Determination of elemental constituents for three herbal plants that are traditionally used to cure cancer

Elemental constituents of fresh leaves of the three herbal plants used traditionally for treatment of cancer namely: Guera Senegalense, Boswellia and Mangifera Indica were analyzed. Results show that all the three samples contain the highest amounts of calcium in parts per million (Guiera Senegalensis 5991 ppm, Boswellia 9413 ppm and Mangifera Indica 2405 ppm) as compared to other constituents. Further studies reveal that presence of calcium in appreciable amount within the metabolic system of human being helps to reduce the risk of cancer and related ailments. Other benefits of calcium in man include strengthening bones and teeth.Keywords: Herbal Medicine, Cancer, Constituents, Carcinoge

Deregulated expression of TCL1 causes T cell leukemia in mice

The TCL1 oncogene on human chromosome 14q32.1 is involved in the development of T cell leukemia in humans. These leukemias are classified either as T prolymphocytic leukemias, which occur very late in life, or as T chronic lymphocytic leukemias, which often arise in patients with ataxia telangiectasia (AT) at a young age. The TCL1 oncogene is activated in these leukemias by juxtaposition to the α or β locus of the T cell receptor, caused by chromosomal translocations t(14:14)(q11:q32), t(7:14)(q35:q32), or by inversions inv(14)(q11:q32). To show that transcriptional alteration of TCL1 is causally involved in the generation of T cell neoplasia we have generated transgenic mice that carry the TCL1 gene under the transcriptional control of the p56(lck) promoter element. The lck-TCL1 transgenic mice developed mature T cell leukemias after a long latency period. Younger mice presented preleukemic T cell expansions expressing TCL1, and leukemias developed only at an older age. The phenotype of the murine leukemias is CD4-CD8+, in contrast to human leukemias, which are predominantly CD4+CD8-. These studies demonstrate that transcriptional activation of the TCL1 protooncogene can cause malignant transformation oft lymphocytes, indicating the role of TCL1 in the initiation of malignant transformation in T prolymphocytic leukemias and T chronic lymphocytic leukemias

Acute Toxicity Study and Hepatocurative Effect of Aqueous Stem Bark Extract of Parkia Biglobosa in Wister albino Rats

Parkia biglobosa plant is widely is used in folk medicinal practices to treat and/or manage various diseases including diabetes, malaria, diarrhea and pains. The current research seek to establish the toxicity profile and hepatocurative ability of aqueous stem bark extract of the plant. Twelve (12) rats were used for Oral LD50 determination, and were grouped into four (4) groups of three rats (3) each. The first three groups were administered with 10 mg/kg, 100 mg/kg and 1000 mg/kg body weight of the extract respectively, while the last group was subdivided into three groups of one rat each and were administered with 2500mg/kg, 3500mg/kg and 5000mg/kg body weight of the extract respectively. For the hepatocurative studies, twenty five (25) experimental rats were divided into five groups of five (5) rats each. Group I served as normal rats, Group II served as test Control while Groups III to V were induced with liver damage and administered with 50mg/kg, 100mg/kg and 150mg/kg of the extract respectively. The LD50 was found to be greater than 5000mg/kg, while phytochemical screening revealed the presence of Flavanoids, Glycosides, Tanins, Saponins, Steroids and Phenols, with the absence of Anthraquinones. For the hepatocurative study, a significant (p<0.0.5) increase in serum albumin and liver enzymes (AST, ALT and ALP) was observed in test control compared to normal control. Upon administration of the extract, a significant (p<0.0.5) fall in Albumin, AST, ALT and ALP was recorded in a dose dependent pattern. No significant difference (p>0.05) was observed between groups in total protein, direct and total bilirubin. The research concludes that the extract is practically non-toxic and possess strong hepatocurative ability which might be due to the phytochemicals present. Keywords: Acute toxiicity; CCl4; Liver; P. biglobosa; Phytochemical and wistar rats. DOI: 10.7176/JNSR/13-16-04 Publication date:September 30th 202

Fludarabine modulates composition and function of the T cell pool in patients with chronic lymphocytic leukaemia

The combination of cytotoxic treatment with strategies for immune activation represents an attractive strategy for tumour therapy. Following reduction of high tumour burden by effective cytotoxic agents, two major immune-stimulating approaches are being pursued. First, innate immunity can be activated by monoclonal antibodies triggering antibody-dependent cellular cytotoxicity. Second, tumour-specific T cell responses can be generated by immunization of patients with peptides derived from tumour antigens and infused in soluble form or loaded onto dendritic cells. The choice of cytotoxic agents for such combinatory regimens is crucial since most substances such as fludarabine are considered immunosuppressive while others such as cyclophosphamide can have immunostimulatory activity. We tested in this study whether fludarabine and/or cyclophosphamide, which represent a very effective treatment regimen for chronic lymphocytic leukaemia, would interfere with a therapeutic strategy of T cell activation. Analysis of peripheral blood samples from patients prior and during fludarabine/cyclophosphamide therapy revealed rapid and sustained reduction of tumour cells but also of CD4+ and CD8+ T cells. This correlated with a significant cytotoxic activity of fludarabine/cyclophosphamide on T cells in vitro. Unexpectedly, T cells surviving fludarabine/cyclophosphamide treatment in vitro had a more mature phenotype, while fludarabine-treated T cells were significantly more responsive to mitogenic stimulation than their untreated counterparts and showed a shift towards TH1 cytokine secretion. In conclusion, fludarabine/cyclophosphamide therapy though inducing significant and relevant T cell depletion seems to generate a micromilieu suitable for subsequent T cell activation

The Novel Deacetylase Inhibitor AR-42 Demonstrates Pre-Clinical Activity in B-Cell Malignancies In Vitro and In Vivo

While deacetylase (DAC) inhibitors show promise for the treatment of B-cell malignancies, those introduced to date are weak inhibitors of class I and II DACs or potent inhibitors of class I DAC only, and have shown suboptimal activity or unacceptable toxicities. We therefore investigated the novel DAC inhibitor AR-42 to determine its efficacy in B-cell malignancies.In mantle cell lymphoma (JeKo-1), Burkitt's lymphoma (Raji), and acute lymphoblastic leukemia (697) cell lines, the 48-hr IC(50) (50% growth inhibitory concentration) of AR-42 is 0.61 microM or less. In chronic lymphocytic leukemia (CLL) patient cells, the 48-hr LC(50) (concentration lethal to 50%) of AR-42 is 0.76 microM. AR-42 produces dose- and time-dependent acetylation both of histones and tubulin, and induces caspase-dependent apoptosis that is not reduced in the presence of stromal cells. AR-42 also sensitizes CLL cells to TNF-Related Apoptosis Inducing Ligand (TRAIL), potentially through reduction of c-FLIP. AR-42 significantly reduced leukocyte counts and/or prolonged survival in three separate mouse models of B-cell malignancy without evidence of toxicity.Together, these data demonstrate that AR-42 has in vitro and in vivo efficacy at tolerable doses. These results strongly support upcoming phase I testing of AR-42 in B-cell malignancies