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Recent Advances in the Therapeutic Approaches of Glioblastoma Multiforme_Crimson Publishers

Abstract

Glioblastoma Multiforme (GBM, WHO grade IV) is one of the most aggressive, invasive, and lethal intracranial neoplasms, with a low post-diagnosis survival rate. Standard-of-care treatment regimens involving maximal surgical resection, radiotherapy, and genetic anti-tumor compounds like Temozolomide have only been marginally effective in improving overall survival and quality of life. Cell fusion, autophagy, and other complex biological processes affecting GBM pathophysiology are being studied to improve GBM treatment. This paper therefore focuses on oncolytic virus therapy combined with surgical resection, photodynamic therapy, and novel gene therapy, demonstrating how GBM treatment for patients could result in immediate and authentic tumor cytotoxicity and removal, rather than treatment of recurrent GBM. Standard therapy for GBM, including surgery, radiotherapy, and chemotherapy, is called the Stupp regime with the inclusion of Temozolomide (TMZ). It is extremely difficult to design new and effective therapeutic approaches because of the numerous complex biological pathways involved in GBM pathogenesis. Even Stupp regime clinical outcomes have only shown modest benefits with less than 10% of overall 5-year survivorship. A major contributing factor in GBM development is also its interaction with the patient’s host immune system.

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Unstipulated and InexactIndeterminate Dendritic Cell Tumour_Crimson Publishers

Opinion

Indeterminate dendritic cell tumour emerges as an extremely exceptional tumefaction composed of proliferation of dendritic cells or cells of histiocytic lineage. Additionally designated as indeterminate cell histiocytosis, indeterminate cell tumour or indeterminate dendritic cell tumour, true cutaneous dendritic cell tumour may depict solitary or multifocal lesions. Generally, tumefaction is confined to diverse cutaneous surfaces wherein deep seated visceral or regional lymph node involvement is exceptional. Tumour forming indeterminate cells simulate Langerhans cells vis-à-vis morphological and antigenic features. However, indeterminate cells appear devoid of Birbeck granules and lack immune reactivity to langerin (CD207). Median age of disease emergence is 45 years although no age of disease occurrence is exempt. An almost equivalent gender predilection is encountered. Indeterminate dendritic cell tumour predominantly(~88%) implicates diverse cutaneous surfaces. Infrequently, regional lymph nodes (9%) or spleen (2.3%) may be involved [1,2]. Of obscure a etiology, neoplasm expounds varied concurrence between indeterminate cells and Langerhans cells as ~indeterminate cells manifest as Langerhans cells devoid of Birbeck granules ~indeterminate cells represent as immature Langerhans cells. A subset of neoplasms express dendritic cell marker ZBTB46, thereby indicating the emergence of neoplasms directly from bone marrow progenitors, in contrast to embryonic precursors which undergo localized cutaneous regeneration [1,2].

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Deciphering the Ras/MAPK Signaling Pathway in the Progression and Treatment of Hepatocellular Carcinoma_Crimson Publishers

Abstract

Hepatocellular Carcinoma (HCC) is a serious health issue and its frequency is rapidly escalating throughout the world therefore researchers have focused more attention to the Ras/MAPK signaling pathway. The signaling pathways are linked to develop tumors and the Ras/MAPK pathway is one of these pathways, activated in 60% of HCCs with poor prognosis. A number of different proteins causes the abnormal regulation of the MAPK pathway in HCC. Ras, a small GTPase and Raf are the most commonly mutated oncogene supports the critical function of this pathway in oncogenesis. The genetic mutations leading to effector molecule to permanently activated in the Ras/MAPK signaling cascades. The inappropriate activation of this pathway is primarily due to the downregulation of various Ras/MAPK pathway inhibitors including RASSF proteins, GAPs, DUSP1, Spred and Sprouty proteins. The post-transcriptional or epigenetic processes downregulate these cancer suppressor genes. The aim of current study on the primary mutations resulting in aberrant activation of Ras/MAPK pathway and their role on the initiation and progression of HCC. It also offers an update on the various inhibitors to target this central signaling pathway including various Ras, Raf, MEK inhibitors in the context of HCC. Finally, we evaluate the available options for treatment in this context.

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Twirl and Whirl-Myopericytoma _Crimson Publishers

Opinion

Myopericytoma emerges as a distinct myoid neoplasm delineating perivascular distribution of tumour cells. The neoplasm configures a morphological continuum with myofibroma. Myopericytoma is comprised of bland, spindle shaped myoid cells configuring a concentric pattern circumscribing innumerable, miniature vascular articulations. Myofibroma expounds a biphasic tumour pattern and exhibits primitive cellular zones admixed with frequent mitotic figures, tumour necrosis and focal calcification. Aforesaid cellular elements are encompassed within hyalinised nodules constituted of myoid spindle shaped cells. Myopericytoma and myofibroma expound chromosomal mutations within PDGFRB gene. Cellular myofibroma or myopericytoma exemplifies SRF-RELA genetic fusion. Nomenclature of infantile hemangiopericytoma is not recommended. Myopericytoma commonly arises within adult subjects although no age of disease emergence is exempt. Myofibroma may emerge as a congenital lesion or occur within 2 years or within adults and expounds a male predilection [1,2]. Myofibromatosis preponderantly implicates infants and young children wherein majority (~88%) of neoplasms occur <2 years. Solitary infantile myofibromatosis is commonly encountered within male subjects whereas multi-centric infantile myobromatosis expounds a female predilection [1,2]. Myopericytoma and myofibroma preponderantly emerge as cutaneous lesions or may be confined to subcutaneous tissues of extremities, trunk or head and neck region. Exceptionally, neoplasm is encountered within diverse viscera or intracranial sites. Infants with myofibromatosis delineate lesions within various visceral locations as hepatic parenchyma, cardiac muscle, gastrointestinal tract, bone or brain [1,2].

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Myopericytoma emerges as a distinct myoid neoplasm delineating perivascular distribution of tumour cells..

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The Miniscule Eaves-Micro-papillary Carcinoma Breast_Crimson Publishers

Abstract Micro-papillary carcinoma breast emerges as an invasive, exfoliative neoplasm delineating characteristic pseudo-papillary, tubular or morula-like epithelial structures with an inverted or ‘inside out’ tumour pattern. Tumefaction exhibits upregulation of various nutrient transporters as glucose transporter 1 (GLUT1) through activation of transcription factor as hypoxia-inducible factor or upregulation of BC-1514 (C21 or f118), especially within micro-papillary areas. Tumour cells exhibit gains of chromosome 1q, 8q, 17q, 20q and loss of chromosome 1p, 8p, 13q, 16q and 20q. Cellular cytological smears delineate angulated clusters, abortive papillae and isolated malignant cells. Densely cellular tufts of cells configure pseudo-papillae, hollow tubules or morula with circumscribing clear spaces and minimal encompassing fibro-collagenous stroma. Characteristic reverse polarity or an ‘inside out’ pattern of tumour cells pervaded with abundant, eosinophilic cytoplasm, intracytoplasmic mucin and nuclei with a peripheral bulge, knobby or serrated appearance is observed. Neoplastic cells appear immune reactive to Epithelial Membrane Antigen (EMA), CD15s, E-cadherin, p120 catenin, oestrogen receptor(ER), Progesterone Receptor (PR), HER2 or GATA3.

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Micro-papillary carcinoma breast emerges as an invasive, exfoliative neoplasm delineating characteristic pseudo-papillary, tubular or morula

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Synergistic Power of Phytochemicals and Nanotechnology in Cancer Treatment_Crimson Publishers

Abstract Bioactive Phytocompounds (BPCs) naturally found in plants, hold immense potential for cancer treatment. However, their limitations like poor solubility, bioavailability and stability hinder their effectiveness. This review explores how nanotechnology can overcome these limitations and empower phytochemicals in the fight against drug-resistant cancer. Despite advancements, conventional therapies (surgery, radiation, chemotherapy) often suffer from side effects and drug resistance. Understanding the complex signaling pathways involved in cancer development is crucial for designing targeted therapies. Phytochemicals offer diverse biological activities against cancer, but their inherent limitations restrict their use. They can induce apoptosis, inhibit growth, modulate inflammation, and bolster the immune response. Nanocarriers encapsulating phytochemicals enhance their solubility, stability, and bioavailability, enabling targeted delivery to cancer cells while minimizing harm to healthy tissues. Intricate nanocarriers are programmed for controlled release and specific targeting based on cancer cell markers. Although phytochemicals exhibit diverse anti-cancer activities, their limitations restrict their use. Nanotechnology offers a game-changer, enhancing solubility, and stability, and enabling targeted delivery to cancer cells, minimizing harm to healthy tissues. Exciting future advancements include intricate nanocarriers programmed for controlled release and personalized therapy tailored to individual patients. This intersection of phytochemicals, cancer research, and nanotechnology offers a beacon of hope, paving the way for personalized, safe, and effective therapies, bringing us closer to a world free from the devastating effects of drug-resistant cancer.

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Bioactive Phytocompounds (BPCs) naturally found in plants, hold immense potential for cancer treatment.

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Qualitative and Quantitative Detection of Runt-Related Transcription Factor 1 and Eight-Twenty-One Oncoprotein Gene Fusion Products using Thermal Fingerprint and Cycle Threshold Value by Employing a DNA Intercalating Dye and Fluorescent PCR for Detecting Acute Myeloid Leukaemia (AML)_Crimson Publishers

Abstract

An intercalating dye-based qualitative and quantitative real time PCR assay was developed to detect and estimate the AML1/ETO fusion transcript in patients suffering from Acute myeloid leukaemia. Quantitation standard was prepared by molecular cloning of the fusion transcript in a multicopy cloning vector followed by its propagation in Escherichia coli. Nucleotide sequencing confirmed the AML1/ETO fusion point within the cloned insert and further, its serial dilution resulted in a predicted increase in cycle threshold value which was used to generate a standard curve. Secondary calibration of the standard with an CE-IVD approved, quantified control DNA allowed quantitative detection of AML1/ETO and ABL copy numbers of an AML1/ETO testing panel of samples and the percentage of the AML1/ETO was successfully ascertained. Qualitative detection data of the fusion transcripts from the panel indicated 100% concordance of data when compared with a published protocol that used hydrolysis probes (TaqMan) for detecting the AML1/ETO fusion transcript percentage in clinical samples. The study indicated the potential of using Evagreen as an intercalating dye for qualitative and quantitative detection of AML1/ETO and ABL transcripts for estimating Minimal Residual Disease (MRD) in AML patients.

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An intercalating dye-based qualitative and quantitative real time PCR assay was developed to detect and estimate the AML1/ETO fusion transcr

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A Review on Malignant Transformation_Crimson Publishers

Abstract

Multiple genetic alterations must accumulate within a cell in order for it to become malignant throughout the development and growth of a tumour. One must identify as many of the genetic changes that occur during cancer development in order to comprehend the biology that underlies the disease. Our current understanding of the chromosomal basis of cancer was built on that chromosome aberrations play a crucial role in the malignant transformation of a normal cell. Numerous genomic tools, the transcriptional activity of protein-coding genes is regulated by these tiny non-coding RNA molecules in mammals. When present in amounts above a particular threshold, the heavy metals cadmium, arsenic, and nickel are all cancer-causing.

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Multiple genetic alterations must accumulate within a cell in order for it to become malignant throughout the development and growth of a tu

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Nutrient Deprivation: A Cancer Treatment of Last Resort_Crimson Publishers

Opinion

A West Hartford high school senior was diagnosed with brain cancer, “a high-grade glioma.” Her parents brought her to Dana Farber Institute in Boston Massachusetts seeking the world’s best treatment. They took an apartment in Boston to support her through the ordeal. The patient received surgery and radiation, and, at five months after diagnosis, showed improvement, but, at seven months, relapsed. She received more surgery and radiation but died nine months after diagnosis [1]. It’s a tragic horror story that plays out in this way for some 3,000 young and many more, older adults each year. The patient’s parents did all they could to get their daughter the best treatment. But, in the end, it was inadequate. And it would have been inadequate at any cancer center. There simply is no dependable treatment for end-stage glioma. “Clearly, there exists an unmet need for innovative approaches” [2].

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A West Hartford high school senior was diagnosed with brain cancer, “a high-grade glioma.”

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Hypoxic Cancer Cells Protect Themselves Against Damage: Search for a Single-Cell Indicator of This Protective Response_Crimson Publishers

Abstract

Tumor hypoxia is accompanied by resistance to many damaging therapeutic effects. This effect is often attributed to the loss of the ability of normal and benign tumor cells to adapt their metabolism to hypoxia, whereas cancer cells, on the contrary, acquire the ability to survive and avoid an immune response under hypoxic conditions. Moreover, cancer cells use hypoxia to reprogram their metabolism and induce antioxidant protection, in particular by increasing the production of antioxidant molecules [NAD(P)H and glutathione], which protect hypoxic cancer cells from the damaging effects of free radicals. However, hypoxic cancer cells may differ one from another by the efficiency of protection against damage; an indicator is required to assess this efficiency. The goal of our work is the search for such a single-cell endogenous indicator. For this, we measured endogenous NAD(P)H fluorescence in single hypoxic cancer cells during their UV-induced damage [NAD(P)H photodegradation], as well as determined their ability to restore NAD(P)H fluorescence intensity after the damage/(photo)degradation. Most hypoxic cancer (but not normal) cells were experimentally found to be capable of partially restoring the damage with different efficiencies. Some hypoxic cancer cells possess increased resistance to UV-induced damage. Such cells retained the ability to partially restore NAD(P)H intensity even after 5-6 cycles of repeated damage. Our studies enable recommending the NAD(P)H regenerative response observed in hypoxic tumor cells as a prognostic indicator to assess their potential resistance to damage. This indicator can be useful in choosing new antitumor capabilities of specifically destroying cancer cells with increased resistance to damage.

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Tumor hypoxia is accompanied by resistance to many damaging therapeutic effects.

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Frontiers of Research on cGAS-STING Signaling Pathway Activation by Mitochondrial DNA_Crimson Publishers

Abstract

In addition to their role in cellular metabolism, mitochondria regulate a range of biological processes such as cell death and inflammation. Mitochondrial DNA (mitochondrial DNA, mtDNA) is the genome of the mitochondria themselves, and when leaked from stressed mitochondria into the cytosol, is able to activate the cyclized GMP-AMP synthase (cGAS)-stimulator of interferon genes STING innate immune signaling pathway, leading to the production of type I interferons and inflammatory cytokines. These products are capable of not only resisting invasion by pathogenic microorganisms but also leading to the development of inflammatory diseases. In this review, we review the role of mtDNA in the activation of the cGAS-STING innate immune signaling pathway.

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In addition to their role in cellular metabolism, mitochondria regulate a range of biological processes such as cell death and inflammation.

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Could Neoadjuvant Cabozantinib plus Nivolumab followed by Cytoreductive Nephrectomy be the Future Treatment Strategy for Advanced Renal Cell Carcinoma?_Crimson Publishers

Abstract

Over time, works from oncologists and scientists have contributed to the development of systemic therapies for metastatic renal cell carcinoma (mRCC) with contemporary studies showing superior disease free and overall survival benefits in mRCC patients treated with tyrosine kinase inhibitors (TKI) combined with immune checkpoint inhibitors (ICI). The role of cytoreductive nephrectomy is however still controversial. Here we present with a 57-year-old female patient who suffered from mRCC with left renal vein tumor thrombus, left adrenal, right upper lobe lung and left hip metastases. After 6 months of combination systemic therapy with cabozantinib plus nivolumab, the patient achieved a partial response and received robot assisted laparoscopic cytoreductive nephrectomy (CN). Pathology report of the primary tumor in the left kidney was 85% necrotic and the resected specimens involving the left renal vein thrombus and left adrenal revealed exclusively necrotic tissues. Three months postoperative, an image study showed no evidence of recurrence. Radical nephrectomy after neoadjuvant cabozantinib plus nivolumab in selected patients may achieve disease free status.

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Over time, works from oncologists and scientists have contributed to the development of systemic therapies for metastatic renal cell carcino

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Iodine-125 Seed Combined with Stent Placement and Transarterial Chemoembolization for Treatment of Hepatocellular Carcinoma with Portal Vein Tumor Thrombosis: A Systematic Review and Meta-Analysis_Crimson Publishers

Abstract

Background: Portal vein tumor thrombus plays an important role in indicating the poor prognosis of hepatocellular carcinoma. Purpose: To assess the safety and efficiency of iodine-125 seed combined with stent placement and transarterial chemoembolization for treatment of hepatocellular carcinoma with portal vein tumor thrombosis. Materials and methods: We searched Cochrane library, PubMed, EMBASE, CNKI, Wang fang Data and CQVIP. We assessed the qualities of included studies. We analyzed the characteristic data, tested heterogeneity, explored heterogeneity and tested publication bias by software-Review Manger 3.5. Result: Totally 7 clinical controlled trials were selected with the inclusion criterion. The results showed that the pressure of main portal vein after stent placement was significantly lower than no stent placement. The cumulative stent patency rates and survival rates in 6 and 12 months of iodine-125 seed combined with stent placement and transarterial chemoembolization were higher than conventional transarterial chemoembolization, transarterial chemoembolization combined with stent and 3-dimensional conformal radiotherapy. Conclusion: For hepatocellular carcinoma patients with portal vein tumor thrombosis, iodine-125 seed combined with stent placement and transarterial chemoembolization was safety. The efficiency of iodine-125 seed combined with stent placement and transarterial chemoembolization were better than conventional transarterial chemoembolization, transarterial chemoembolization plus stent and transarterial chemoembolization combined with stent and 3-dimensional conformal radiotherapy.

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Portal vein tumor thrombus plays an important role in indicating the poor prognosis of hepatocellular carcinoma.

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A Prostate Cancer Specific Telomerase Repressor Region on Human Chromosome 11q_Crimson Publishers

Abstract

Telomerase reactivation is one of the key events in the development of cancer. More than 90% of all cancers de-repress sequences within the genome, which results in the overexpression of hTERT and telomerase. In doing so, telomeres at the ends of human chromosomes, which would naturally shorten after each round of replication, are maintained indefinitely giving rise to immortalized cells. The actual mechanisms responsible for telomerase depression in cancer are still under intense investigation and the elucidation of this process would represent a major therapeutic target. The literature has pointed to genes on different chromosomes being responsible for telomerase repression in specific cancers. Microcell Mediated Chromosome Transfer (MMCT) was used to transfer human chromosomes 3, 8, 10, 11, 13, and 17 into the prostate cancer cell line PC3. In doing so, we observed robust and sustained hTERT and telomerase repression for chromosome 11. We then fragmented chromosome 11 using 25G of gamma radiation before repeating the transfer into PC3. We found that 70% of the hybrid clones picked expressed very low levels of hTERT and telomerase when compared to the controls. STS mapping of the clones identified 3 distinct regions on chromosome 11q which could harbour sequences responsible for telomerase repression specific to prostate cancer. Identification of this telomerase repressor could lead to new chemotherapeutic drugs to target prostate cancer or a highly specific biomarker for the disease.

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Telomerase reactivation is one of the key events in the development of cancer.

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Age to Begin Cigarettes Smoking and Factors Associated with it Among Youths (Age 15- 24 Years) in Hawassa, Ethiopia_Crimson Publishers

Abstract Background:Inhaling the fumes and hydrocarbon vapors produced by slowly burning tobacco in cigarettes is referred to as cigarette smoking. As a result, the study’s goal was to find out when young people in Hawassa, Ethiopia, started smoking and what reasons influenced them to do so.

Methods: From April 1 to April 30/2022, a community-based cross-sectional study was conducted in Hawassa, Ethiopia. Kaplan-Meier (KM) analyses were used to assess the likelihood of cigarette smoking at a particular age. With the outcome variable of having ever smoked a cigarette before and the follow-up period of age, the Cox proportional hazards model was used. In addition, logistic regression was used to assess potential cigarette smoking predictors.

Result: Age (AOR, 95%CI 1.56 (1.03, 2.38), believing that smoke from other people does not affect me (AOR, 95%CI, 0.03 (0.001, 0.85), and living with people who smoke (AOR, 95%CI, 0.02 (0.002, 0.242), are all characteristics linked to cigarette smoking, according to multivariate analysis. Cox proportional hazards model for youth who had ever smoked cigarettes using age as a follow-up period showed the youth who drink alcohol is more likely to have a shorter time to begin smoking than those who did not ever drink alcohol (AHR) (95%CI)) =6.22 (1.60, 24.21)

Conclusion: Cigarette smoking is found to be substantially associated with factors such as age, believing smoke from other people does not damage me and living with individuals who smoke. Knowledge of the health implications of cigarette smoking did not prevent smoking, and we propose that more research be done on the relationship between knowledge of the health impacts of smoking and smoking behavior. More research is needed to determine the impact of living with smokers on one’s smoking status.

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Inhaling the fumes and hydrocarbon vapors produced by slowly burning tobacco in cigarettes is referred to as cigarette smoking.

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Does HMBG1 Level Measured in Bronchoalveolar Lavage Liquid Contribute to Cytology?_Crimson Publishers

Abstract

Lung cancer is the leading cause of cancer-related death. Due to the poor prognosis, intensive research continues for early diagnosis and treatment. High Mobility Group Box (HMGB) proteins are nonhistone nuclear proteins with very different functions in the cell. HMGB1 can be released into the extracellular matrix, where it performs important functions in inflammation and carcinogenesis, such as promoting angiogenesis, preventing apoptosis, and promoting tissue invasion and metastasis. Patients who underwent bronchoscopy due to lung pathologies in Private Medical Park Gaziantep Hospital Thoracic Surgery Clinic were included in the study. Age, gender, bronchoscopy biopsy, cytology results, and clinicopathological evaluation results were obtained by scanning the patient files. Samples were obtained from the lavage fluid taken for Bronchoalveolar (BAL) cytology from patients who underwent bronchoscopy due to lung pathologies. After cytological evaluation, the remaining samples were stored at -80 °C. HMGB1 levels were measured from these samples [1]. Statistical analyzes were performed using SPSS for Windows 15.0 software. Before the study, approval was obtained from the SANKO University Clinical Research Ethics Committee. A total of 95 patients, 33 (34.7%) female, and 62 (65.3%) males, with a mean age of 59±15.2 (Range 17-86) were included in the study. When the final pathology results were evaluated together with clinical findings, 29 (30.5%) patients were diagnosed with primary lung cancer, 12 (12.6%) with metastatic lung cancer, 7 with COPD, and 47 with pneumonia. There was no statistically significant difference between the clinicopathological diagnosis groups in terms of hmgb1 level measured in bronchoalveolar lavage fluid (p=0.306). Clinicopathological diagnosis groups were grouped as malignant or benign. Benign lesions were detected in 54 (56.8%) patients, and malignant lesions were found in 41 (43.2%) patients. In terms of malignant and benign lesions, the level of hmgb1 measured in the bronchoalveolar lavage fluid was not statistically significant (p=0.146). When cytology was used to differentiate the lesions, 88 (92.6%) were reported as malignant and 7 (7.4%) as benign [2]. It was not statistically significant in terms of cytological results and hmgb1 level measured in bronchoalveolar lavage fluid (p=0.819). The sensitivity of cytology was 17%, the specificity was 100%, and the accuracy was 74.7%

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Towards a Holistic Approach in the Immunotherapy of Cancer_Crimson Publishers

Abstract

The immune response against malignant tumors is performed through multiple immune cell types; each of them has been shown to be effective in its antitumor activity; this has inspired many therapeutic approaches such as adoptive cells transfers or stimulation through antitumoral antibodies or cytokines. The present opinion article is approaching the immune response in cancer from a holistic perspective, exploring the possibility that it may be used in integrated approaches, in cancer immunotherapy.

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The immune response that the organism mounts against malignant tumors involves many types of immune cells, both innate, such as macrophages,

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