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Nathan Goodyear

Artemether suppresses cell proliferation and induces apoptosis in diffuse large B cell ... - 0 views

www.spandidos-publications.com/...etm.2017.5063

artemisinin artesunate artemether cancer lymphoma B cell lymphoma

shared by Nathan Goodyear on 14 Jun 19 - No Cached
  • Nathan Goodyear on 14 Jun 19
     
    Artemether, a derivative of artemisinin found to be effective agains B cell Lymphoma in cell study.
Nathan Goodyear

Artesunate shows potent anti-tumor activity in B-cell lymphoma - 0 views

www.ncbi.nlm.nih.gov/...PMC5819282

Artesunate B cell lymphoma lymphoma

shared by Nathan Goodyear on 23 May 19 - No Cached
  • Nathan Goodyear on 23 May 19
     
    Study finds artesunate triggers apoptosis in NHL B-cell lymphoma type.
Nathan Goodyear

Vitamin C increases viral mimicry induced by 5-aza-2′-deoxycytidine | PNAS - 0 views

www.pnas.org/10238

AML leukemia acute myeloid leukemia MDS vitamin C cancer

shared by Nathan Goodyear on 12 May 18 - No Cached
  • Vitamin C alone at concentrations up to 57 μM had little effect on cell growth but was toxic at 228 μM (SI Appendix, Fig. S1B), in line with recent studies of high vitamin C concentrations (125–2,000 μM)
  • In our combination approach, vitamin C increased the effects of low doses of 5-aza-CdR, with 57 μM vitamin C almost doubling the growth inhibition
  • Using the Chou–Talalay method (28), we found that the two compounds indeed acted synergistically, rather than additively, to inhibit cancer cell growth over the physiological ranges of vitamin C in healthy individuals (26–84 μM)
  • ...12 more annotations...
  • These results show that targeting the cancer DNA methylome by combining low-dose 5-aza-CdR and vitamin C stimulates the expression of ERVs, the induction of a cell-autonomous immune activation response, and increased apoptosis of cancer cells
  • The addition of vitamin C to treatment protocols therefore may be a straightforward way to increase the clinical efficacy of such drugs in MDS and leukemia patients
  • Vitamin C deficiency has been seen previously in patients with multiple types of cancer, including hematological malignancies (35⇓–37). We predict that these patients might receive the most benefits from the combination treatment.
  • induction of an innate immune response
  • We therefore measured plasma concentrations of vitamin C in a small number of patients with miscellaneous hematologic malignancies. Strikingly, 58% of patients with hematological neoplasia who were not taking vitamin C supplements had severe vitamin C deficiency (serum concentration <11.4 μM, at which clinical features of scurvy may be manifested) (34), and 33% had vitamin C levels below the normal range
  • it is possible that vitamin C was oxidized to DHA before it was transported into the cells
  • Oral administration of vitamin C should be sufficient for the therapeutic strategy, because the concentrations reported in this study would not require i.v. administration.
    • Nathan Goodyear
      Nathan Goodyear on 12 May 18
       
      This statement lacks a basic understanding of vitamin C pharmacokinetics.
  • Vitamin C is an essential nutrient for humans and has been reported to increase IFN levels in human cells upon virus infection
  • daily treatment with vitamin C alone at physiological concentrations enhanced the expression of viral-defense genes relative to untreated cells
  • When combined with low-dose 5-aza-CdR, physiological concentrations of vitamin C synergistically inhibited cancer-cell growth and induced apoptosis. Such synergy was associated with increased ERV expression and dsRNA in treated cells. The mechanism of action differs from that of vitamin C at higher doses, which involves its pro-oxidant activity, including GSH inhibition, to generate reactive oxygen species
  • This activity has been shown to induce DNA damage and to enhance the sensitivities of myeloid malignancies, multiple myeloma, and cutaneous T-cell lymphoma to arsenic trioxide (41⇓⇓–44). It also can increase chemosensitivity of ovarian cancer cells (27) and selectively kill KRAS or BRAF mutant colorectal cancer cells by inhibiting GAPDH
  • reactive oxygen species
  • Nathan Goodyear on 12 May 18
     
    91% of patients with hematologic malignancies have vitamin C levels that are either low or severly deficient. This study found that vitamin C plus low dose DNA methyltransferase inhibitors have synergistic inhibition of cancer cell proliferation and increased apoptosis.  Unfortunately, the authors claimed that oral vitamin C would be sufficient which indicates an incredible lack of understanding of vitamin C pharmacokinetics.
Nathan Goodyear

The current state and future perspectives of cannabinoids in cancer biology - 0 views

www.ncbi.nlm.nih.gov/...PMC5852356

Cancer CBD THC cannabinoids

shared by Nathan Goodyear on 19 Sep 18 - No Cached
hoangkimchi liked it
  • The activation of each of them leads to an inhibition of adenylyl cyclase via G proteins (Gi/o), which in turn activates many metabolic pathways such as mitogen‐activated protein kinase pathway (MAPK), phosphoinositide 3‐kinase pathway (PI3K), cyclooxygenase‐2 pathway (COX‐2), accumulation of ceramide, modulation of protein kinase B (Akt), and ion channels
  • phytocannabinoids, endocannabinoids, and synthetic cannabinoids
  • Action of THC in human organism relies on mimicking endogenous agonists of CB receptors—endocannabinoids
  • ...8 more annotations...
  • The upregulated expression of CB receptors and the elevated levels of endocannabinoids have been observed in a variety of cancer cells (skin, prostate, and colon cancer, hepatocellular carcinoma, endometrial sarcoma, glioblastoma multiforme, meningioma and pituitary adenoma, Hodgkin lymphoma, chemically induced hepatocarcinoma, mantel cell lymphoma)
  • concentration of endocannabinoids, expression level of their receptors, and the enzymes involved in their metabolism frequently are associated with an aggressiveness of cancer
  • CB2 receptor contributes to human epidermal growth factor receptor (HER2) pro‐oncogenic signaling and an overexpression of CB2 increases susceptibility for leukemia development after leukemia viral infection
  • endocannabinoid‐degrading enzymes are upregulated in cancer cell lines and in human tumors
  • Many cannabinoids, ranging from phytocannabinoids (THC, CBD), endocannabinoids (2‐arachidonoylglycerol, anandamide), to synthetic cannabinoids (JWH‐133, WIN‐55,212‐2), have shown ability to inhibit proliferation, metastasis, and angiogenesis in a variety of models of cancer
  • Despite some inconsistent data, the main effect of cannabinoids in a tumor is the inhibition of cancer cells’ proliferation and induction of cancer cell death by apoptosis
  • CB1 and CB2 receptor agonists stimulate apoptotic cell death in glioma cells by induction of de novo synthesis of ceramide, sphingolipid with proapoptotic activity
  • process of autophagy is upstream of apoptosis in mechanism of cell death induced by cannabinoids
Nathan Goodyear

CD3+/CD16+CD56+ cell numbers in peripheral blood are correlated with higher tumor burde... - 0 views

www.ncbi.nlm.nih.gov/...21526506

NK cells CD16_56 cancer lymphoma natural killer cells

shared by Nathan Goodyear on 28 Sep 18 - No Cached
  • Nathan Goodyear on 28 Sep 18
     
    Only abstract available here.  Study finds association between high tumor burden, more aggressive disease, and lower NK cell numbers.  In addition, inverse assocation with CD16/56 and LDH found.  Most likely direct tumor suppression as cause.
Nathan Goodyear

The emerging role of estrogen in B cell malignancies: Leukemia & Lymphoma: Vol 58, No 3 - 0 views

www.tandfonline.com/...10428194.2016.1213828

estrogen leukemia lymphoma ER ER beta estrogen receptor cancer

shared by Nathan Goodyear on 27 Nov 17 - No Cached
  • Nathan Goodyear on 27 Nov 17
     
    Evidence that Estrogen and ER status plays role in hematological cancer.  ER-beta agonist inhibited cell growth and induced cell death. Similar to prostate cancer.
Nathan Goodyear

Gamma-linolenic acid induces apoptosis in B-chroni... [Leuk Lymphoma. 2001] - PubMed re... - 0 views

www.ncbi.nlm.nih.gov/...11426562

gamma linolenic acid GLA cancer dexamethasone

shared by Nathan Goodyear on 11 Feb 11 - No Cached
  • n the presence of GLA 5 microg/ml and dexamethasone the degree of apoptosis was 86%
  • These results demonstrate that GLA induces apoptosis in B-CLL B- and T-cells cells in vitro and that they are more susceptible to GLA-induced apoptosis than normal peripheral blood B- and T-cells.
  • Nathan Goodyear on 11 Feb 11
     
    GLA, omega-6 found in plant based oils,  kills 42% of leukemia cells; with dexamethasone, the kill rate increases to 86%
Nathan Goodyear

Utility of MYD88 in the Differential Diagnosis and Choice of Second-Line Therapy in a C... - 0 views

www.hindawi.com/...5183646

Waldenstrom lymphoma "waldenstrom's macroglobulinemia" Cancer

shared by Nathan Goodyear on 30 Oct 18 - No Cached
  • Nathan Goodyear on 30 Oct 18
     
    Interesting study that highlights the complexities between Waldenstrom's Macroglobulinemia and other B-cell lymphoma's. These authors concluded that sFLC's correlated better with treatment outcomes than IgM levels.
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