Evidence map›Paper›PMID 37675821›Full record

ReviewCancer reports (Hoboken, N.J.)2023

Unraveling the signaling mechanism behind astrocytoma and possible therapeutics strategies: A comprehensive review.

Chowdhury Lutfun Nahar Metu, Sunita Kumari Sutihar, Md Sohel, Fatematuz Zohora, Akayed Hasan, Md Thandu Miah, Tanu Rani Kar, Md Arju Hossain, Md Habibur Rahman

Open access · goldAbstract readReview
In one paragraph

Review in Cancer reports (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Chowdhury Lutfun Nahar MetuBiochemistry and Molecular Biology, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, Bangladesh.
Sunita Kumari SutiharBiochemistry and Molecular Biology, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, Bangladesh.
Md SohelBiochemistry and Molecular Biology, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.ORCID 0000-0001-8344-1976
Fatematuz ZohoraDepartment of Pharmacy, Faculty of Pharmacy, University of Dhaka, Dhaka, Bangladesh.
Akayed HasanDepartment of Pharmacy, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.
Md Thandu MiahDepartment of Pharmacy, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.
Tanu Rani KarDepartment of Biochemistry and Molecular Biology, Primeasia University, Dhaka, Bangladesh.
Md Arju HossainDepartment of Biotechnology and Genetic Engineering, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.
Md Habibur RahmanDepartment of Computer Science and Engineering, Islamic University, Kushtia, Bangladesh.ORCID 0000-0002-5068-2690
Mawlana Bhashani Science and Technology University · BDGopalganj Science and Technology University · BDIslamic University · BDPrimeasia University · BDUniversity of Dhaka · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA form of cancer called astrocytoma can develop in the brain or spinal cord and sometimes causes death. A detailed overview of the precise signaling cascade underlying astrocytoma formation has not yet been revealed, although various factors have been investigated. Therefore, our objective was to unravel and summarize our current understanding of molecular genetics and associated signaling pathways with some possible therapeutic strategies for astrocytoma. RECENT

findingsIn general, four different forms of astrocytoma have been identified in individuals, including circumscribed, diffuse, anaplastic, and multiforme glioblastoma, according to a recent literature review. All types of astrocytoma have a direct connection with some oncogenic signaling cascade. Common signaling is MAPK cascade, including Ras-Raf-ERK, up-regulated with activating EGFR/AKT/PTEN/mTOR and PDGFR. Recent breakthrough studies found that BRAF mutations, including KIAA1549: BRAF and BRAF V600E are responsible for astrocytoma progression. Additionally, cancer progression is influenced by mutations in some tumor suppressor genes, such as the Tp53/ATRX and MGMT mutant. As synthetic medications must cross the blood-brain barrier (BBB), modulating signal systems such as miRNA is the primary option for treating patients with astrocytoma. However, available surgery, radiation therapy, and experimental therapies such as adjuvant therapy, anti-angiogenic therapy, and EGFR-targeting antibody drug are the usual treatment for most types of astrocytoma. Similar to conventional anticancer medications, some phytochemicals slow tumor growth by simultaneously controlling several cellular proteins, including those involved in cell cycle regulation, apoptosis, metastatic spread, tyrosine kinase, growth factor receptor, and antioxidant-related proteins.

conclusionIn conclusion, cellular and molecular signaling is directly associated with the development of astrocytoma, and a combination of conventional and alternative therapies can improve the malignancy of cancer patients.

Indexed as

AstrocytomaBrain NeoplasmsGlioblastomaErbB ReceptorsHumansProto-Oncogene Proteins B-rafErbB ReceptorsProto-Oncogene Proteins B-rafastrocytomagrademutationnatural productssignaling mechanismtreatment

Identifiers

PMID37675821
PMCPMC10598261
OpenAlexW4386507620

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.