miR-21 as a diagnostic and prognostic biomarker in glioma: tissue and serum expression analysis in a Pakistani cohort

May combine two claims.

No miR-21 expression was detected in adjacent non-malignant brain tissue, indicating its elevated expression was localized to tumor cells.

“No miR-21 expression was detected in adjacent non-malignant brain tissue, indicating its elevated expression was localized to tumor cells [28]”

• cites [28] Piwecka M et al (2015) Comprehensive analysis of MicroRNA expression profile in malignant glioma tissues. Mol Oncol 9(7):1324–1340 sourceDisputed

  Section 3.1 identifies miR-21 as up-regulated in both tumor and adjacent peritumoral tissue, contrary to the claim that it was undetected in adjacent tissue. Section 4.1 likewise reports miR-21 overexpression among changes in adjacent brain, so the paper does not support localization of its elevated expression to tumor tissue. (LLM, conf=0.91)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured

May combine two claims.

Extracellular microRNAs are stable and detectable in body fluids such as serum, plasma, urine, and cerebrospinal fluid, making them suitable as biomarkers.

“Extracellular miRs are notably stable and detectable in various body fluids such as serum, plasma, urine, and cerebrospinal fluid (CSF), making them ideal for use as biomarkers [8].”

• cites [8] Jiang G et al (2020) Prognostic value of miR-21 in gliomas: comprehensive study based on meta-analysis and TCGA dataset validation. Sci Rep 10(1):4220 sourcePartly supported

  The Discussion (page not available in our copy) says miRNAs can be easily and stably detected in plasma, serum, and cerebrospinal fluid and are therefore potential tumor biomarkers. It does not mention urine, so the full list of body fluids in the citing sentence is not supported. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

miR-21 impacts the PI3K/AKT/mTOR pathway in gliomas.

“Additionally, miR-21 impacts the PI3K/AKT/mTOR pathway, a central regulator of cell survival, growth, and metabolism, might contributing to the aggressive nature of gliomas [13].”

• cites [13] Zirak G (2022) The role of micro RNAs in regulating PI3K/AKT signaling pathways in glioblastoma. Iran J Pathol Vol 17(2):122–136 sourceSupported

May combine two claims.

miR-21 is significantly upregulated in glioma tissues and strongly correlates with tumor characteristics and invasiveness.

“miR-21, an oncomiR in glioma, showed significant upregulation in glioma tissues, strongly correlating with tumor characteristics and invasiveness [26].”

• cites [26] Wu L et al (2013) MicroRNA-21 expression is associated with overall survival in patients with glioma. Diagn Pathol 8:1–5 sourcePartly supported

  The Results section reports significantly higher miR-21 expression in glioma tissues than in non-neoplastic brain tissues, and the Discussion reports a significant correlation with aggressive clinicopathological features. The Abstract Background says miR-21 is associated with glioma invasion, but the paper does not establish the claimed strong correlation between expression and invasiveness specifically. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The prognosis of glioma remains poor despite advances in treatment strategies and surgical interventions.

“Despite advances in treatment strategies and surgical interventions, the diagnosis and overall survival of glioma patients remain poor [22].”

• cites [22] Sharma A, Graber JJ (2021) Overview of prognostic factors in adult gliomas. Annals Palliat Med 10(1):86374–86874 sourcePartly supported

  The High grade glioma section (page unavailable) says that treatment research has not dramatically changed survival and that grade IV astrocytoma survival remains 16–22 months despite surgical resection being standard care. The claim extends that poor-survival assessment to glioma patients generally, whereas the Survival and prognostication section reports substantially variable survival for low-grade glioma. The paper also discusses difficulty predicting outcomes, not that diagnosis itself remains poor. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The latest WHO CNS5 2021 glioma tumor classification emphasizes the use of genetic alterations in IDH, ATRX, Ki-67, and p53 in association with glioma patient overall survival.

“The latest WHO CNS5 2021 glioma tumor classification emphasizes the use of genetic alterations in IDH, ATRX, Ki-67, and p53 in association with glioma patient overall survival.”

• cites [2] Torp SH, Solheim O, Skjulsvik AJ (2022) The WHO 2021 classification of central nervous system tumours: a practical update on what neurosurgeons need to know—a minireview. Acta Neurochir 164(9):2453–2464 sourcePartly supported

  In “Specific tumour updates > Gliomas, glioneuronal and neuronal tumours” (page unavailable), Table 5 links IDH mutations to better prognosis, and the discussion uses ATRX and TP53 findings in glioma diagnosis. It does not link ATRX or TP53 alterations to overall survival; it describes Ki-67 as a proliferative index, not a genetic alteration, and says it lacks a reliable threshold for risk stratification. The claim therefore overstates the role of these four markers in relation to overall survival. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

IDH, ATRX, Ki-67, and p53 markers are significantly associated with disease prognosis and play a crucial role in designing treatment strategies for better glioma outcomes.

“These markers are significantly associated with disease prognosis and play a crucial role in designing treatment strategies for better glioma outcomes [2].”

• cites [2] Torp SH, Solheim O, Skjulsvik AJ (2022) The WHO 2021 classification of central nervous system tumours: a practical update on what neurosurgeons need to know—a minireview. Acta Neurochir 164(9):2453–2464 sourcePartly supported

  In ‘Gliomas, glioneuronal and neuronal tumours’ (page not provided), Table 5 associates IDH mutations with better prognosis, and the text says Ki-67 increases with tumour grade. But it says Ki-67 has no reliable threshold for identifying patients at increased risk of recurrence; it presents ATRX and TP53 chiefly as diagnostic markers, not as prognostic markers. The paper does not establish that these four markers guide treatment strategies to improve glioma outcomes. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

miR-21 also regulates STAT3 gene activation and expression of hTERT in a STAT3-dependent manner.

“miR-21 also regulates STAT3 gene activation and expression of hTERT in a STAT3dependent manner [45].”

• cites [45] Bian Z et al (2021) Noncoding RNAs involved in the STAT3 pathway in glioma. Cancer Cell Int 21:1–15 sourceSupported

May combine two claims.

miR-21 is associated with autophagy in glioma through the PI3K/AKT/mTOR pathway, and its high expression is linked to high-grade glioma.

“miR-21 is associated with autophagy in glioma through the PI3K/AKT/mTOR pathway, and its high expression is linked to high-grade glioma [44].”

• cites [44] Amin W et al (2024) Autophagy-associated biomarkers ULK2, UVRAG, and MiRNAs miR-21, miR-126, and miR-374: prognostic significance in glioma patients. PLoS ONE 19(9):e0311308 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

PIK3R1 acts as a tumor suppressor by inhibiting the PI3K/AKT signaling pathway, which promotes cell proliferation, migration, and invasion in cancer.

“Studies have shown that PIK3R1, coding for the protein p85α, acts as a tumor suppressor by inhibiting the PI3K/AKT signaling pathway, which is known for promoting cell proliferation, migration, and invasion in cancer [38].”

• cites [38] Danish F et al (2024) Investigating the association between the autophagy markers LC3B, SQSTM1/p62, and DRAM and autophagy-Related genes in glioma. Int J Mol Sci 25(1):572 sourcePartly supported

  The Discussion (page unavailable) associates abnormal PI3K/AKT/mTOR activation with tumor development, progression, and invasion, supporting the pathway-related part of the sentence. Our copy does not mention PIK3R1 or p85α, or say that PIK3R1 suppresses tumors by inhibiting that pathway; searches for both terms returned no matching passage. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

STAT3 binds to miR-21 promoter and regulates its expression.

“STAT3 binds to miR-21 promoter and regulates its expression.”

• cites [45] Bian Z et al (2021) Noncoding RNAs involved in the STAT3 pathway in glioma. Cancer Cell Int 21:1–15 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

PIK3R1 is directly targeted and negatively regulated by miR-21.

“PIK3R1 is directly targeted and negatively regulated by miR-21.”

• cites [39] Yan L-X et al (2015) PIK3R1 targeting by miR-21 suppresses tumor cell migration and invasion by reducing PI3K/AKT signaling and reversing EMT, and predicts clinical outcome of breast cancer. Int J Oncol 48(2):471–484 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

GAB1 is a direct target of miR-21 and is important for tumor angiogenesis and metastasis.

“GAB1 a direct target of miR-21, is an important gene for tumor angiogenesis and metastasis, it is also involved in diverse biological processes such as cellular proliferation and differentiation, survival, angiogenesis, and inflammation.”

• cites [43] Pérez-Baena MJ et al (2023) The role of GAB1 in cancer. Cancers 15(16):4179 sourcePartly supported

  Section 3, “Role of GAB1 in Cancer” (page not provided), says GAB1 is involved in biological processes fundamental to tumor angiogenesis and metastasis; sections 3.2 and 3.3 give examples of those roles. The passages do not identify GAB1 as a direct target of miR-21, so that part of the attributed claim is unsupported. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

May combine two claims.

When miR-21 is overexpressed, it leads to downregulation of PIK3R1, resulting in more aggressive tumor behavior.

“When miR-21 is overexpressed, it leads to the downregulation of PIK3R1, resulting in more aggressive tumor behavior, this relationship is further evidenced by miR-21 knockout models, where the removal of miR-21 restores PIK3R1 activity, leading to reduced PI3K/AKT pathway signaling and, consequently, the inhibition of tumor growth and invasion [39].”

• cites [39] Yan L-X et al (2015) PIK3R1 targeting by miR-21 suppresses tumor cell migration and invasion by reducing PI3K/AKT signaling and reversing EMT, and predicts clinical outcome of breast cancer. Int J Oncol 48(2):471–484 sourcePartly supported

  The Results section reports that miR-21 overexpression reduced PIK3R1 levels, while inhibiting miR-21 increased PIK3R1 and reduced PI3K/AKT signaling; the paper also links miR-21 targeting of PIK3R1 to breast cancer cell growth and invasion. However, the cited sentence describes miR-21 knockout models, whereas the Methods describe transient knockdown using LNA-antimiR-21, not knockout models. Page numbers are unavailable in our copy. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

PTEN acts as a tumor suppressor through inhibiting PI3K/AKT pathway and is a well-established miR-21 target.

“PTEN acts as a tumor suppressor through inhibiting PI3K/AKT pathway, is a wellestablished miR-21 target.”

• cites [44] Amin W et al (2024) Autophagy-associated biomarkers ULK2, UVRAG, and MiRNAs miR-21, miR-126, and miR-374: prognostic significance in glioma patients. PLoS ONE 19(9):e0311308 sourceSupported

May combine two claims.

Serum can be a source of microRNAs as they can pass through the blood-brain barrier and remain stable in the blood.

“Serum can be a source of microRNAs as they can pass through the blood-brain barrier and remain stable in the blood [36].”

• cites [36] Ahmed SI et al (2018) CD133 expression in glioblastoma multiforme: A literature review. Cureus 10(10):e3439 sourceCould not verify

  The Introduction and Review discuss CD133 expression in glioblastoma, including mRNA levels and shRNA-mediated suppression, but do not address serum microRNAs. Searches for microRNAs crossing the blood-brain barrier and for circulating serum biomarkers found no passage supporting the claim. (LLM, conf=0.77)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

These pathways are well known to be linked with GBM pathogenesis.

“These pathways are well known to be linked with GBM pathogenesis [37].”

• cites [37] Șovrea AS et al (2022) Multiple faces of the glioblastoma microenvironment. Int J Mol Sci 23(2):595 sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

miR-21 enhances NF-κB and IL-6 upregulation, forming a positive feedback loop in response to inflammatory stimulus or DNA damage.

“After which miR-21 enhances NF-κB and IL-6 upregulation.This upregulation of NF-κB and IL-6 induces miR-21 expression and forms a positive feedback loop in response to any inflammatory stimulus or DNA damage [46].”

• cites [46] Aloizou A-M et al (2020) The role of MiRNA-21 in gliomas: hope for a novel therapeutic intervention? Toxicol Rep 7:1514–1530 sourcePartly supported

  In “MiRNA-21-induced glioma proliferation” (page unavailable), the review says miR-21 suppresses an inhibitor of NF-κB, allowing NF-κB overactivation. “MiRNA-21 upregulation factors” (page unavailable) links IL-6/STAT3 signaling to miR-21 expression and describes feedback between miR-21 and STAT3. It does not establish that miR-21 upregulates IL-6 or that NF-κB and IL-6 form the claimed feedback loop in response to any inflammatory stimulus or DNA damage. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The increase of IL-6 causes STAT3 to translocate to nucleus and induce miR-21 through binding to its upstream enhancer region.

“The increase of IL-6 the master TF, STAT3 translocate to nucleus and induces miR-21 through binding to its upstream enhancer region.”

• cites [46] Aloizou A-M et al (2020) The role of MiRNA-21 in gliomas: hope for a novel therapeutic intervention? Toxicol Rep 7:1514–1530 sourcePartly supported

  The “MiRNA-21 upregulation factors” section says the miR-21 gene has conserved STAT3 binding sites and that IL-6/STAT3 signaling could explain miR-21 upregulation. It does not say that increased IL-6 causes STAT3 to translocate to the nucleus or specify an upstream enhancer as the binding location; the claimed mechanism is more definite and detailed than the review’s account. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

May combine two claims.

miR-21 tissue expression shows a slight positive correlation with tumor volume, but the correlation is not statistically significant (r=0.15, p=0.163).

“While tissue expression of miR-21 showed a positive trend with tumor volume, this correlation did not reach statistical significance.”

• Also stated in: § MicroRNA 21 Expression in Tumor Regions and Volume of Glioma Patients · plain

  “Our findings revealed a pattern of slight positive correlation between miR-21 expression levels and tumor volume, although this correlation was not statistically significant (r=0.15,p=0.163) (Figure 2B).”

May combine two claims.

Serum miR-21 expression shows a positive correlation with tumor volume, but the correlation is not statistically significant (r=0.37, p=0.139).

“Similarly, mean expression value of miR-21 according to tumor region are represented in Figure 8A and miR-21 expression shows positive correlation using pearson's method with tumor volume, although this correlation was not significant (r=0.37,p=0.139) in Figure 8B.”

May combine two claims.

miR-21 tissue expression varies across tumor regions, with high expression in Bi-Frontal, right intraventricular, right parietal, and right temporal regions, and down-regulation in supra sellar and left temporal parietal regions.

“High expression levels were observed in the Bi-Frontal, right intraventricular region, followed by the right parietal and right temporal regions.Conversely, miR-21 expression was down-regulated in tumors located within the supra sellar and left temporal parietal regions (Figure 2A).”

May combine two claims.

miR-21 target genes are notably involved in MAPK signaling, cancer pathways, EGF/EGFR signaling, glioma, Glioblastoma signaling, Ras signaling, and EGFR tyrosine kinase.

“Notable pathways included were MAPK signaling, cancer pathways, EGF/EGFR signaling, glioma, Glioblastoma signaling, Ras signaling, EGFR tyrosine kinase (Figure 11).”

May combine two claims.

miR-21 expression is related to IDH, ATRX, p53, and Ki-67 index in gliomas.

“Additionally, miR-21 expression is related to IDH (mutation/wildtype), ATRX (lost/retained), p53 (mutation/wildtype), and Ki-67 (high/low) index in gliomas, which can help improve cancer prognosis.”

May combine two claims.

There is a significant correlation between low miR-21 expression and IDH mutant gliomas, which are associated with a good prognosis.

“Moreover, study findings distinctively revealed the significant correlation between low miR-21 expression and IDH mutant gliomas, which are associated with a good prognosis of disease.”

May combine two claims.

76% of patients in the low miR-21 expression group remained alive until the 30th month of survival follow-up, whereas in the high miR-21 expression group, 50% of patients had died by the 20th month of follow-up.

“It is important to note that 76% of patients in the low miR-21 expression group remained alive until the 30 th month of survival follow-up, whereas in the high miR-21 expression group, 50% of patients had died by the 20 th month of follow-up.”

May combine two claims.

There was no significant difference between low and high miR-21 expression groups in terms of overall survival in serum samples (p=0.8), with an AUC curve of 0.48.

“Consequently, the study result may partly reflect a high miR-21 expression in low grade groups and our result showed no significant difference between low and high miR-21 expression groups in terms of overall survival (p=0.8), with an AUC curve of 0.48.”

May combine two claims.

IDH wildtype patients with low miR-21 expression had a survival probability of 50% at the 30th month, while IDH wildtype patients with high miR-21 expression had a survival probability of only 30% (p<0.0001).

“Additionally, IDH wildtype patients with low miR-21 expression had a survival probability of 50% at the 30 th month, while IDH wildtype patients with high miR-21 expression had a survival probability of only 30% (p<0.0001).”

May combine two claims.

miR-21 is closely associated with poor clinical outcomes and aggressive molecular features.

“In summary, our study demonstrates that miR-21 is significantly upregulated in glioma tissues and serum, particularly in high-grade and IDH-wildtype tumors, and is closely associated with poor clinical outcomes and aggressive molecular features.”

May combine two claims.

miR-21 is significantly upregulated in glioma tissues and serum.

“In summary, our study demonstrates that miR-21 is significantly upregulated in glioma tissues and serum, particularly in high-grade and IDH-wildtype tumors, and is closely associated with poor clinical outcomes and aggressive molecular features.”

Probably not a substantial claim: may not pass S3 (load-bearing).

In gliomas, miR-21 exerts oncogenic effects by downregulating tumor suppressor genes PTEN and PDCD4.

“In the context of gliomas, miR-21 exerts its oncogenic effects by downregulating several key tumor suppressor genes, such as PTEN (Phosphatase and Tensin Homolog) and PDCD4 (Programmed Cell Death Protein 4) [11].”

• cites [11] Chawra, HS et al (2024) MicroRNA-21’s role in PTEN suppression and PI3K/AKT activation: implications for cancer biology. Pathol Res Pract 254:55091. https://doi.org/10.1016/j.prp.2024.155091 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

miR-21 modulates the Wnt/β-catenin and STAT3 signaling pathways.

“This miRNA modulates essential oncogenic pathways, including the Wnt/β-catenin signaling pathway, which is crucial for cell proliferation and differentiation, and the STAT3 (Signal Transducer and Activator of Transcription 3) pathway, which plays a significant role in tumorigenesis and immune evasion [12].”

• cites [12] Hashemi M et al (2023) Pre-clinical and clinical importance of miR-21 in human cancers: Tumorigenesis, therapy response, delivery approaches and targeting agents. Pharmacol Res 187:106568 sourceNot checked — no full text of the source

May combine two claims.

miR-21 is significantly upregulated in both glioma tissue and serum, particularly in high-grade and IDH-wildtype tumors.

“miR-21 is significantly upregulated in both glioma tissue and serum, particularly in high-grade and IDH-wildtype tumors.”

May combine two claims.

miR-21 expression is strongly associated with poor clinical outcomes and aggressive molecular features.

“It is strongly associated with poor clinical outcomes and aggressive molecular features.”

May combine two claims.

miR-21 serves as a strong tissue-based prognostic marker in gliomas and a promising serum biomarker for tumor monitoring.

“miR-21 serves as a strong tissue-based prognostic marker in gliomas and a promising serum biomarker for tumor monitoring.”

May combine two claims.

miR-21 prognostic value is robust both alone and in combination with established markers.

“Its prognostic value is robust both alone and in combination with established markers.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Tissue findings align with global data.

“While tissue findings align with global data, further studies are required to validate the serum results.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Written informed consent was obtained from all participants prior to surgery.

“Written informed consent was obtained from all participants prior to surgery.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The study was approved by the Institutional Ethical Review Committee at Aga Khan University Hospital.

“This study was approved by the Institutional Ethical Review Committee (AKU-ERC # 2019-1945-5110, AKU-ERC # 2021-1945-17282; AKU-ERC # 2021-6265-18766) at Aga Khan University Hospital, Karachi, Pakistan.”

Classified as probably not a substantial claim.

U6 expression was used as an endogenous control to normalize miR-21 expression in both tissue and serum samples.

“U6 expression served as housekeeping genes to normalize miR-21 expression in both tissue and serum samples.”

Classified as probably not a substantial claim.

Histological samples of glioma FFPE tissues were examined and graded by a histopathologist.

“Histological samples of glioma formalin-fixed paraffin-embedded (FFPE) tissues were examined and graded by a histopathologist at Aga Khan University Hospital.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Each qPCR reaction was conducted in duplicate, with non-template control and non-primer control included as experimental controls.

“Each reaction was conducted in duplicate, with non-template control (NTC) and non-primer control (NPC) included as experimental controls.”

May combine two claims.

The serum sample cohort (n=42) was less than half the size of the tissue sample group (n=90), which reduces statistical power to detect survival differences.

“First, the serum sample cohort (n=42) was less than half the size of the tissue sample group (n=90), which reduces statistical power to detect survival differences.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

miR-21 targets Spry2, a negative feedback regulator of Ras, and consequently amplifies Ras/MAPK signaling particularly in conjunction with dysfunctional PTEN.

“Studies have found that miR-21 targets Spry2, a negative feedback regulator of Ras, and consequently amplifies Ras/MAPK signaling particularly in conjunction with dysfunctional PTEN.”

• cites [40] Kwak H et al (2011) Downregulation of Spry2 by miR-21 triggers malignancy in human gliomas. Oncogene 30(21):2433–2442 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

miR-21 overexpression may promote glioma growth via overactivation of Ras/MAPK.

“Therefore, miR-21 overexpression may promote glioma growth via overactivation of Ras/MAPK [40].”

• cites [40] Kwak H et al (2011) Downregulation of Spry2 by miR-21 triggers malignancy in human gliomas. Oncogene 30(21):2433–2442 sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

FASLG serves as a direct miR-21 target in GSCs regulating its proliferation.

“Thus, FASLG serves as a direct miR-21 target in GSCs regulating its proliferation [42].”

• cites [42] Shang C et al (2015) MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG. Mol Biol Rep 42:721–727 sourceNot checked — no full text of the source

May combine two claims.

miR-21 acts as an oncogene, binding to FOXO1 transcripts and terminating its translation.

“Here, miR-21 acts as an oncogene, binding to FOXO1 transcripts and terminating its translation.”

• cites [41] Lei B-X et al (2014) miR-21 induces cell proliferation and suppresses the chemosensitivity in glioblastoma cells via downregulation of FOXO1. Int J Clin Exp Med 7(8):2060Not checked — no full text of the source

May combine two claims.

There was a notable difference in grade distribution between the serum and tissue cohorts: serum had a higher proportion of grade 4 gliomas (61.90% vs 48.8%) and a lower proportion of grade 2 tumors (11.90% vs 26.6%).

“Second, there was a notable difference in grade distribution between the cohorts.The serum sample cohort had a substantially higher proportion of grade 4 gliomas (61.90% vs 48.8% in tissue samples) and a lower proportion of grade 2 tumors (11.90% vs 26.6% in tissue samples).”

Probably not a substantial claim: may not pass S3 (load-bearing).

This mechanism could account for the association of poor prognosis in glioma with miR-21 overexpression by inducing chemoresistance in tumor cells.

“This mechanism could also account for the association of poor prognosis in glioma with miR-21 overexpression by inducing chemoresistance in tumor cells [41].”

• cites [41] Lei B-X et al (2014) miR-21 induces cell proliferation and suppresses the chemosensitivity in glioblastoma cells via downregulation of FOXO1. Int J Clin Exp Med 7(8):2060Not checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

miR-21 is involved in regulating apoptosis and growth of Glial Stem Cells (GSCs) through downregulating FASLG proteins.

“miR-21 is involved in regulating apoptosis and growth of Glial Stem Cells (GSCs) through downregulating FASLG proteins.”

• cites [42] Shang C et al (2015) MiR-21 up-regulation mediates glioblastoma cancer stem cells apoptosis and proliferation by targeting FASLG. Mol Biol Rep 42:721–727 sourceNot checked — no full text of the source

May combine two claims.

miR-21 exhibits strong prognostic value, both independently and in combination with established biomarkers, making it a promising tool for glioma diagnosis and prognosis.

“miR-21 exhibits strong prognostic value, both independently and in combination with established biomarkers, making it a promising tool for glioma diagnosis and prognosis.”