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Nathan Goodyear

Substantial contribution of extrinsic risk factors to cancer development - 0 views

www.ncbi.nlm.nih.gov/...PMC4836858

cancer lifestyle

shared by Nathan Goodyear on 03 Jan 18 - No Cached
  • Here we provide evidence that intrinsic risk factors contribute only modestly (<10~30%) to cancer development
  • we conclude that cancer risk is heavily influenced by extrinsic factors. These results carry immense consequences for strategizing cancer prevention
  • cancers are proposed to originate from the malignant transformation of normal tissue progenitor and stem cells
  • ...14 more annotations...
  • “Intrinsic processes” include those that result in mutations due to random errors in DNA replication whereas “extrinsic factors” are environmental factors that affect mutagenesis rates (such as UV radiation, ionizing radiation, and carcinogens
  • intrinsic factors do not play a major causal role.
  • intrinsic cancer risk should be determined by the cancer incidence for those cancers with the least risk in the entire group controlling for total stem cell divisions
  • if one or more cancers would feature a much higher cancer incidence, for example, lung cancer among smokers vs. non-smokers, then this most likely reflects additional (and probably extrinsic) risk factors (smoking in this case)
  • Particularly, for breast and prostate cancers, it has long been observed that large international geographical variations exist in their incidences (5-fold for breast cancer, 25-fold for prostate cancer)14, and immigrants moving from countries with lower cancer incidence to countries with higher cancer rates soon acquire the higher risk of their new country
  • Colorectal cancer is another high-incidence cancer that is widely considered to be an environmental disease17, with an estimated 75% or more colorectal cancer risk attributable to diet
  • melanoma, its risk ascribed to sun exposure is around 65–86%
  • non-melanoma basal and squamous skin cancers, ~90% is attributable to UV
  • 75% of esophageal cancer, or head and neck cancer are caused by tobacco and alcohol
  • HPV may cause ~90% cases in cervical cancer23, ~90% cases in anal cancer24, and ~70% in oropharyngeal cancer
  • HBV and HCV may account for ~80% cases of hepatocellular carcinoma
  • H pylori may be responsible for 65–80% of gastric cancer
  • While a few cancers have relatively large proportions of intrinsic mutations (>50%), the majority of cancers have large proportions of extrinsic mutations, for example, ~100% for Myeloma, Lung and Thyroid cancers and ~80–90% for Bladder, Colorectal and Uterine cancers, indicating substantial contributions of carcinogen exposures in the development of most cancers
  • onsistent estimate of contribution of extrinsic factors of >70–90% in most common cancer types. This concordance lends significant credibility to the overall conclusion on the role of extrinsic factors in cancer development
  • Nathan Goodyear on 03 Jan 18
     
    Really great read.  Cancer is a majority lifestyle disease.
Nathan Goodyear

Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views

www.ncbi.nlm.nih.gov/...PMC5686300

nagalase Gc-MAF cancer

shared by Nathan Goodyear on 29 Jan 18 - No Cached
  • MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
  • This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Nagalase has been detected in many cancer patients, but not in healthy individuals
  • ...31 more annotations...
  • Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
  • It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
  • The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
  • It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
  • The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
  • Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
  • Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
  • The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
  • Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
  • Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
  • It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
  • Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
  • Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
  • weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
  • this treatment has been suggested for non-anemic patients
  • Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
  • Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
  • In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
  • individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
  • Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
  • Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
  • There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
  • It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
  • it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
  • The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
  • Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
  • Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
  • It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
  • inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
  • macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
  • Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
  • Nathan Goodyear on 29 Jan 18
     
    great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
Nathan Goodyear

Hypercalcemia of malignancy and new treatment options - 0 views

www.ncbi.nlm.nih.gov/...PMC4675637

hypercalcemia calcium cancer

shared by Nathan Goodyear on 11 Sep 18 - No Cached
  • Hypercalcemia of malignancy occurs as the result of direct bone metastasis and via humoral mechanisms such as parathyroid hormone-related protein (PTHrP) or 1,25-dihydroxyvitamin D mediated pathways
  • ectopic secretion of parathyroid hormone (PTH) has been implicated
  • Hypercalcemia due to osteolytic bone lesions is common in multiple myeloma, leukemia, and breast cancer
  • ...22 more annotations...
  • Humoral hypercalcemia is predominant in squamous cell, renal cell and ovarian cancers, and lymphomas are associated with 1,25-dihydroxyvitamin D mediated hypercalcemia
  • 20% of cases of hypercalcemia of malignancy and is frequently encountered in multiple myeloma, metastatic breast cancer, and to a lesser extent in leukemia and lymphoma
  • Physiologic bone turnover requires the complementary activity of osteoblasts – mesenchymal stem cell-derived bone-forming cells – and bone-resorbing cells of monocyte and macrophage lineage known as osteoclasts
  • In local osteolytic hypercalcemia, the RANKL/RANK interaction results in excessive osteoclast activation leading to enhanced bone resorption and thus hypercalcemia
  • In addition, osteoclast activation is also mediated by malignancy secreted cytokines, including interleukin-1, initially termed “osteoclast stimulating factor”
  • Macrophage inflammation protein 1-alpha (MIP 1-alpha)
  • hypercalcemia is through extra-renal 1,25-dihydroxyvitamin D (calcitriol) production
  • 1% of cases
  • increased production of 1,25-dihydroxyvitamin D occurs nearly exclusively in Hodgkin and non-Hodgkin lymphoma with case reports of the same in ovarian dysgerminoma
  • 1-α-hydroxylase in the kidney, a process regulated by PTH
  • in 1,25-dihydroxyvitamin D induced hypercalcemia, malignant cells likely recruit and induce adjacent macrophages to express 1-α-hydroxylase, converting endogenous calcidiol into calcitriol.31 Calcitriol then binds to receptors in the intestine leading to heightened enteric calcium reabsorption with resultant hypercalcemia
  • this mechanism of disease is best conceptualized as an absorptive form of hypercalcemia
  • Ectopic production of PTH by malignant cells has been described in a handful of cases involving cancer of the ovary and lung, as well as neuroendocrine tumors and sarcoma
  • primary hyperparathyroidism and malignancy comprising nearly 90% of cases of hypercalcemia
  • an initial panel consisting of PTH, PTHrP, phosphorus, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D should be obtained
  • Lymphoma, a hypercalcemia due to 1,25-dihydroxyvitamin D mediated pathways, is implied by elevations in 1,25-dihydroxyvitamin D without concomitant elevations in 25-hydroxyvitamin D. In such cases, PTH is low and PTHrP undetectable
  • Treatment of hypercalcemia of malignancy is aimed at lowering the serum calcium concentration by targeting the underlying disease, specifically by inhibiting bone resorption, increasing urinary calcium excretion, and to a lesser extent by decreasing intestinal calcium absorption
  • mildly symptomatic disease
  • marked symptoms
  • hydration with isotonic fluid (if admitted), avoidance of thiazide diuretics, and a low-calcium diet
  • denosumab
  • Denosumab is an RANKL antibody that inhibits osteoclast maturation, activation, and function
  • Nathan Goodyear on 11 Sep 18
     
    hypercalcemia in cancer and treatments.
Nathan Goodyear

Quercetin Suppresses Drug-Resistant Spheres via the p38 MAPK-Hsp27 Apoptotic Pathway in... - 0 views

www.ncbi.nlm.nih.gov/...PMC3495857

Quercetin HSP heat shock proteins HSP27

shared by Nathan Goodyear on 23 Feb 19 - No Cached
  • Nathan Goodyear on 23 Feb 19
     
    Quercetin found to inhibit HSP27 expression
Nathan Goodyear

FDG-PET/CT imaging biomarkers in head and neck squamous cell carcinoma - 0 views

www.ncbi.nlm.nih.gov/...PMC3587845

PET scan cancer PET_CT scan maxSUV

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • F-fluoro-2-deoxyglucose (FDG) PET/CT is sensitive for the diagnosis and initial staging of several types of malignancies
  • SUV is a semiquantitative measure of the normalized concentration of radioactivity in a tumor or lesion
  • As FDG is the most common radiotracer used clinically and reflects tumor glucose metabolism, SUV is used as a surrogate marker for tumor metabolism.
  • ...9 more annotations...
  • primary tumor SUVmax >10 predicted survival, independent of the tumor stage and diameter
  • advanced tumors tend to have higher FDG uptake (and thus higher SUV values)
  • the impact of the SUV on treatment outcome has been observed even within a given tumor stage
  • The association between FDG uptake and tumor burden or stage has been well documented
  • FDG uptake not only reflects tumor burden/stage but also expresses, at least in part, some intrinsic biologic characteristic(s) of the tumor
  • SUVmax reflects the highest voxel value within the ROI or VOI. It is the most widely used parameter to measure metabolic tumor activity in oncologic FDG-PET/CT imaging
  • Several studies suggest that primary tumor baseline SUVmax also has predictive value in assessing the tumor burden, lymph node involvement and local extension
  • According to EORTC, a drop (delta between baseline and post-therapy) of 15–25% in SUVmax may represent a good treatment response
  • PERCIST criteria was proposed by the investigators at the Johns Hopkins Medical Institutions and suggested that a decrease in SUV normalized to lean body mass of at least 30% should be achieved before considering partial tumor response
  • Nathan Goodyear on 19 Mar 18
     
    Good review of PET/CT scan and MaxSUV in head and neck cancers.
Nathan Goodyear

Effect of tumor microenvironment on pathogenesis of the head and neck squamous cell car... - 1 views

molecular-cancer.biomedcentral.com/...s12943-019-0983-5

TME cancer tumor microenvironment

shared by Nathan Goodyear on 21 Nov 19 - No Cached
  • Nathan Goodyear on 21 Nov 19
     
    To be read
Nathan Goodyear

Effect of tumor microenvironment on pathogenesis of the head and neck squamous cell car... - 1 views

www.ncbi.nlm.nih.gov/...PMC6441173

tumor microenvironment cancer TME

shared by Nathan Goodyear on 28 Aug 20 - No Cached
  • Nathan Goodyear on 28 Aug 20
     
    Nice review of the tumor microenvironment in the treatment of cancer.
Nathan Goodyear

Cannabinoids Promote Progression of HPV-Positive Head and Neck Squamous Cell Carcinoma ... - 0 views

aacrjournals.org/...te-Progression-of-HPV-Positive

head and neck cancer THC p38 MAPK

shared by Nathan Goodyear on 15 Nov 22 - No Cached
  • Nathan Goodyear on 15 Nov 22
     
    THC stimulates p38/MAPK signaling to inhibit apoptosis via CB agonism; good thing CBD is a reverse agonist on CB receptors.
Nathan Goodyear

Quercetin Inhibits Cell Survival and Metastatic Ability via the EMT-Mediated Pathway in... - 0 views

www.ncbi.nlm.nih.gov/...PMC7037689

EMT epithelial to mesenchymal transition cancer quercetin

shared by Nathan Goodyear on 08 Mar 21 - No Cached
  • Nathan Goodyear on 08 Mar 21
     
    Quercetin inhibits EMT.
Nathan Goodyear

Role of toll-like receptor 4 on the immune escape of human oral squamous cell carcinoma... - 0 views

www.ncbi.nlm.nih.gov/...PMC3496658

toll-like receptors TLR-4 chemoresistance TLR4 chemotherapy cancer

shared by Nathan Goodyear on 12 Jun 20 - No Cached
  • Nathan Goodyear on 12 Jun 20
     
    TLR-4 receptor increase increases chemotherapy resistance.
Nathan Goodyear

Health-related quality of life in patients with metastatic, relapsed, or inoperable squ... - 0 views

link.springer.com/...s00520-015-2937-9

metronomic chemotherapy quality of life QOL low-dose chemotherapy cancer

shared by Nathan Goodyear on 20 Sep 20 - No Cached
  • Nathan Goodyear on 20 Sep 20
     
    Overall QOL, but pain associated QOL was improved with metronomic very MTD.
Nathan Goodyear

Effect of local hyperthermia on metastases in oral squamous cell carcinoma | Request PDF - 0 views

www.researchgate.net/...n_oral_squamous_cell_carcinoma

metastasis cancer hyperthermia

shared by Nathan Goodyear on 25 Feb 21 - No Cached
  • Nathan Goodyear on 25 Feb 21
     
    Hyperthermia inhibits LN metastasis.
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