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Nathan Goodyear

Niclosamide Suppresses Cancer Cell Growth By Inducing Wnt Co-Receptor LRP6 De... - 0 views

journals.plos.org/...article

Niclosamide cancer Wnt apoptosis

shared by Nathan Goodyear on 16 Apr 18 - No Cached
  • Nathan Goodyear on 16 Apr 18
     
    Niclosamide, a common antilemintic/anti-parasitic medication, inhibits Wnt/Beta-catenin signaling involved in carcinogenesis and metastasis. the mechanism is through LRP6 degradation to provide antiproliferative and apoptosis activity.
Nathan Goodyear

Immune responses to malignancies - 0 views

www.ncbi.nlm.nih.gov/...PMC3721350

cancer immune system

shared by Nathan Goodyear on 18 Apr 18 - No Cached
  • increased densities of T-cell infiltrates with a high proportion of CD8+ T cells within primary colorectal carcinomas were associated with a significant protection against tumor recurrence
  • coexpression of genes mediating cytotoxicity and TH1 adaptive immune responses accurately predicted survival in patients with colorectal carcinoma independently of the metastatic status.
  • tumor-specific cytolytic T lymphocytes (CTLs)
  • ...10 more annotations...
  • tumor-associated antigens (TAs)
  • Proinflammatory cytokines secreted by inflammatory cells can contribute to tumor progression, and soluble factors produced by the tumor in response to nonspecific or tumor-specific signals, such as prostaglandin E2 (PGE2), adenosine, or TGF-β, downregulate functions of immune cells
  • they are largely ineffective in arresting tumor growth, although they can proliferate and mediate antitumor cytotoxicity on their removal from the tumor bed and ex vivo IL-2 activation.42
  • DCs (HLA-DR+CD86+CD80+CD14−) are nature’s best APCs
  • They are a common component of tumor immune infiltrates and are responsible for the uptake, processing, and cross-presentation of TAs to naive or memory T cells, thus playing a crucial role in the generation of tumor-specific effector T cells
  • DCs control the induction of Treg cells. In patients with cancer, cellular interactions between antigen-presenting DCs and T cells lead to expansion and accumulation of Treg cells at the tumor site and in the periphery
  • NK cells (CD3−CD56+CD16+), which mediate innate immunity and contain both perforin-rich and granzyme-rich granules, are well equipped to mediate lysis of tumor cells
  • B cells (CD19+, CD20+) are also rare in most human tumors, with the exception of breast cancer and melanoma
  • The initial acute inflammation involving the recruitment and influx of antitumor effector cells is replaced by chronic inflammation in later stages of tumor progression
  • Tissue hypoxia plays a major role in shaping the nature of immune infiltrates in tumors
  • Nathan Goodyear on 18 Apr 18
     
    Another great review of the immune system during different stages of carcinogenesis; how the cancer manipulates the immue system to cloak itself from the immune system.
Nathan Goodyear

Wnt Signaling in Cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC3331705

Wnt cancer

shared by Nathan Goodyear on 07 Jun 18 - No Cached
  • Nathan Goodyear on 07 Jun 18
     
    Wnt signaling promotes carcinogenesis through positive and negative effects.
Nathan Goodyear

Growth hormone is permissive for neoplastic colon growth - 0 views

www.pnas.org/...E3250

colorectal cancer HGH colon cancer growth hormone

shared by Nathan Goodyear on 14 Aug 19 - No Cached
  • Nathan Goodyear on 14 Aug 19
     
    Elevated GH levels favor carcinogenesis and spread of colorectal cancer.
Nathan Goodyear

Role of the growth hormone-IGF-1 axis in cancer: Expert Review of Endocrinology & Metab... - 0 views

www.tandfonline.com/...eem.10.73

cancer growth hormone HGH

shared by Nathan Goodyear on 14 Aug 19 - No Cached
  • Nathan Goodyear on 14 Aug 19
     
    Great read on the different mechanisms by which GH promotes carcinogenesis and growth via STATs, P13K/Akt, mTOR, IGF-1...
Nathan Goodyear

Chemotherapeutic potential of curcumin for colorectal cancer. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12171541

curcumin tumeric cancer

shared by Nathan Goodyear on 11 Sep 17 - No Cached
  • Nathan Goodyear on 11 Sep 17
     
    Only abstract available here.  Good discussion of the effects of curcumin: curcumin inhibits carcinogenesis, increases glutathione production, inhibits promotion and progression (mets) of cancer, induces cell apoptosis (cell death).
Nathan Goodyear

NF-κB, an Active Player in Human Cancers | Cancer Immunology Research - 0 views

cancerimmunolres.aacrjournals.org/...823

tumor microenvironment NF-kappaB angiogenesis metastasis

shared by Nathan Goodyear on 10 Jan 21 - No Cached
  • Nathan Goodyear on 10 Jan 21
     
    NF-kappaB plays integral role in carcinogenesis
Nathan Goodyear

Integrin αvβ3-Targeted Cancer Therapy - 0 views

www.ncbi.nlm.nih.gov/...PMC2901818

angiogenesis tumor microenvironment metastasis TME cancer Integrin αvβ3

shared by Nathan Goodyear on 20 Jan 22 - No Cached
  • Nathan Goodyear on 20 Jan 22
     
    Integrin αvβ3 play key role in angiogenesis, carcinogenesis, and metastasis.
Nathan Goodyear

Stress-induced epinephrine enhances lactate dehydrogenase A and promotes breast cancer ... - 0 views

www.ncbi.nlm.nih.gov/...PMC6391112

glycolytic shift LDH lactate dehydrogenase Stress immunosuppression Fear cancer

shared by Nathan Goodyear on 17 Apr 23 - No Cached
  • Nathan Goodyear on 17 Apr 23
     
    Mood, i.e., fear and stress push glycolytic shift and immunosuppression favoring carcinogenesis. Medicine must revisit how it approaches cancer diagnosis and movement forward. Propagation of fear only accelerates cancer progression.
Nathan Goodyear

Frequent Loss of Estrogen Receptor-β Expression in Prostate Cancer - 0 views

cancerres.aacrjournals.org/...5331.long

ER beta prostate cancer prostate cancer estrogen receptor estrogen receptor receptors hormone hormones

shared by Nathan Goodyear on 05 Feb 13 - No Cached
  • Nathan Goodyear on 05 Feb 13
     
    Loss of ER-beta expression in the prostate associated with increased progression from a normal prostate to prostate cancer.
Nathan Goodyear

Telomerase reactivation reverses tissue degeneration in aged telomerase deficient mice - 0 views

www.ncbi.nlm.nih.gov/...PMC3057569

telomerase telomerase activator telomere aging

shared by Nathan Goodyear on 18 May 16 - No Cached
  • age-progressive loss of telomere function in mice has been shown to provoke widespread p53 activation resulting in activation of cellular checkpoints of apoptosis, impaired proliferation and senescence, compromised tissue stem cell and progenitor function, marked tissue atrophy and physiological impairment in many organ systems
  • Despite chromosomal instability, the brief course of telomerase reactivation was not sufficient to promote carcinogenesis (data not shown), a finding consistent with a role for telomerase in promoting progression of established neoplasms
  • Nathan Goodyear on 18 May 16
     
    another mouse study that found that increasing telomerase activity in shortened telomere mice improved tissue regeneration.
Nathan Goodyear

Progesterone metabolites regulate induction, growth, and suppression of estrogen- and p... - 0 views

www.ncbi.nlm.nih.gov/...PMC3706910

progesterone metabolites metabolite 5-alpha pregnene 5-alpha pregnenes 5alpha-dihydroprogesterone 4-pregnene 4-pregnenes 3alpha-dihydroprogesterone breast cancer ER PR hormone hormones receptors estrogen

shared by Nathan Goodyear on 28 Jan 14 - No Cached
  • in vitro studies had shown that the progesterone metabolites, 5α-dihydroprogesterone (5αP) and 3α-dihydroprogesterone (3αHP), respectively, exhibit procancer and anticancer effects on receptor-negative human breast cell lines
  • Onset and growth of ER/PR-negative human breast cell tumors were significantly stimulated by 5αP and inhibited by 3αHP
  • When both hormones were applied simultaneously, the stimulatory effects of 5αP were abrogated by the inhibitory effects of 3αHP and vice versa
  • ...31 more annotations...
  • Treatment with 3αHP subsequent to 5αP-induced tumor initiation resulted in suppression of further tumorigenesis and regression of existing tumors
  • Tumorigenesis of ER/PR-negative breast cells is significantly enhanced by 5αP and suppressed by 3αHP, the outcome depending on the relative concentrations of these two hormones in the microenvironment in the breast regions
  • The findings show that the production of 5αP greatly exceeds that of 3αHP in ER/PR-negative tumors and that treatment with 3αHP can effectively block tumorigenesis and cause existing tumors to regress
  • hypothesis that a high 3αHP-to-5αP concentration ratio in the microenvironment may foster normalcy in noncancerous breast regions.
  • a large proportion (about 30% to 60%) of breast tumors are ER and/or PR negative
  • about 90% of normal proliferating breast epithelial cells are receptor negative
  • Our previous in vitro studies had shown that breast tissues and cell lines readily convert progesterone to 5α-pregnanes, such as 5αP, and delta-4-pregnenes, such as 3αHP (Figure ​(Figure1),1), and that tumorous breast tissues [15] and tumorigenic breast cell lines [16] produce higher levels of 5αP and lower levels of 3αHP than do normal breast tissues and nontumorigenic cell lines
  • The progesterone metabolism studies suggested that increases in 5αP and decreases in 3αHP production accompany the shift toward breast cell neoplasia and tumorigenicity
  • In vitro studies on five different human breast cell lines showed that cell proliferation and detachment are significantly increased by 5αP and decreased by 3αHP
  • the prevailing theory of hormonal regulation of breast cancer, as well as hormone-based therapies, revolves around estrogen and/or progesterone and ER/PR-positive breast cells and tumors.
  • Not only do these "receptor-negative" breast cancers fail to benefit from current hormonal therapies, but they also generally exhibit more-aggressive biologic behaviors and poorer prognosis than the receptor-positive ones
  • The results of the studies reported here show for the first time that the progesterone metabolites, 5αP and 3αHP, act as hormones that regulate ER/PR-negative breast tumor formation, growth, and regression
  • The onset of the ER/PR-negative human breast cell tumors in mice was considerably accelerated, and the growth significantly stimulated, by just one or two applications of 5αP
  • In contrast, 3αHP retarded onset of tumor formation, suppressed tumor growth, and inhibited or regressed existing 5αP-induced tumors
  • When both hormones were administered simultaneously, the effects of one were abrogated by the effects of the other.
  • The 5αPR and 3αHPR (which are associated with the plasma membranes of both ER/PR-positive [19] and ER/PR-negative [29] cells) are distinct from each other and from known ER, PR, androgen, and corticosteroid receptors, and lack affinity for other steroids, such as progesterone, estrogen, androgens, corticosteroids, and other progesterone metabolites
  • Levels of 5αPR are upregulated by 5αP itself and estradiol, and downregulated by 3αHP in both ER/PR-positive and -negative cells
  • ndications are that 5αP acts via the surface receptor-linked mitogen-activated protein kinase (MAPK; Erk1/2) pathway; 5αP significantly stimulates activation of Erk1/2 [30], increases the Bcl-2/Bax expression ratio [18] and actin depolymerization [31], and decreases expression of actin and adhesion plaque-associated vinculin [31], resulting in decreased apoptosis and increased mitosis and cell detachment
  • 3αHP appears to suppress protein kinase C (PKC), phospholipase C (PLC), Ca2+ mobilization (unpublished observations), and the Bcl-2/Bax expression ratio [18], and increases expression of the cell-cycle inhibitor p21 [18], resulting in increased apoptosis and decreased proliferation and detachment of breast cell lines.
  • serum from mice with tumors had significantly more 5αP than 3αHP
  • the tumors, which on average had about threefold higher concentrations of 5αP than the respective sera, and >10-fold higher 5αP than 3αHP levels
  • Previous in vitro metabolism studies showed that human breast tumor tissues convert significantly more progesterone to 5α-pregnanes like 5αP and less to 4-pregnenes like 3αHP than do paired normal (nontumorous) tissues
  • Similar differences in progesterone metabolism and enzyme gene expressions were observed between tumorigenic and nontumorigenic breast cell lines
  • breast carcinomas are able to synthesize progesterone
  • The current findings, along with the previous in vitro studies, suggest that the relative concentrations of 5αP and 3αHP in the breast microenvironment constitute important autocrine/paracrine determinants not only for tumorigenesis but also for potential regression of tumors and the maintenance of normalcy of ER/PR-negative breast cells/tissues.
  • Evidence presented here shows that a high concentration of 5αP, relative to 3αHP in the microenvironment, promotes initiation and growth of tumors, whereas a higher concentration of 3αHP, relative to 5αP, suppresses tumorigenesis and promotes normalcy
  • 5α-reductase and 5αPR levels are upregulated by 5αP
  • in the 3αHP-treated mice, the elevated 3αHP levels, relative to 5αP, in the microenvironment could have opposed progression to xenograft neoplasia by its inherent anticancer actions and the suppression of 5αP synthesis and 5αPR expression
  • the opposing actions of the progesterone metabolites also appear to exert some control over the estrogen-regulated effects on breast cancer by their ability to modulate ER numbers in ER-positive cells
  • because both ER/PR-negative and ER/PR-positive, as well as normal and tumorigenic human breast cell lines, have been shown to respond to 5αP and 3αHP in vitro, it is suggested that these endogenously produced progesterone metabolites may also play regulatory hormonal roles in ER/PR-positive breast cancers, as well as in the maintenance of normalcy in nontumorous breast tissues.
  • The in vivo data provide further evidence that progesterone metabolites, such as 5αP and 3αHP, deserve to be considered as active hormones in their own right, rather than inactive waste products
  • Nathan Goodyear on 28 Jan 14
     
    Progesterone metabolites and breast cancer
Nathan Goodyear

Estrogen and prostate cancer: An eclipsed truth in an androgen-dominated scenario - Car... - 0 views

onlinelibrary.wiley.com/...abstract

aromatase aromatase activity Estradiol Estrogen ER alpha prostate cancer prostate cancer disease

shared by Nathan Goodyear on 21 Aug 13 - No Cached
  • Aberrant aromatase expression and activity has been reported in prostate tumor tissues and cells, implying that androgen aromatization to estrogens may play a role in prostate carcinogenesis or tumor progression
  • imbalance of their expression may be critical to determine the ultimate estrogen effects on prostate cancer cells
  • In prostate cancer, ERβ activation appears to limit cell proliferation directly or through ERα inhibition, and loss of ERβ has been consistently associated with tumor progression
  • Nathan Goodyear on 21 Aug 13
     
    High aromatase activity and ER alpha expression/signaling associated with prostate disease.
Nathan Goodyear

The Role of Estrogens in Prostate Carcinogenesis: A Rationale for Chemoprevention - 0 views

www.ncbi.nlm.nih.gov/...PMC1477605

prostate cancer hormone hormones estrogen estrogen receptors aromatase men

shared by Nathan Goodyear on 16 Sep 13 - No Cached
  • Nathan Goodyear on 16 Sep 13
     
    Good review of the mixed pathway of hormones in cancer development--prostate.  Estrogens, through estrogen receptors, promote prostate cancer development and growth.
Nathan Goodyear

Modulation of arachidonic acid metabolism by ... [Carcinogenesis. 2004] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15073046

curcumin tumeric inflammation

shared by Nathan Goodyear on 13 Sep 13 - No Cached
  • Nathan Goodyear on 13 Sep 13
     
    curcumin found to inhibit LOX and COX and thus inflammatory leukotrienes, thromboxanes, and prostaglandins.  
Nathan Goodyear

Estrogen Receptors in Colorectal Cancer: Goalkeepers, Strikers, or Bystanders? - 0 views

cancerpreventionresearch.aacrjournals.org/...897.full

estrogen colon cancer ER beta ER-beta breast

shared by Nathan Goodyear on 19 Nov 13 - No Cached
  • one can conclude that ERβ has an overall antiproliferative effect, thereby inhibiting cancer cell proliferation and antagonizing ERα function in the breast
  • HRT with estrogen alone did not increase the risk of breast cancer in the Women's Health Initiative clinical trials program
  • colorectal normal or cancer epithelium does not coexpress ERα and ERβ
  • ...7 more annotations...
  • ERβ expression resulted in the inhibition of proliferation and G1 phase cell-cycle arrest
  • ERβ expression strongly inhibited cMyc and tumor growth in a xenograft mouse model
  • induced ERβ in CRC cells has an antiproliferative, tumor-suppressive function that is independent of ERα
  • ERs also have the ability to bind many other compounds with an estrogen-like structure, including phytoestrogens and xenoestrogens (or endocrine disruptors)
  • Phytoestrogens are a diverse class of natural compounds with structural similarity to estradiol
  • Barone et al. recently found that two ERβ-selective phytoestrogens effectively counteracted CRC tumorigenesis and surprisingly increased ERβ expression in mice with mutations of the tumor-suppressor gene adenomatous polyposis coli
  • We can conclude that estrogens are important in protecting against CRC initiation and progression, and that the protective effect most likely is mediated by ERβ
  • Nathan Goodyear on 19 Nov 13
     
    ER beta is a new potential mode of therapy in colon cancer.  ER beta stimulation has been shown to inhibit colon cancer cell growth.
Nathan Goodyear

Sex Steroids and Prostate Carcinogenesis Integrated, Multifactorial Working Hypothesis - 0 views

www.ncbi.nlm.nih.gov/...PMC2821822

prostate cancer estradiol Testosterone aromatase hormone hormones

shared by Nathan Goodyear on 23 Sep 13 - No Cached
  • Nathan Goodyear on 23 Sep 13
     
    The genesis of cancer is complex.  To simply say that cancer is genetic is both niave and uninformed.  This study displays the complexity of the timing of hormones and cancer genesis.  This rat study found that Estradiol added to Testosterone increased "markedly".  Estrogen plays a role in the genesis of prostate disease.  However, this varies among individuals.  The response of prostate cancer to estradiol appears to change according to the progression of the cancer.
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