Affordable in home care | starts at $28 per hr
My answer to Can Alzheimer's be prevented? How? Could it be cured with stem cell research?
Answer by Connie b. Dellobuono:
It can be slowed down with nurture (massage,love,loving environment), whole foods (probiotic, sulfur rich foods), social interaction, sufficient sleep and exercise.
Can Alzheimer's be prevented? How? Could it be cured with stem cell research?
My answer to Do repeated seizures trigger Alzheimer's a few years (less than 6) later in life?
Answer by Connie b. Dellobuono:
Unprovoked seizures develop in 10%-22% of people with Alzheimer disease, a disorder that affects more than 5 million Americans.
Consequently, as many as 1 million people with Alzheimer disease in the United States may develop seizures. The likelihood of seizures increases in familial and early-onset cases of Alzheimer disease.
After cerebrovascular disease and brain tumors, Alzheimer disease and other dementias are the most common etiologies of seizures in elderly persons.
In recent retrospective study by Vossel and colleagues covering a 5-year period (2007-2012) reported on 12 patients with amnestic mild cognitive impairment (aMCI) and 35 patients with Alzheimer disease, all of whom had epilepsy. Another 7 patients with Alzheimer disease plus subclinical epileptiform activity were included. Patients with epilepsy beginning before age 30 years or known etiologies of seizures (eg, subdural hematoma, stroke) that were presumably unrelated to the development of aMCI or Alzheimer disease were excluded.
Study findings. Patients with aMCI and epilepsy presented with cognitive decline 6.8 years earlier (at age 64.3 years vs 71.1 years) than those with aMCI without epilepsy (P=.02). Those with Alzheimer disease and epilepsy presented with cognitive decline 5.5 years earlier (at age 64.8 years vs 70.3 years) than those with Alzheimer disease without epilepsy (P=.001). Patients with Alzheimer disease and subclinical epileptiform activity had an early onset of cognitive decline (at age 58.9 years).
Do repeated seizures trigger Alzheimer's a few years (less than 6) later in life?
My answer to Is everyone naturally immune to some disease?
Answer by Connie b. Dellobuono:
Environmental influences have greater impact to our immune system than our genes.
The researchers also looked for genetic influence in the twins’ responses to flu vaccines. Some people react more strongly to vaccines than others, producing more antibodies: proteins that our bodies manufacture to identify and protect us from invading microbes. If this trait were genetic, identical twins would have similar responses. Instead, the variation in responses was almost entirely the result of environmental differences—presumably, what strains of flu the twins had previously been exposed to.
The researchers also studied the immune system impact of cytomegalovirus, which lies dormant in a large fraction of the population, rarely causing symptoms. Pairs of identical twins with different infection statuses—one was infected and the other was not—had more divergent immune systems than sets of twins in which both were uninfected. In fact, cytomegalovirus infection influenced nearly 60% of the parameters the scientists measured. “That’s kind of a smoking gun” that the variation is environmental, Davis says.
The work goes beyond previous research in its scope, says immunologist Jean-Laurent Casanova of Rockefeller University in New York City, who was not involved with the research. “To do a twin study and measure a tremendous number of immunological parameters, that is very novel.”
“There’s nothing here that is revolutionary or requires rethinking of our assumptions about how the immune system functions,” says David Baltimore, a biologist at the California Institute of Technology in Pasadena. But, he says, “I found it very impressive … that as we age, our immune systems become molded in increasingly individual ways.”
Introduction Risk factors for Alzheimer’s disease (AD) affecting the rate of cognitive decline and brain shrinkage include nonmodifiable factors such as age, low education levels, and genetic…
Source: Vit B12, folate, homocysteine and Alzheimer’s disease
Risk factors for Alzheimer’s disease (AD) affecting the rate of cognitive decline and brain shrinkage include nonmodifiable factors such as age, low education levels, and genetic factors, whereas modifiable risk factors have also been identified. One such modifiable risk factor is homocysteine (Hcy), an amino acid that is produced in the methylation cycle of protein metabolism. The association between elevated plasma Hcy and cognitive impairment has been well established (Budge et al., 2002, McCaddon et al., 2001 and Seshadri, 2006), although the underlying mechanisms to explain the association are still being researched.
Hcy is produced via protein metabolism. The conversion of Hcy to useful metabolites, S-adenosyl methionine and glutathione, requires vitamins B9 (methyl folate), B12 (cobalamin), and B6 (pyridoxine) as cofactors ( Morris, 2012a and Refsum et al., 2006). Hence, if the B-vitamin supply through the diet is suboptimal, remethylation of Hcy via the enzyme methionine synthase is reduced, and plasma levels of Hcy rise. The importance of the remethylation process is the regeneration of the active form of folate, tetrahydrofolate, needed for thymidine synthesis, DNA replication, and neurogenesis. S-adenosyl methionine is a methyl donor for the central nervous system and important to neurotransmitter synthesis. Vitamin B12 is also important for fatty acid metabolism, acting as a cofactor for the enzyme methylmalonyl-CoA mutase and also promoting neural membrane formation. Buildup of methylmalonic acid (MMA) indicates the loss of this B12 function. Disruption of any of these pathways is likely to lead to loss of cognitive function and contribute to neuronal atrophy. Increased oxidative stress occurs in the brain when Hcy is elevated ( Birch et al., 2009) and may increase the permeability of blood brain barrier. It is well known that vitamin B12 deficiency is a cause of pernicious or megaloblastic anemia, peripheral neuropathy, lack of energy, and poor memory.
Hcy levels rise with age (Nygård et al., 1998), possibly because of poor absorption of B vitamins from the diet and other factors including male sex, smoking, high blood pressure, and other clinical conditions (Refsum et al., 2006). However, studies in AD patients showed that blood levels of total Hcy are higher than in healthy controls, whereas folate and B12 levels are lower (Clarke et al., 1998).
Brain shrinkage because of cortical atrophy occurs with normal aging (Fjell et al., 2009 and Thambisetty et al., 2010). The rate of brain atrophy has been shown to be a marker of cognitive decline (Fox et al., 1999) in domains such as memory, processing speed, and executive function (Fjell and Walhovd, 2010).
A 5-year study of people older than 60 years showed that percentage brain volume loss occurred at an average rate of 0.7% ± 0.3% per year (Vogiatzoglou et al., 2008). However, the decrease in brain volume was greater among those with lower vitamin B12 levels and markers of functional B12 including holo-transcobalamin at baseline. Brain volume loss was also associated with higher plasma total Hcy and MMA levels at baseline. For those with the lowest tertile of baseline vitamin B12 (<308 pmol/L), there was a 6-fold increase in the rate of brain volume loss. Elevated total Hcy is also associated with a smaller hippocampus in community-dwelling older adults (Williams et al., 2002). Minimal hippocampal width was shown to decline by 0.7 mm for each 10 micromolar increment in Hcy.
The rate of brain atrophy is known to be increased with neurodegenerative diseases such as AD. Atrophy in the medial temporal lobes becomes detectable by brain imaging at an early stage and is followed by increasing atrophy spreading to other regions of the brain in a sequential pathway (Smith, 2002). Rates of atrophy in those with AD can reach up to 12% per year and have been directly associated with cognitive decline starting in the domain of episodic memory and later involving domains of attention, executive function, processing speed, language, visuospatial skills, and orientation.
Hcy levels have also been associated with cognitive decline. For example, the Hordaland Homocysteine Study found that a rise in Hcy levels over time (6 years of follow-up) predicted cognitive decline (Nurk et al., 2005). This association has been confirmed in other studies (McCaddon et al., 2001) and reviews (Sachdev, 2005) and shown to be age dependent (Oulhaj et al., 2010). Controversies to these findings have been discussed by Morris (2012a).
Summary
Elevated Hcy is a risk factor for brain atrophy, cognitive decline, and AD. Hcy can be lowered with B vitamins that are important cofactors in the methylation cycle of Hcy. Together, these cofactors play a role in DNA repair and integrity of the neural membranes; thus, deficiencies will result in damage and brain atrophy.
Treatment with B vitamins can reduce the rate of brain shrinkage in older adults, especially in those with elevated Hcy. The treatment can also delay cognitive decline if taken long term (over 1 year) in those with high Hcy levels. Treatment is likely to be more beneficial in those whose brain shrinkage has not yet reached critical levels and in those who do not yet have dementia.
http://www.sciencedirect.com/science/article/pii/S0197458014003583
https://ods.od.nih.gov/factsheets/Folate-HealthProfessional/
J Natl Cancer Inst. 2008 Jul 16;100(14):996-1002. doi: 10.1093/jnci/djn209. Epub 2008 Jul 8. Decreased cancer risk after iron reduction in patients with peripheral arterial disease: results from a …
J Natl Cancer Inst. 2008 Jul 16;100(14):996-1002. doi: 10.1093/jnci/djn209. Epub 2008 Jul 8.
Decreased cancer risk after iron reduction in patients with peripheral arterial disease: results from a randomized trial. Zacharski LR1, Chow BK, Howes PS, Shamayeva G, Baron JA, Dalman RL, Malenka DJ, Ozaki CK, Lavori PW.
Excess iron has been implicated in cancer risk through increased iron-catalyzed free radical-mediated oxidative stress.
A multicenter randomized, controlled, single-blinded clinical trial (VA Cooperative Study #410) tested the hypothesis that reducing iron stores by phlebotomy would influence vascular outcomes in patients with peripheral arterial disease. Patients without a visceral malignancy in the last 5 years (n = 1277) were randomly assigned to control (n = 641) or iron reduction (n = 636). Occurrence of new visceral malignancy and cause-specific mortality data were collected prospectively. Cancer and mortality outcomes in the two arms were compared using intent-to-treat analysis with a Cox proportional hazards regression model. Statistical tests were two-sided.
Patients were followed up for an average of 4.5 years. Ferritin levels were similar in both groups at baseline but were lower in iron reduction patients than control patients across all 6-month visits (mean = 79.7 ng/mL, 95% confidence interval [CI] = 73.8 to 85.5 ng/mL vs 122.5 ng/mL, 95% CI = 115.5 to 129.5 ng/mL; P < .001). Risk of new visceral malignancy was lower in the iron reduction group than in the control group (38 vs 60, hazard ratio [HR] = 0.65, 95% CI = 0.43 to 0.97; P = .036), and, among patients with new cancers, those in the iron reduction group had lower cancer-specific and all-cause mortality (HR = 0.39, 95% CI = 0.21 to 0.72; P = .003; and HR = 0.49, 95% CI = 0.29 to 0.83; P = .009, respectively) than those in the control group. Mean ferritin levels across all 6-monthly visits were similar in patients in the iron reduction and control groups who developed cancer but were lower among all patients who did not develop cancer than among those who did (76.4 ng/mL, 95% CI = 71.4 to 81.4 ng/mL, vs 127.1 ng/mL, 95% CI = 71.2 to 183.0 ng/mL; P = .017).
Iron reduction was associated with lower cancer risk and mortality. Further studies are needed to define the role of body iron in cancer risk.
http://www.cell.com/cell-metabolism/references/S1550-4131(16)30361-8
Authors -> Title –> Source
Anderson, E.R., Taylor, M., Xue, X., Ramakrishnan, S.K., Martin, A., Xie, L., Bredell, B.X., Gardenghi, S., Rivella, S., and Shah, Y.M. Intestinal HIF2α promotes tissue-iron accumulation in disorders of iron overload with anemia.
Crossref | PubMed | Scopus (15)
Proc. Natl. Acad. Sci. USA. 2013; 110: E4922–E4930
Ashmore, J.H., Rogers, C.J., Kelleher, S.L., Lesko, S.M., and Hartman, T.J. Dietary iron and colorectal cancer risk: a review of human population studies.
Crossref
Crit. Rev. Food Sci. Nutr. 2016; 56: 1012–1020
Bao, Z.Q., Jacobsen, D.M., and Young, M.A. Briefly bound to activate: transient binding of a second catalytic magnesium activates the structure and dynamics of CDK2 kinase for catalysis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30)
Structure. 2011; 19: 675–690
Bastide, N.M., Chenni, F., Audebert, M., Santarelli, R.L., Taché, S., Naud, N., Baradat, M., Jouanin, I., Surya, R., Hobbs, D.A. et al. A central role for heme iron in colon carcinogenesis associated with red meat intake.
Crossref | Scopus (10)
Cancer Res. 2015; 75: 870–879
Blachier, F., Vaugelade, P., Robert, V., Kibangou, B., Canonne-Hergaux, F., Delpal, S., Bureau, F., Blottière, H., and Bouglé, D. Comparative capacities of the pig colon and duodenum for luminal iron absorption.
Crossref | Scopus (16)
Can. J. Physiol. Pharmacol. 2007; 85: 185–192
Brady, D.C., Crowe, M.S., Turski, M.L., Hobbs, G.A., Yao, X., Chaikuad, A., Knapp, S., Xiao, K., Campbell, S.L., Thiele, D.J., and Counter, C.M. Copper is required for oncogenic BRAF signalling and tumorigenesis.
Crossref | PubMed | Scopus (46)
Nature. 2014; 509: 492–496
Brookes, M.J., Hughes, S., Turner, F.E., Reynolds, G., Sharma, N., Ismail, T., Berx, G., McKie, A.T., Hotchin, N., Anderson, G.J. et al. Modulation of iron transport proteins in human colorectal carcinogenesis.
Crossref | PubMed | Scopus (73)
Gut. 2006; 55: 1449–1460
Brookes, M.J., Boult, J., Roberts, K., Cooper, B.T., Hotchin, N.A., Matthews, G., Iqbal, T., and Tselepis, C. A role for iron in Wnt signalling.
Crossref | PubMed | Scopus (37)
Oncogene. 2008; 27: 966–975
Cadieux, J.A., Zhang, Z., Mattice, M., Brownlie-Cutts, A., Fu, J., Ratkay, L.G., Kwan, R., Thompson, J., Sanghara, J., Zhong, J., and Goldberg, Y.P. Synthesis and biological evaluation of substituted pyrazoles as blockers of divalent metal transporter 1 (DMT1).
Crossref | Scopus (11)
Bioorg. Med. Chem. Lett. 2012; 22: 90–95
Cancer Genome Atlas, N. and Cancer Genome Atlas Network. Comprehensive molecular characterization of human colon and rectal cancer.
Crossref | PubMed | Scopus (1595)
Nature. 2012; 487: 330–337
Carballo, M., Conde, M., El Bekay, R., Martín-Nieto, J., Camacho, M.J., Monteseirín, J., Conde, J., Bedoya, F.J., and Sobrino, F. Oxidative stress triggers STAT3 tyrosine phosphorylation and nuclear translocation in human lymphocytes.
Crossref | PubMed | Scopus (163)
Cerami, E., Gao, J., Dogrusoz, U., Gross, B.E., Sumer, S.O., Aksoy, B.A., Jacobsen, A., Byrne, C.J., Heuer, M.L., Larsson, E. et al. The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data.
Crossref | PubMed | Scopus (1077)
Cancer Discov. 2012; 2: 401–404
Cross, A.J., Ferrucci, L.M., Risch, A., Graubard, B.I., Ward, M.H., Park, Y., Hollenbeck, A.R., Schatzkin, A., and Sinha, R. A large prospective study of meat consumption and colorectal cancer risk: an investigation of potential mechanisms underlying this association.
Crossref | PubMed | Scopus (127)
Cancer Res. 2010; 70: 2406–2414
Dame, M.K., Jiang, Y., Appelman, H.D., Copley, K.D., McClintock, S.D., Aslam, M.N., Attili, D., Elmunzer, B.J., Brenner, D.E., Varani, J., and Turgeon, D.K. Human colonic crypts in culture: segregation of immunochemical markers in normal versus adenoma-derived.
Crossref | Scopus (4)
Lab. Invest. 2014; 94: 222–234
Dixon, S.J. and Stockwell, B.R. The role of iron and reactive oxygen species in cell death.
Crossref | PubMed | Scopus (117)
Nat. Chem. Biol. 2014; 10: 9–17
Dixon, S.J., Lemberg, K.M., Lamprecht, M.R., Skouta, R., Zaitsev, E.M., Gleason, C.E., Patel, D.N., Bauer, A.J., Cantley, A.M., Yang, W.S. et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (211)
Cell. 2012; 149: 1060–1072
Donovan, A., Lima, C.A., Pinkus, J.L., Pinkus, G.S., Zon, L.I., Robine, S., and Andrews, N.C. The iron exporter ferroportin/Slc40a1 is essential for iron homeostasis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (421)
Cell Metab. 2005; 1: 191–200
Feng, Y., Sentani, K., Wiese, A., Sands, E., Green, M., Bommer, G.T., Cho, K.R., and Fearon, E.R. Sox9 induction, ectopic Paneth cells, and mitotic spindle axis defects in mouse colon adenomatous epithelium arising from conditional biallelic Apc inactivation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (12)
Am. J. Pathol. 2013; 183: 493–503
Gunshin, H., Fujiwara, Y., Custodio, A.O., Direnzo, C., Robine, S., and Andrews, N.C. Slc11a2 is required for intestinal iron absorption and erythropoiesis but dispensable in placenta and liver.
Crossref | PubMed
Hinoi, T., Akyol, A., Theisen, B.K., Ferguson, D.O., Greenson, J.K., Williams, B.O., Cho, K.R., and Fearon, E.R. Mouse model of colonic adenoma-carcinoma progression based on somatic Apc inactivation.
Crossref | PubMed | Scopus (111)
Cancer Res. 2007; 67: 9721–9730
Jarnicki, A., Putoczki, T., and Ernst, M. Stat3: linking inflammation to epithelial cancer – more than a “gut” feeling?.
Crossref | PubMed | Scopus (104)
Cell Div. 2010; 5: 14
Jenkitkasemwong, S., Wang, C.Y., Coffey, R., Zhang, W., Chan, A., Biel, T., Kim, J.S., Hojyo, S., Fukada, T., and Knutson, M.D. SLC39A14 is required for the development of hepatocellular iron overload in murine models of hereditary hemochromatosis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (4)
Cell Metab. 2015; 22: 138–150
Johnson, R.L. and Fleet, J.C. Animal models of colorectal cancer.
Crossref | PubMed | Scopus (16)
Cancer Metastasis Rev. 2013; 32: 39–61
Le, N.T. and Richardson, D.R. The role of iron in cell cycle progression and the proliferation of neoplastic cells.
PubMed
Biochim. Biophys. Acta. 2002; 1603: 31–46
Merk, K., Mattsson, B., Mattsson, A., Holm, G., Gullbring, B., and Björkholm, M. The incidence of cancer among blood donors.
Crossref | PubMed | Scopus (46)
Int. J. Epidemiol. 1990; 19: 505–509
Nelson, R.L. Iron and colorectal cancer risk: human studies.
Crossref | PubMed
Nutr. Rev. 2001; 59: 140–148
Nurtjahja-Tjendraputra, E., Fu, D., Phang, J.M., and Richardson, D.R. Iron chelation regulates cyclin D1 expression via the proteasome: a link to iron deficiency-mediated growth suppression.
Crossref | PubMed | Scopus (74)
Blood. 2007; 109: 4045–4054
O’Shea, J.J., Holland, S.M., and Staudt, L.M. JAKs and STATs in immunity, immunodeficiency, and cancer.
Crossref | PubMed | Scopus (164)
Osborne, N.J., Gurrin, L.C., Allen, K.J., Constantine, C.C., Delatycki, M.B., McLaren, C.E., Gertig, D.M., Anderson, G.J., Southey, M.C., Olynyk, J.K. et al. HFE C282Y homozygotes are at increased risk of breast and colorectal cancer.
Crossref | PubMed | Scopus (61)
Hepatology. 2010; 51: 1311–1318
Putoczki, T.L., Thiem, S., Loving, A., Busuttil, R.A., Wilson, N.J., Ziegler, P.K., Nguyen, P.M., Preaudet, A., Farid, R., Edwards, K.M. et al. Interleukin-11 is the dominant IL-6 family cytokine during gastrointestinal tumorigenesis and can be targeted therapeutically.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (80)
Cancer Cell. 2013; 24: 257–271
Radulescu, S., Brookes, M.J., Salgueiro, P., Ridgway, R.A., McGhee, E., Anderson, K., Ford, S.J., Stones, D.H., Iqbal, T.H., Tselepis, C., and Sansom, O.J. Luminal iron levels govern intestinal tumorigenesis after Apc loss in vivo.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (27)
Cell Rep. 2012; 2: 270–282
Salh, B., Bergman, D., Marotta, A., and Pelech, S.L. Differential cyclin-dependent kinase expression and activation in human colon cancer.
Anticancer Res. 1999; 19: 741–748
Satyanarayana, A. and Kaldis, P. Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms.
Crossref | PubMed | Scopus (272)
Oncogene. 2009; 28: 2925–2939
Seril, D.N., Liao, J., Yang, G.Y., and Yang, C.S. Oxidative stress and ulcerative colitis-associated carcinogenesis: studies in humans and animal models.
Crossref | PubMed | Scopus (256)
Carcinogenesis. 2003; 24: 353–362
Shah, Y.M., Matsubara, T., Ito, S., Yim, S.H., and Gonzalez, F.J. Intestinal hypoxia-inducible transcription factors are essential for iron absorption following iron deficiency.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (158)
Cell Metab. 2009; 9: 152–164
Shen, J., Sheng, X., Chang, Z., Wu, Q., Wang, S., Xuan, Z., Li, D., Wu, Y., Shang, Y., Kong, X. et al. Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (12)
Cell Rep. 2014; 7: 180–193
Shi, H., Bencze, K.Z., Stemmler, T.L., and Philpott, C.C. A cytosolic iron chaperone that delivers iron to ferritin.
Crossref | PubMed | Scopus (176)
Science. 2008; 320: 1207–1210
Siegel, R., Ma, J., Zou, Z., and Jemal, A. Cancer statistics, 2014.
Crossref | PubMed | Scopus (4908)
CA Cancer J. Clin. 2014; 64: 9–29
Song, S., Christova, T., Perusini, S., Alizadeh, S., Bao, R.Y., Miller, B.W., Hurren, R., Jitkova, Y., Gronda, M., Isaac, M. et al. Wnt inhibitor screen reveals iron dependence of β-catenin signaling in cancers.
Crossref | PubMed | Scopus (37)
Cancer Res. 2011; 71: 7628–7639
Tak, Y.S., Tanaka, Y., Endo, S., Kamimura, Y., and Araki, H. A CDK-catalysed regulatory phosphorylation for formation of the DNA replication complex Sld2-Dpb11.
Crossref | PubMed | Scopus (56)
EMBO J. 2006; 25: 1987–1996
van de Wetering, M., Francies, H.E., Francis, J.M., Bounova, G., Iorio, F., Pronk, A., van Houdt, W., van Gorp, J., Taylor-Weiner, A., Kester, L. et al. Prospective derivation of a living organoid biobank of colorectal cancer patients.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (49)
Cell. 2015; 161: 933–945
Xue, X. and Shah, Y.M. Hypoxia-inducible factor-2α is essential in activating the COX2/mPGES-1/PGE2 signaling axis in colon cancer.
Crossref | PubMed | Scopus (17)
Carcinogenesis. 2013; 34: 163–169
Xue, X. and Shah, Y.M. Intestinal iron homeostasis and colon tumorigenesis.
Crossref | PubMed | Scopus (9)
Nutrients. 2013; 5: 2333–2351
Xue, Y., Ren, J., Gao, X., Jin, C., Wen, L., and Yao, X. GPS 2.0, a tool to predict kinase-specific phosphorylation sites in hierarchy.
Crossref | PubMed | Scopus (282)
Mol. Cell. Proteomics. 2008; 7: 1598–1608
Xue, X., Taylor, M., Anderson, E., Hao, C., Qu, A., Greenson, J.K., Zimmermann, E.M., Gonzalez, F.J., and Shah, Y.M. Hypoxia-inducible factor-2α activation promotes colorectal cancer progression by dysregulating iron homeostasis.
Crossref | PubMed | Scopus (35)
Cancer Res. 2012; 72: 2285–2293
Xue, X., Ramakrishnan, S.K., and Shah, Y.M. Activation of HIF-1α does not increase intestinal tumorigenesis.
Crossref | PubMed | Scopus (8)
Am. J. Physiol. Gastrointest. Liver Physiol. 2014; 307: G187–G195
Yu, H., Pardoll, D., and Jove, R. STATs in cancer inflammation and immunity: a leading role for STAT3.
Crossref | PubMed | Scopus (1251)
Nat. Rev. Cancer. 2009; 9: 798–809
Zacharski, L.R., Chow, B.K., Howes, P.S., Shamayeva, G., Baron, J.A., Dalman, R.L., Malenka, D.J., Ozaki, C.K., and Lavori, P.W. Decreased cancer risk after iron reduction in patients with peripheral arterial disease: results from a randomized trial.
Crossref | PubMed | Scopus (133)
Zeestraten, E.C., Maak, M., Shibayama, M., Schuster, T., Nitsche, U., Matsushima, T., Nakayama, S., Gohda, K., Friess, H., van de Velde, C.J. et al. Specific activity of cyclin-dependent kinase I is a new potential predictor of tumour recurrence in stage II colon cancer.
Crossref | PubMed | Scopus (18)
Br. J. Cancer. 2012; 106: 133–140
Zhong, Z., Wen, Z., and Darnell, J.E. Jr. Stat3: a STAT family member activated by tyrosine phosphorylation in response to epidermal growth factor and interleukin-6.
Crossref | PubMed
Science. 1994; 264: 95–98
A man complained of breathing problems and died later. Only after death and upon learning of his bagpipe hobby, that the doctor discovered fungus in his bagpipe.
Source: Inhaled fungus from a bagpipe
To effectively starve cancer, increase brain growth and to lose weight, a diet mimicking fasting has proven to work in combo with some chemo that it is now being used. To begin to understand the ef…
Source: Diet that mimics fasting for brain growth and starves cancer
To effectively fight cancer, increase brain growth and to lose weight, a diet mimicking fasting has proven to work that in some chemo it is now used. To begin to understand the effects of a fasting…
Source: Diet that mimics fasting for brain growth and anti-tumor growth
Copyright © 2026 KRM Digital Solutions
