 primary, 41 metastatic, and 17 recurrent fresh-frozen tumors from 77 patients along with matched normal DNA, by whole-exome sequencing (WES). We also sequenced 13 pairs of synchronous bilateral ovarian cancer (SBOC) to evaluate the evolutionary history. Lastly, to search for therapeutic targets, we evaluated the activity of the Bromodomain and Extra-Terminal motif (BET) inhibitor GS-626510 on primary tumors and xenografts harboring c-MYC amplifications. In line with previous studies, the large majority of germline and somatic mutations were found in BRCA1/2 (21%) and TP53 (86%) genes, respectively. Among mutations in known cancer driver genes, 77% were transmitted from primary tumors to metastatic tumors, and 80% from primary to recurrent tumors, indicating that driver mutations are commonly retained during ovarian cancer evolution. Importantly, the number, mutation spectra, and signatures in matched primary–metastatic tumors were extremely similar, suggesting transcoelomic metastases as an early dissemination process using preexisting metastatic ability rather than an evolution model. Similarly, comparison of SBOC showed extensive sharing of somatic mutations, unequivocally indicating a common ancestry in all cases. Among the 17 patients with matched tumors, four patients gained PIK3CA amplifications and two patients gained c-MYC amplifications in the recurrent tumors, with no loss of amplification or gain of deletions. Primary cell lines and xenografts derived from chemotherapy-resistant tumors demonstrated sensitivity to JQ1 and GS-626510 (P = 0.01), suggesting that oral BET inhibitors represent a class of personalized therapeutics in patients harboring recurrent/chemotherapy-resistant disease.

Rapid/warm autopsy to reveal APOBEC-mutagenesis as driver of heterogeneity of metastatic thoracic tumors.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 9023-9023
Author(s):  
Nitin Roper ◽  
Tapan K Maity ◽  
Shaojian Gao ◽  
Abhilash Karavattu Venugopalan ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Copy Number ◽  
Thymic Carcinoma ◽  
Driver Mutations ◽  
Patient Specific ◽  
Primary Tumors ◽  
Metastatic Lung ◽  
Organ Specific ◽  
Proteomic Analyses ◽  
Copy Number Changes

9023 Background: Intratumor heterogeneity has been characterized among multiple cancer types. In lung adenocarcinoma, APOBEC-mutagenesis has been shown to be a source of heterogeneity. However, these data are largely limited to early stage primary tumors. There is limited information about the role of APOBEC-mutagenesis and somatic variants, copy number changes, transcript and protein expression in influencing tumor heterogeneity in metastatic lung adenocarcinoma and other thoracic tumors. Methods: We applied whole exome sequencing, RNA-seq, OncoScan CNV and mass spectrometry-based proteomic analyses on 46 tumor regions from metastatic sites including lung, liver and kidney, obtained by rapid/warm autopsy from 4 patients (pts) with stage IV lung adenocarcinoma, 1 pt each with pleural mesothelioma and thymic carcinoma. The autopsy procedure was initiated between 2-4 hours of death. Results: All tumors displayed organ-specific, branched evolution that was consistent across exome, transcriptome and proteomic analyses. The degree of heterogeneity at the genomic and proteomic level was patient-specific. There was extensive heterogeneity within the tumors of one of four patients with lung adenocarcinoma and in the thymic carcinoma patient (both non-smokers) with multiple driver mutations and copy number changes occurring in only some of the tumors suggesting ongoing late tumor evolution. Further examination of the heterogenous thymic and lung adenocarcinoma tumors showed strong enrichment with the APOBEC-mutagenesis pattern and high associated levels of APOBEC3B mRNA. Conclusions: Metastatic lung adenocarcinoma, thymic carcinoma and mesothelioma evolve through a branched, organ-specific process with marked differences in the acquisition of significant driver mutations and copy number changes. APOBEC3B is a potential driver of heterogeneity in pts with advanced, heterogeneous metastatic lung adenocarcinoma and thymic carcinoma and needs to be evaluated further.

scholarly journals The evolutionary history of 2,658 cancers

2017 ◽  
Author(s):  
Moritz Gerstung ◽  
Clemency Jolly ◽  
Ignaty Leshchiner ◽  
Stefan C. Dentro ◽  
Santiago Gonzalez ◽  
...  
Keyword(s):  
Copy Number ◽  
Timing Analysis ◽  
Point Mutations ◽  
Life History Evolution ◽  
Driver Mutations ◽  
Driver Genes ◽  
Somatic Evolution ◽  
History Of ◽  
Small Set ◽  
Trisomy 7

SummaryCancer develops through a process of somatic evolution. Here, we use whole-genome sequencing of 2,778 tumour samples from 2,658 donors to reconstruct the life history, evolution of mutational processes, and driver mutation sequences of 39 cancer types. The early phases of oncogenesis are driven by point mutations in a small set of driver genes, often including biallelic inactivation of tumour suppressors. Early oncogenesis is also characterised by specific copy number gains, such as trisomy 7 in glioblastoma or isochromosome 17q in medulloblastoma. By contrast, increased genomic instability, a nearly four-fold diversification of driver genes, and an acceleration of point mutation processes are features of later stages. Copy-number alterations often occur in mitotic crises leading to simultaneous gains of multiple chromosomal segments. Timing analysis suggests that driver mutations often precede diagnosis by many years, and in some cases decades, providing a window of opportunity for early cancer detection.

scholarly journals Hepato curative effects of Silymarin and Cymbopogoncitratus stem infusion: RCT

2021 ◽  
Vol 15 (6) ◽  
pp. 1966-1969
Author(s):  
Sidra Mumal ◽  
Abdul Azeem ◽  
Talal Zafar ◽  
Hina Aslam ◽  
Tasneem Murad ◽  
...  
Keyword(s):  
Synergistic Effects ◽  
Serum Markers ◽  
Control Group ◽  
P Value ◽  
Trial Methodology ◽  
Adult Rats ◽  
Sinusoidal Dilatation ◽  
Group 4 ◽  
Group 3 ◽  
Group 2

People all around the world suffer from liver diseases, which is a serious health problem. Purpose: To observe the synergistic effects of Silymarin and Cymbopogoncitratus stem infusion on liver in acetaminophen induced hepatotoxicity in rats. Study Design: Laboratory-Based Randomized Control Trial. Methodology: Total forty adult rats were divided into four groups (10 each). Group 1 was taken as control group. After initial sampling at day 0, Acetaminophen (300 mg/kg) was injected to 30 rats via intra-peritoneal route. At day 8, rats were further divided into three groups. Group 2 was a disease control group. Group 3 was given Silymarin (100 mg/kg) and group 4 was treated with Silymarin (100 mg/kg) plus Cymbopogoncitratus stem infusion (130 mg/kg) through gavage method for fourteen days. At day 21, rats were sacrificed for histological examination after terminal sampling. Statistical Analysis: Mean± SEM was calculated and analyzed through SPSS 20. P-value less than 0.05 was considered statistically significant. Results: Rats from group 2 showed marked elevation (p<0.05) in serum markers. There was marked sinusoidal dilatation and necrosis present in group 2 rats.Silymarinin group 3 and Silymarin plus Cymbopogoncitratus stem infusion in group 4 significantly lowered the biochemical enzymes as well as considerably reversed the histological changes in comparison to group 2 rats. Conclusion: We concluded in present study that synergism was observed in group 4 rats. There was more reversal of hepatic injury in group 4 rats. Key words: Cymbopogoncitratus, Silymarin and Synergism.

scholarly journals MET amplification identified by next-generation sequencing and its clinical relevance for MET inhibitors

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Lun-Xi Peng ◽  
Guang-Ling Jie ◽  
An-Na Li ◽  
Si-Yang Liu ◽  
Hao Sun ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Copy Number ◽  
Kinase Inhibitor ◽  
De Novo ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Precision Oncology ◽  
Next Generation ◽  
Driver Genes ◽  
Generation Sequencing

Abstract Background MET amplification plays an important role in the development of non-small-cell lung cancer (NSCLC) either de novo or in resistance to epidermal growth factor receptor tyrosine–kinase inhibitor (EGFR-TKI) settings. Fluorescence in situ hybridization (FISH) is the standard method for MET amplification. With more and more discoveries of oncogenic driver genes, next-generation sequencing (NGS) plays a significant role in precision oncology. Meanwhile, the role of NGS in MET amplification remains uncertain. Methods Forty patients diagnosed with advanced NSCLC were included. FISH and NGS were conducted prior to MET inhibitors treatment. MET amplification by FISH was defined as a MET/CEP7 ratio of  >  2.0 and/or copy number (CN)  >  5. MET amplification by NGS was defined as gene copy number (GCN)  ≥  5. Results The concordance rate among FISH and NGS was 62.5% (25/40). MET amplification identified by FISH showed the optimal predictive value. The partial response (PR) rate was 68.0% (17/25 with MET amplification) vs. 6.7% (1/15 without MET amplification); the median progression-free survival (PFS) was 5.4 months versus 1.0 months (P  < 0.001). MET amplification identified by NGS failed to distinguish significant clinical outcomes. The PR rate was 60.0% (6/10, with MET GCN  ≥ 5) vs. 40.0% (12/30, with MET GCN  < 5); the median PFS was 4.8 months vs. 2.2 months (P  = 0.357). The PR rate was 68.8% (11/16) and the median PFS was 4.8 months in patients with focal amplification by NGS. Conclusions MET amplification identified by FISH remains the optimal biomarker to identify suitable candidates for MET-TKI therapy. In comparison, amplification identified by NGS seems not as robust to be effective predictive biomarker. Further exploration is needed regarding the focal amplification by NGS in predicting the efficacy.

scholarly journals Serum Procalcitonic (PCT) Versus Serum C - Reactive Protein (CRP) for Severity of Organ Dysfunction in Sepsis

2020 ◽  
Vol 3 (2) ◽  
pp. 24-27
Author(s):  
Sirikonda Aishwarya ◽  
Karankoti Raj Kumar ◽  
Rallabhandi Sai Sri Harsha ◽  
Patnala Chakradhar
Keyword(s):  
Intensive Care ◽  
Organ Dysfunction ◽  
Plasma Concentrations ◽  
Age Groups ◽  
P Value ◽  
C Reactive Protein ◽  
Adequate Treatment ◽  
Reactive Protein ◽  
Group 4 ◽  
Group 3

Background: Intensive care units (ICUs), despite advances in critical care nursing, have frequent issues with early diagnosis and adequate treatment. Recently discovered world-class procalcitonin (PCT), a revolutionary laboratory marker, has been shown to be useful in this regard. The objective is to Comparison of concentrations of serum procalcitonin (PCT) and c-reactive protein (CRP) with a comparable level of organ malfunction during sepsis and evaluation of the interaction between serum PCT and CRP concentrations with different organ malfunction occurrence in sepsis. Design: It is a Hospital-Based Prospective study. Participants and Setting: Fifty people were admitted to the intensive care unit of Gandhi Medical College. Subjects and Methods: The extent of sepsis-related organ impairment was evaluated with the sequential organ failure assessment (SOFA) on day 1. Patients were identified by category 1(0-6), category 2(7-12), group 3(13-18), and group 4(19-24) in 4 separate classes with varying organ impairment seriousness of sepsis. Serum PCT and CRP concentrations have been measured. Results: The majority of the patients belonged to the age groups of 60-69 years (30%) and 50-59 years (22%) Majority of the patients belonged to the Sofa group 1 around 42% followed by sofa group 2 with 38%, sofa group 3 with 16% and the least belonged to the sofa group 4 with 4%. The mean PCT and CRP concentration in those who survived was 14.73 ng/ml and 149.916mg/L respectively and in those who died were 45.76 ng/ml (p-value <0.001) and 183.584 mg/L (p-value 0.172) respectively. The linear correlation between PCT plasma concentrations and the four groups was significantly stronger than with CRP. Conclusion: In SOFA and serum PCT, The level of organ dysfunction and complications in sepsis patients is closely related to serum CRP levels.

Serum and Bronchoalveolar Lavage Fluid 25(OH)Vitamin D3 Levels in HIV-1 and Tuberculosis: A Cross-Sectional Study from a Tertiary Care Center in North India

2018 ◽  
Vol 16 (2) ◽  
pp. 167-173
Author(s):  
Sanjeev Sinha ◽  
Kartik Gupta ◽  
Dibyakanti Mandal ◽  
B.K. Das ◽  
R.M. Pandey
Keyword(s):  
Vitamin D ◽  
Lavage Fluid ◽  
Cross Sectional Study ◽  
P Value ◽  
Vitamin D Metabolites ◽  
Cross Sectional ◽  
Group 4 ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Background: Vitamin D is an immunomodulator, and its deficiency is associated with Tuberculosis (TB) infection. Bronchoalveolar lavage fluid (BALF) is a rich milieu of macrophages that form the first line of defense against invading TB bacilli. As there is an increased prevalence of vitamin D deficiency in TB and human immunodeficiency virus-1 (HIV-1) subjects, we intend exploring the possibility of a localized deficiency of vitamin D metabolites in BALF of these patients. Objective: The primary objective was to assess the level of 25D3 in serum and BALF of subjects and look for a significant difference among patients and controls. The secondary objective was to find a correlation between serum and BALF 25D3 levels. Methods: We performed a cross-sectional study with subjects divided into four groups: Controls (group 1), HIV positive without active TB (group 2), active TB without HIV (group 3), and HIV-TB coinfection (group 4). BALF and serum 25D3 levels were compared between the groups. Results: Among the 149 (an immunomodulator) successive subjects enrolled, there were 40 subjects in group 1 (HIV-TB-), 48 in group 2 (HIV+TB-), 37 in group 3 (HIV-TB+), and 24 in group 4 (HIV+TB+). Females constituted 31.6% of the study subjects. In groups 3 and 4, there were significantly lower serum 25D3 levels compared to group 1 (p-value group 3: 0.002; group 4: 0.012). In groups 2, 3, and 4, there were significantly lower BALF 25D3 levels compared to group 1 (p-value group 2: 0.000; group 3: 0.000; group 4: 0.001). There was a significant correlation between serum and BALF 25D3 levels (Spearman’s rank correlation coefficient 0.318, p-value = 0.0001). Conclusion: Lower levels of serum and BALF 25D3 were observed in HIV, TB, and HIV-TB coinfected patients. Localized deficiency of vitamin D metabolites might be associated with increased vulnerability to TB infection.

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