Omah is the native Prince from the enchanted empire of Jicotea, a kingdom expanded from the spiritual beginnings of harmonious tribes. Omah has everything one could want or inherit except the two things that would make him the ideal royal…adventure and a portrait worthy smile. Following the appearance of the mysterious Moilinere’s magical key, Omah is transported to an incredulous land where intelligent sheep reign over the giants. The Prince forms an unlikely friendship with a fashionable but misunderstood giant called Mook. The two companions Omah and Mook devise a plan to save the land of ShRATI from the single colour obsessed hooves of the sheep.
I have followed an awesome Haiku writer for quite some time now but I haven’t made a slot on my schedule to read beyond work material for about 9 months or more. YIKES!!! If…no when I find their page I’ll insert it here (https://trashcanbard.wordpress.com).
Why do I like a Haiku or few? They encourage deeper thinking and sometimes elicit emotions. Subjective interpretation. Overall, Haikus are great additions to your daily reading as life becomes more robotic. 🙂
I recently had a conversation about the small animals I sponsored on a monthly basis and it had me thinking about my contributions to help the homeless. Why is it easier to give to animals on a regular basis but with the homeless there is such scrutiny about whether they truly need financial assistance? Perhaps it comes from the experiences with homeless people who in fact have not been homeless but working as a homeless person and finishing the working day to go to their place of residence. Therefore, duping strangers by appealing to their emotions. Does the layperson know enough about the many forms of homelessness to decide who are those in needs in comparison to those looking to profit off of other’s generosity? Homelessness is not just based on the central focus of rough sleepers we see on TV.
From the Public Health Module of my course we explored the homelessness figures that included estimates of hidden forms such as those living on friends’ or relatives’ sofas for long or short periods of time. How can we meet the needs of others or serve our community both humans or animals when we do not know what or where their needs are?
In the past when I have carried cash (as I don’t like to carry physical money), I have offered whatever change I had at the time. Depending who I was with it was met with a smile or furrowed brows. Sometimes it’s difficult when you give to the homeless and you see or smell signs of substance abuse and you give because you want to help but you’re concerned and later hope that your donation was not part of the funds that allowed them to buy their last hit before an overdose.
On the other hand, who are we as human beings to judge another living the way they choose to live. I don’t know their struggles, what they could be trying to numb or escape from. Also, maybe it’s an assumption on my part to think they want to escape what if they simply like the way substances make them think or feel. Sometimes behaviours are also habits. Whether consciously we know what’s right or wrong, good or bad or the constructs are formed by our own experiences or and government laws. Sometimes we just fail to challenge our own actions. Human beings can and do continue along the same path somewhere in some aspect of their lives. Whether that’s routines like eating the same meals from different restaurants, getting irritated if something has not been returned to the location where you usually store it or what brands you like to buy.
I think our differences: in terms of quirks, drives or habits are what make humans so fascinating. There are entire schools of thought, which includes research designated to understanding human behaviour. I think this understanding has led me to give with good intentions and hope for the best for that person not because I am such a good person or want others to think I am such a good person but because at the time I saw a need, I had to means to fill the need so I did. Also, probably because I can pull from my own experiences that as quickly as someone rises, they can also fall. Life is an unseen journey, perhaps there is some selfish thought behind the act of generosity though delayed, as in am I giving to others in the instance that I am in their predicament someone might also make a gesture in kind towards me? As I am writing this, this is what I have just thought about but then would I need to think this way if wealth was more distributed in society and there was no one percent. Will I still give so readily when I have the means to support others? Is giving to others, animals or general altruism a nature or nurture expression? They say money attracts money but what about greed? What about poverty? Do we have these sayings to soothe ourselves from the reality that keeps some destitute and others economically flourishing despite the scales of changes from tax breaks to global disasters.
In a sense, I guess it is easier to sponsor an animal. The cute photographs or fluffy friends and email updates of seasonal activities in comparison are more manageable and make for a pleasant experience. They do not come with the sense of responsibility to increase your contribution if it is shared that the recipient has children that would also be in need. Nor the afterthoughts of what next for the person you meet. Then again who’s to say I am not in need? To reiterate life is complex I think interpretation helps us feel better or worse with time. A group pf people could look at the same person and make completely different or similar assumptions. It depends on who’s looking or judging. I do not currently own a fast car or a grand estate but I am happy and wake up every morning excited about life and the people in my life.
How can I expect much else if instead I sat in a lack mentality? Surely, I would miss the opportunities popping up from unexpected places whilst feeling sorry for myself or disheartened. This written reflection is probably why I always advise people to do what they can live with.
I got it from my Mama. Well, that’s what my Mum always said to me “Do what you can live with” and it stuck so now it’s all I will say to you…
Okay so long story short I was asked to complete a 6000 word literature review on any topic so I chose….
Salivary Biomarkers for Oral Squamous Cell Carcinoma.
*sigh*
I mean YAAAAY!!!!
Okay so I started all interested reading so much and getting the background information ready when I realised there were LOADS of scientific abbreviations I didn’t understand.
Yes, I did read the journals several times over but…
So I decided to find the function of every significant salivary biomarker from the 10 papers reviewed.
I have provided a wonderful list of the significant biomarkers, just for you.
Besties!!!
Name and Function of Significant Salivary Biomarkers for OSCC
( ) = Alternative scientific names or abbreviations for biomarkers
Cristaldi et al (2019)
ctDNA:
KIF1A: Kinesin Family Member 1A – Protein that transports synaptic vesicles and nutrients across axons.
Promoter hypermethylation:
NID2: Nidogen 2 – Cell adhesion protein.
HOXA9: Homeobox A9 – Protein coding gene (commonly associated with acute leukaemia).
Hypermethylation:
CCNA1: Cyclin A1 – Regulates cell cycles.
DAPK: Death Associated Protein Kinase – Regulator of cell death and autophagy (elimination of dysfunctional structures or products from cells).
MGMT: O6-methylguanine DNA methyltransferase – converts information for a DNA repair protein but prevents the addition of alkyl groups so may inhibit alkylating chemotherapy.
TIMP3: Tissue Inhibitor of Metalloproteinases 3 – Protein coding gene that inhibits proteolytic enzymes or matrix metalloproteinases.
C-deletion in exon 4 codon 63 of p53 gene – Mutation of p53 gene codon 63.
p53 gene codon 63 is a tumour suppressor, consequently there is proliferation or maturation of OSCC.
ctDNA somatic mutations and HPV genes – Tumour DNA and Human Papillomavirus DNA.
MicroRNAs: Regulate RNA genes
miR-31: MicroRNA-31 – Tumour suppressor inhibits cell invasion and metastasis.
DUSP1: Dual Specificity Phosphatase 1 – Protein coding gene initiated by response to damage to fibroblasts e.g. heat, oxidative stress reduces cell proliferation.
H3F3A: H3 Histone, Family 3A – Protein that produces the nucleosome or packages of chromosomal fibres. This process results in DNA coils.
IL1B: Interleukin 1 Beta – Protein mediator made by many cells including white blood cells is a proinflammatory cytokine for monocytes.
IL8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis.
OAZ1: Ornithine Decarboxylase Antizyme 1 – Regulates polyamines that are responsible for cell growth and repair.
S100P: S100 Calcium Binding Protein P – A protein from the S100P gene that regulates cell processes and binds inorganic compounds like calcium, zinc and magnesium.
SAT: Spermidine/Spermine N1-acetyltransferase – Regulates polyamine (a natural compound) and normal or neoplastic growth related to polyamine.
IL-8 mRNA: Interleukin 8 messenger RNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making IL8.
Apolipoprotein E protein – Metabolises fats by binding with fat to create lipoproteins that transport fats in the body.
Gualtero and Suarez Castillo (2016)
Cyfra 21- 1 – Protein fragment a soluble cytokeratin 19/CK19 and epithelial marker.
ZNF510: Zinc Finger Protein 510 – Protein coding gene for associated with gene expression and regulates transcription.
IL-8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis.
SAT: Spermidine/Spermine N1-acetyltransferase – Regulates polyamine (a natural compound) and normal or neoplastic growth related to polyamine.
H3F3A: H3 Histone, Family 3A – Protein that produces the nucleosome or packages of chromosomal fibres. This process results in DNA coils.
Saxena et al (2017)
Microbiota:
Porphyromonas gingivalis – Gram negative, proteolytic, anaerobic bacteria. Involved in many conditions including periodontal disease, invades gingival epithelium.
Tannerella forsythia – Gram negative, proteolytic, anaerobic bacteria Involved in periodontal disease. Initiates alveolar bone connective tissues destruction.
Candida albicans – A common fungal infection causing yeast.
Bacteriodes melaninogenica – Gram negative, anaerobic bacteria that is ‘haemolytic’ kills red blood cells and creates biofilm to spread.
Streptococcus mitis – Gram negative, facultative anaerobic bacteria. Can colonise hard tissues like enamel and mucosa.
Genomics:
p53 exon 4 codon 63 mutations – Mutation of p53 gene codon 63. p53 gene codon 63 is a tumour suppressor, consequently there is proliferation or maturation of OSCC.
Transcriptome:
mRNA: interleukin-8 (IL-8) mRNA –Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making IL8.
mRNA: H3F3A (H3 histone family 3A) mRNA – Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making H3F3A.
IL-1-b: Interleukin 1 Beta – Protein mediator made by many cells including white blood cells is a proinflammatory cytokine for monocytes.
S100P: S100 Calcium Binding Protein P – A protein from the S100P gene that regulates cell processes and binds inorganic compounds like calcium, zinc and magnesium.
mRNA: DUSP1: Dual Specificity Phosphatase 1 mRNA – Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making DUSP1.
OAZ1: Ornithine Decarboxylase Antizyme 1 – Regulates polyamines that are responsible for cell growth and repair.
SAT Spermidine/Spermine N1-acetyltransferase – Regulates polyamine (a natural compound) and normal or neoplastic growth related to polyamine.
Soluble CD44 – Cell surface glycoprotein that regulates metastasis.
Chattopadhyay and Panda (2019)
Transcriptome:
miR-31: MicroRNA-31 – Tumour suppressor inhibiting some stages of metastasis e.g. invasion and colonisation.
miR-136: MicroRNA-136 – Tumour suppressor for invasion and metastasis.
miR-147: MicroRNA-147 – Down regulates the inflammatory response of macrophages.
miR-1250: MicroRNA-1250 – Tumour suppressor affecting Gene GPC3 that produces Glypican-3 a protein for cell proliferation.
miR-148a: MicroRNA-148a – Tumour suppressor inhibiting many stages of tumour growth and initiating apoptosis.
miR-632: MicroRNA-632 – Gene associated with breast cancer, blood cancer, hepatocellular cancer and angiogenesis in gastric cancer.
miR-668: MicroRNA-668 – Regulates mitochondrial function andNLRP3 NLR Family Pyrin Domain Containing 3 that plays a role in T helper cells detection of pathogens.
miR-877: MicroRNA-877 – Tumour suppressor that inhibits cell proliferation, invasion, colonisation, migration and stimulates apoptosis.
miR-503: MicroRNA-503 – Reduces cell proliferation and migration and encourages apoptosis of endothelial cells.
miR-323-5p: MicroRNA-323-5p – Tumour suppressor linked to the inhibition of proliferation and migration of cancerous glial cells or glioma of the brain and spinal cord.
miR-24: MicroRNA-24 – Promotes tumour invasion and metastasis.
miR-27b – Tumour suppressor regulates proliferation invasion and migration. Associated with endothelial cells and breast cancer.
Proteomics:
IL-1µ: Interleukin Alpha – Pro-inflammatory cytokine made by macrophages that stimulates the proliferation and maturation of B-cells.
IL-6: Interleukin 6 – Proinflammatory cytokine that stimulates bone resorption by osteoclasts.
IL-8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis.
VEGF-A: Vascular Endothelial Growth Factor-A – Initiates tumour angiogenesis, formation of new blood vessels and stimulates proliferation and migration of endothelial cells.
TNF-µ: Tissue Necrosis Factor Alpha – Proinflammatory cytokine stimulated by macrophages and monocytes, cell mediator for necrosis and apoptosis. Cell death.
Cyfra 21-1: Cytokeratin 19 protein fragment – Epithelial marker that remains despite malignant changes.
TPA: Tissue Plasminogen Activator – Enzyme produced by endothelial cells and responsible for the breakdown of clots by conversion of plasminogen to plasmin.
CA-125: Cancer Antigen -125 – Tumour marker found on the surface of ovarian cancer cells and associated with diagnosis of ovarian cancer.
bFGF: Basic fibroblast growth factor – Protein for tissue repair, regeneration and differentiation by stimulating fibroblast proliferation. Can also trigger tumorigenesis in dysfunction.
Microbiome:
Haemopilus – Bacteria linked to numerous bacterial infections including: meningitis, sepsis, pneumonia, pericarditis, epiglottitis, septic arthritis, cellulitis and osteomyelitis.
Neisseria – Gram-negative, non-motile bacteria that colonises the surface of mucosa, this genus is responsible for meningitis and gonorrhoea diseases.
Aggregatibacter – Gram-negative genus that can lead to infective endocarditis and periodontal disease specifically periodontitis.
Lactobacillus and Lactobacillaceae – Rod-shaped gram-positive bacteria that metabolises glucose to produce lactic acid. Associated with dental caries.
Metabolomics:
Phenylalanine – Amino acid obtained from food and used by the body to produce proteins and enzymes. Phenylalanine dysfunction linked to gastroesophageal cancer.
Valine – Amino acid inducing protein synthesis as well as the maintenance and repair of the muscles.
lactic acid – A by-product of metabolism e.g. respiration the build-up of lactic acid. In carcinomas lactic acid is thought to support angiogenesis and suppression of the immune system.
Hema Shree et al (2019)
MMP-9: Matrix metalloproteinase 9 – Is a proteolytic enzyme linked to periodontal disease and cancer cell invasion.
Chemerin – An ‘adipokine’ or cytokine released from adipose and other tissues linked to the generation of fat cell, new blood vessels and inflammation.
Choline – Water soluble, natural compound obtained from food like eggs or fish that supports metabolism and cell growth.
Betaine – Compound found in beetroot, some seafood and wheat that regulates water balance within cells, metabolises choline and assists cell metabolism transcription via DNA methylation.
Pipecolinic acid – Product of human metabolism found in urine, cerebrospinal fluid and blood as a result of lysine metabolism. Lysine creates protein.
I-carnitine – Delivers fatty acids to mitochondria to supply the body with energy.
Stuani et al (2016)
Cytokines:
IL-1µ Interleukin Alpha – Pro-inflammatory cytokine made by macrophages that stimulates the proliferation and maturation of B-cells.
IL-1-b: Interleukin 1 Beta – Protein mediator made by many cells including white blood cells is a proinflammatory cytokine for monocytes.
IL-1RA: Interleukin 1 Receptor Antagonist – Competes with Interleukin 1 IL-1 for binding sites to prevent the pro-inflammatory effects of IL-1.
IL-6 Interleukin 6 – Proinflammatory cytokine that stimulates bone resorption by osteoclasts.
IL-8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis.
IL-10: Interleukin 10 – An anti-inflammatory with homeostatic effects on the immune system. Produced by many cells like macrophages, b-cells and cytotoxic T-cells.
IL-13: Interleukin 13 – Anti-inflammatory releasing proteolytic enzymes to respond to allergic reactions involving the airways. Although, IL-13 also stimulates b-cells to release immunoglobulin E to cause the allergic reaction.
TNF-a Tissue Necrosis Factor Alpha – Proinflammatory cytokine and cell mediator for necrosis and apoptosis (cell death), stimulated by macrophages and monocytes.
Growth factors:
VEGF-a Vascular Endothelial Growth Factor-A – Initiates tumour angiogenesis, formation of new blood vessels and stimulates proliferation and migration of endothelial cells.
EGF: Epidermal Growth Factor – Stimulates cell proliferation, growth and differentiation from mesenchyme.
IGF-I: Insulin-like Growth Factor – Liver derived hormone, secreted when growth hormone is released. IGF-I is a cell protecting antioxidant and anti-inflammatory.
Immunoglobulins:
Total IgG: Total Immunoglobulin G – Antibody produced by B-cells that protects the body from bacterial, viral and fungal infections.
Secretory IgA: Secretory Immunoglobin A – Found in many body secretions including saliva, which protects the epithelium from antigens.
Transmembrane tyrosine receptors:
EGF/EGFR: Epidermal Growth Factor/Epidermal Growth Factor Receptor– Stimulates cell proliferation, growth and differentiation from mesenchyme. EGFR is where EGF binds.
Metalloproteinases:
MMP-2: Matrix Metalloproteinase -2/Gelatinase A’ – is a proteolytic enzyme also playing a role in vascular tissue regeneration, new blood vessels and invasion of tumour cells.
MMP-9 Matrix metalloproteinase 9 – Is a proteolytic enzyme linked to periodontal disease and cancer cell invasion.
Antigens:
CA125: Cancer Antigen -125 – Tumour marker found on the surface of ovarian cancer cells and associated with diagnosis of ovarian cancer.
bFGF: Basic fibroblast growth factor – Protein for tissue repair and regeneration.
TPS: Tissue Polypeptide Specific Antigen – Tumour biomarker for monitoring the proliferation of tumour cells.
Ki67- Tumour biomarker for monitoring the proliferation and growth of tumour cells.
Enzymes:
Heparanase –Binds to heparan sulphate that stimulates macrophages causing inflammation as well as growth and metastasis of tumours.
Adenosine deaminase – Made by cells like lymphocytes with homeostatic effects on the immune system.
Lactate dehydrogenase (LDH) –Speed up the conversion of pyruvate to lactate and vice versa. Cancer patients typically have high levels of LDH.
OGG1 (8-oxyguanine Glycosylase) – Removes useful genes from Damaged DNA.
Phospho-Src – Mediates cell adhesion proliferation growth and metastasis.
Peptides:
Endothelin-1 (ET-1) – Increases blood pressure in blood vessels via strong vasoconstrictor properties.
ZNF510: Zinc Finger Protein 510 – Protein coding gene for associated with gene expression and regulates transcription.
HNP-1: Human Neutrophil Peptide1 – Antimicrobial protein secreted from neutrophils.
Aldehyde:
Acetaldehyde production – Considered a carcinogen found in cigarettes, coffee and naturally in fruits, vegetables and plants. Acetaldehyde is also formed when alcohol dehydrogenase an enzyme created by the liver oxidises ethanol found in alcohol.
Hormone:
Cortisol – One of the steroid hormones produced by the adrenal glands. Cortisol is responsible for responding to stress by increasing blood pressure to supply the body with more energy and glucose to the brain. This hormone also suppresses other body systems like digestion so energy and nutrients can be available to manage stress.
Oxidative stress related molecules:
Carbonyls – compound with a single carbon atom double bound to an oxygen atom within a molecule, which allows cells to modify their functions with mutagenic and carcinogen properties e.g. formaldehyde
Antioxidant capacity – The measured ability of the antioxidant to manage free radicals in disease samples.
Total antioxidant status (TAS) – The testing of the antioxidant effects on oxidative stress.
Peroxidase – Enzymes within cells that breakdown harmful by-products of cell metabolism like hydrogen peroxide from into non-toxic hydrogen and water.
Glutathione S-transferase – Detoxification enzymes that speeds up the direct contact gene sharing of the antioxidant Glutathione (GSH) that prevents free radicals in cells.
Superoxide dismutase – Enzyme that accelerates chemical reactions in the body.
Uric acid – Waste product of the body, high levels can be a sign of disease.
NO: Nitric oxide – Colourless gas and a principle oxide on the nitrogen. High levels of NO can halt or kill tumour cells but may not prevent metastasis.
NO2: Nitrogen Dioxide – Bad smelling gas and Nitrogen oxide. Common air pollutant. Highly reactive gas, linked to lung cancer.
NO3: Nitrate – Water soluble compound used as a food preservative; vegetables are natural sources of nitrate for the body. Nitrates dilate blood vessels to lower blood pressure or react with amines with carcinogenic results.
8-OHdG: 8-hydroxy-2′-deoxyguanosine – Oxidised product of deoxyguanosine commonly detected in urine for assessment of oxidative stress. An inconclusive biomarker for carcinogenesis.
Genetic and Epigenetics:
C deletion on exon 4 within p53 gene codon 63 – Mutation of p53 gene codon 63. p53 gene codon 63 is a tumour suppressor, consequently there is proliferation or maturation of OSCC.
Genes expression:
MMP1 (Matrix Metalloproteinase 1/ Interstitial Collagenase/ Fibroblast Collagenase) – Proteolytic enzyme and protein coding gene for tissue mitosis embryonic development, and modification. MMP1 reported to support the metastatic process of cancer cells.
FN: Fibronectin 1 – Liver produced protein coding gene assisting wound healing and the clotting cascade. Research suggests increased numbers of FN1 genes in several cancers and propose FN1 is supportive of cancer cell proliferation.
FAPA: Fibroblast Activation Protein Alpha – Cell surface proteolytic enzyme of somatic cells surfaces (of cells that divide). Tissues remodelling properties. Clinical exploration suggests FAPA assists invasive processes of epithelial cancer cells.
SRPINH2 (Common research abbreviation = SERPINE2): (Serpin Peptidase Inhibitor, Clade E, Member 2) – Protein coding gene for cell neurogenesis, heparin-binding and differentiation. SERPINE2 is an inhibitor of serine proteases involved in the clotting and wound healing: Plasmin Thrombin, Trypsin and Urokinase.
IL8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis. Linked to cancer cell motility and progression.
IgLA: Intracellular Growth Locus Protein A – Mediator of intracellular macrophage processes and human cell processes by release of regulating substances. IgLA potentially assists cancer cell metastasis research links this to bone involvement.
ABCG1: ATP Binding Cassette Subfamily G Member 1 – Protein coding gene for homeostasis of lipids in the body. Associated with tumour immunity.
COL5A1: Collagen Type V Alpha 1 Chain – Protein coding gene for the production of pro-α1(V) an element in collagen V. High levels found in tongue squamous cell carcinoma amongst other cancers also linked to Ehlers Danlos Syndrome.
HBB: Haemoglobin Subunit Beta – Protein coding gene for Beta-globin (b-globin) the oxygen carrying, red pigment protein of haemoglobin in red blood cells. Linked to Thalassaemia, Thyroid Cancer and Sickle Cell Disease. It has been asserted in clinical investigations that adequate levels of HBB inhibits abnormal cell growth.
DNA methylation:
ECAD: Epithelial Cadherin (CAM 120/80/ E-Cadherin /Uvomorulin) – Protein for coding calcium depend protein for the regulation of cell adhesion giving tissues their structure, epithelial cell proliferation and cell motility. Associated with tumour suppression, specifically invasion and metastasis.
MGMT: O-6-Methylguanine-DNA Methyltransferase – Protein coding gene for DNA regeneration. Oncology research has proposed MGMT silencing in cancer patients.
DAPK: Death Associated Protein Kinase 1 (DAPK1) – Tumour suppressor that regulates cell mediation and cell death. Oncology research associates DAPK1 dysfunction with the development of cancer cells.
RARb: Retinoic Acid Receptor Beta (RAR-beta/ NR1B2 Nuclear Receptor Subfamily 1, Group B, Member 2) – Protein coding gene for tumour suppression via use of retinoic acid that assists cell mediation of differentiation, morphogenesis and growth.
p16: Cyclin-Dependent Kinase Inhibitor 2a (CDKN2A) – Protein for tumour suppression, specifically by obstruction of the cell cycle following the initial G1 (growth phase). p16 inhibits cyclin-dependent kinases (CDK) with p16 deletion observed in numerous cancers.
p15: Cyclin-Dependent Kinase 4 Inhibitor B (CDKN2B /p15INK4b/ MTS2/INK4b) – Tumour suppressor via initiation of TGF-β- cell inhibition pathways, capable of inhibiting specific tumour cells.
TMEFF2: Tomoregulin-2 (TENB2) – Protein coding gene for Tomoregulin Transmembrane Proteins, with the ability to operate as both a tumour suppressor and a cancer cell causing gene.
TMEFF3: No further information found.
HIN-1: High in Normal 1 – Inconclusive protein tumour suppressor of cancer cell invasion and growth, adhering to epithelial cells. Research proposes that HIN-1 can arrest the activity of breast cancer cells.
WIF-1: WNT Inhibitory Factor 1 – Protein coding gene that adheres to fat with tumour suppressing properties.
FHIT: Fragile Histidine Triad Diadenosine Triphosphatase – Protein coding gene linked to Breast Cancer and Renal Cancer, with tumour suppression and DNA protection functions.
SPARC: Secreted Protein Acidic and Rich in Cysteine (Osteonectin) – Non-collagenous protein detected in bone. SPARC regulates cell growth and binds to numerous proteins and minerals like calcium and albumin. SPARC aids cancer progression in some cancers (e.g. melanomas) and acts as a tumour suppressor in others (e.g. neuroblastomas).
APC: Adenomatous Polyposis Coli – Tumour suppressing protein preventing proliferation and growth.
ADCYAP1: Adenylate Cyclase Activating Polypeptide 1 – Protein stimulating genome transcriptional activities. Linked to the onset of cervical cancer.
AGTR1: Angiotensin II Receptor Type 1 – Makes the protein that regulates solutes and fluids as part of the Renin-Angiotensin System. Research suggests AGTR1 assists many stages of carcinogenesis including: proliferation, angiogenesis, invasion and metastasis.
BMP3: Bone Morphogenetic Protein 3 – Tumour suppressing protein and coding gene for the mediation of transcription factors.
CEBPA: CCAAT/enhancer-binding protein alpha – Transcription factor that contributes to the differentiation of granulocytes and cell cycles. Inconclusive findings regarding its potential function as an oncogene.
EPHA5: Ephrin Type-A Receptor 5 – Protein that plays a role in ATP binding, nucleotide binding and neurogenesis (formation of new neurons). Clinically associated with tumour invasion, growth and migration.
ERBB4: Erb-B2 Receptor Tyrosine Kinase 4 – A gene, which with factors that initiate cell mitosis and differentiation. Mutations of ERBB4 linked to the development of numerous cancers e.g. lung adenocarcinoma and melanoma.
ESR1: Estrogen Receptor 1 – Gene for coding of oestrogen receptors for tissue growth (e.g. bone), sexual development and reproduction. Mutations of ESR1 clinically associated with Osteoporosis, Endometrial Cancer (cancer of the uterus), Breast Cancer and Oestrogen Resistance.
ETV1: ETS-translocation variant 1 – Transcription factor for the development of dopamine neurons, motor neurons and sensory or proprioceptive neurons. Research links ETV1 to several stages of carcinogenesis: differentiation, proliferation angiogenesis, growth and metastasis.
EYA4: EYA Transcriptional Coactivator and Phosphatase 4 – Protein coding gene for stimulation of transcriptional processes for development of the eyes. It has also been clinically proposed that EYA4 is also an oncogene regulating genome repair, innate immunity following viral and cell damage and cell apoptosis.
FGF3: Fibroblast Growth Factor 3 – Protein coding gene contributing to various healthy cell and tumour cell cycle activities such as: growth, repair development and morphogenesis. Linked to cancers like oesophageal cancer and hepatocellular cancer to name few.
FGF8: Fibroblast growth factor 8 – Protein coding gene for the production of fibroblasts cells that make collagen. Associated with increase in growth and angiogenesis of tumours.
FLT1: Fms Related Receptor Tyrosine Kinase 1 – Protein coding gene for making new endothelial cells and new blood vessels. Linked to many head and neck carcinomas and blood carcinomas.
GABRB3: Gamma-Aminobutyric Acid Type A Receptor Subunit Beta 3 – Protein encoding gene for the receptor the inhibitory neurotransmitter gamma-aminobutyric acid. Research proposes down regulation of GABRB3 to be linked to late stages of cancer and cancer cell motility to lymph nodes.
GALR1: Galanin Receptor 1 (Galanin Receptor Type 1 / GALNR1 / GAL1-R / GALR-1 / GALNR / GALR1) – Proteins utilised by neurons for communication, located in the CNS and autonomic nervous system. GALR1 also functions as a tumour suppressor, halting tumour activity like cancer cell proliferation.
GAS7: Growth Arrest Specific 7 – Protein coding gene for the development of specialised neurons and mature Purkinje Cells of the Cerebellar Cortex that governs movement of the body. Role in tumour suppression associated with Breast Cancer.
HLF: Hepatic Leukaemia Factor (HLF Transcription Factor/ PAR BZIP Family Member) – Gene coding to initiate transcription associated with leukaemia.
IHH: Indian Hedgehog Signalling Molecule – Protein coding gene for growth and differentiation of bone. Tumour suppressing abilities in lung cancer explored as well hereditary developmental conditions like Acrocapitofemoral Dysplasia, which causes dysplasia of the skeleton and results in a narrow chest and short limbs.
IL11: Interleukin 11 – Protein coding gene for cytokines stimulating humoral system production of B-cells (antibodies) mediated by T-cells, blood cell proliferation and Megakaryocytes to increase platelet levels. Reported to support the proliferation and metastasis of cancer cells. Conclusive presence in various cancers but role inconclusive.
INSR: Insulin Receptor – Bound insulin or other molecules turns insulin signalling pathways on to regulate blood glucose levels and assembling of other useful molecules like lipids, carbohydrates and proteins. Reported as detected in all cancers.
IRAK3: Interleukin 1 Receptor Associated Kinase 3 – Located in monocytes and macrophages triggering the inflammatory response. Detected in many cancers. Repressed gene transcription (methylation) of IRAK3 has been reported to be an indicator of poor prognosis or progression of cancer.
KDR: Kinase Insert Domain Receptor – (Vascular Endothelial Growth Factor Receptor / VEGFR2) – Manages the construction and vascularity of new blood vessels. KDR also supports cell processes for endothelium and actin a protein of the cytoskeleton. Dysfunction of KDR associated with several cancers like Cutaneous Melanoma.
NOTCH3: Notch Receptor 3 – Transcriptional gene responsible for cell proliferation, differentiation, cell death and cell pathways for neural development. Reported as a supporting gene for ovarian cancer progression and related cancer cell cycle processes.
NTRK3: Neurotrophic Receptor Tyrosine Kinase 3 – Protein coding gene for motile growth cones that allow developing axons to synapse. NTRK3 linked to differentiation of cells and cancers like Fibrosarcoma.
PKD2: Gene coding for Polycystin-2 a protein regulated by Polycystin-1. Polycystin-2 regulates cell motility and proliferation and transport of molecules within the kidneys. PKD2 has been associated with Renal Cancer, Prostrate Cancer and Breast Cancer, Colorectal (bowel) Cancer and Lung Cancer.
PTCH2: Patched 2 – Tumour suppressor gene with protein binding ability. Reported in connection with cancer such as Basal Cell Carcinoma and development defects like Congenital Macrostomia (facial cleft).
PXN: Paxillin – Gene for coding of the protein that allows actin adhesion to extracellular matrix. Reported as a contributing to Papilloma.
RASGRF1: Ras Protein Specific Guanine Nucleotide Releasing Factor 1 – Protein coding gene for Guanine Nucleotide Exchange Factor (GEF) that activates other proteins for the production of RNA during transcription of genes. Reported as a promoter of cancer cell growth and motility.
TFPI2: Tissue Factor Pathway Inhibitor 2 – Tumour suppressor and inhibitor of proteins involved in the clotting cascade. Linked to epithelial cancer Choriocarcinoma and Fibrosarcoma.
TMEFF1: Transmembrane Protein with EGF Like and Two Follistatin Like Domains 1 (Tomoregulin-1) – Inconclusive tumour suppressor for Brain Cancers.
TNFSF10: TNF Superfamily Member 10 (Tumour Necrosis Factor Ligand Superfamily, Member 10) – Protein encoding gene for cell mediators of Tumour Necrosis Factors. Tumour Necrosis Factors kill tumour cells without affecting healthy cells. Clinically reported in connection with Ameloblastoma (tumours of the jaws caused by enamel forming cells, which can cause facial disfigurement) and Thoracic Cancer.
TWIST1: Twist Family BHLH Transcription Factor 1 – Protein coding gene for proteins converting DNA to RNA during embryonic development. TWIST1 is associated with motility and invasion of tumour cells.
WNT2: Wnt Family Member 2 – Protein coding gene molecules with signalling ability via cell surface receptors. Linked to tumour development and progression in various cancers including oesophageal, lung and colon cancer.
WT1: Wilms Tumour 1 (WT1 Transcription Factor) – Protein coding gene and tumour suppressor, also clinically reported as a contributory variable to rare kidney cancer Wilms Tumour 1 or Nephroblastoma.
LOH (Loss of heterozygosity), loci (markers of where changes on chromosomes have taken place/ microsatellites): Tracks loss of one set of genes by chromosomal changes at specific sites, which are marked.
D3S656: Polymorphic marker (detecting the numerous forms that chromosomes can take)
D3S1293: Polymorphic marker for tumour suppression in head and neck cancer.
D3S1234: Polymorphic marker linked to pulmonary adenocarcinoma and oral squamous cell carcinoma.
D3S1217: Polymorphic marker associated with breast cancer.
D3S126: Polymorphic marker
D8S254: Polymorphic marker, inconclusively reported to be close to tumour suppressor genes.
D8S261: Polymorphic marker, linked to schizophrenia predispositions, Renal Carcinomas, Prostate Cancer and Breast Cancer.
LPL-tet: Polymorphic marker, tumour and invasion in HNSC Head and Neck Squamous Cancer.
D8S298: Polymorphic marker, reported with the progression of Hepatocellular Carcinoma.
D8S283: Polymorphic marker, associated with Colon Cancer.
D9S104: Polymorphic marker for tumour suppression in Oral Cancer.
D9S156: Polymorphic marker clinically related to Oral Squamous Cell Carcinoma.
D9S168: Polymorphic marker for progression of Renal Cancer.
D9S171: Polymorphic marker linked to Pulmonary Adenocarcinoma and Oral Squamous Cell Carcinoma.
D9S199: Polymorphic marker, reported with the progression of Hepatocellular Carcinoma.
D17S513: Polymorphic marker, linked to Colon Cancer and Breast Cancer.
TP53: Tumour Protein 53 – Polymorphic marker, inconclusive tumour suppressor.
D17S799: Polymorphic marker, clinically related to Oral Squamous Cell Carcinoma.
CHRNB1: Cholinergic Receptor Nicotinic Beta 1 Subunit – Protein coding gene that aids the production of acetylcholine receptors for neural synapsing and activity across plasma membranes. Identified in numerous cancers including head and neck cancers.
D17S122: Polymorphic marker, reported in Breast Cancer research.
D18S46: Polymorphic marker for tumour suppression, Ovarian Cancer, Anal Carcinoma and Oral Squamous Cell Carcinoma.
D18S363: Polymorphic marker linked to nerve tissues cancer (Neuroblastoma), and colon cancer.
D18S35: Polymorphic marker associated with metastasis in Prostate Cancer and Colon Cancer.
D18S39: Polymorphic marker for tumour suppression in Head and Neck Squamous Cell Carcinoma.
e D18S41: Polymorphic marker associated with Bipolar Disorder, Male Breast Cancer and Prostate Cancer.
DUSP1 mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Dual Specificity Phosphatase 1.
OAZ1 mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Ornithine Decarboxylase Antizyme 1.
S100P mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making S100 Calcium Binding Protein P.
SAT1 mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Spermidine/Spermine N1-acetyltransferase 1.
Other proteins:
Total protein – Test that measures the quantity of protein in blood serum. High levels associated with cancer or low fluid intake.
Albumin – Liver made protein regulating osmotic pressure within cells. Low levels reported in cancer patients.
Cyclin D1 – Protein produced by gene CCDN1 that regulates the cell cycle. Also, a research suggested oncogene (cancer casing gene).
Maspin – Tumour suppressor gene, inhibiting invasion and metastasis.
Serotransferrin – Iron binding transport glycoprotein found in blood plasma.
Hemopexin (HX /HPX / beta-1B-glycoprotein) – Glycoprotein that collects free haem in the bloodstream, to prevent oxidative damage caused by a decrease in iron levels.
a-1B: Alpha 1 B adrenergic receptor – Binds with amines adrenaline or noradrenaline to cause cellular changes such as non-malignant mutations or transformation to an oncogene (cancer causing gene).
Glycoprotein – Proteins with carbohydrates attached that are found on the surface of a cell membrane. Glycoproteins identify and regulate the transport of substances in and out of the cell. Dysfunction would allow antigens both in and out of cells.
a1-Antitrypsin (α1-AT / AAT) – A protein made in the liver that protects the lungs by inhibiting the production of proteolytic enzymes. Elevated levels reported in clinical tests of numerous cancers including lung adenocarcinoma, prostate cancer and OSCC.
Haptoglobin b Chain (HP) – Binds haemoglobin to plasma to allow proteolytic breakdown, whilst simultaneously prevent kidney mutations and retaining free iron molecules. Reported as present in the early stages of many different cancers including lung cancer.
Fibrinogen b (Fibrinogen Beta Chain/ FGB) – A gene that assists with the production of fibrinogen a protein for blood coagulation. Reported as a biomarker in Oral Cancer diagnostics and suggested to support prognosis.
Complement C3 (Complement Component 3 / C3) – Humoral (immune system) protein that makes direct contact to kill viruses and bacteria. However, it has been reported that C3 supports the cancer cell cycle: angiogenesis (construction of new blood vessels) and cancer cell progression.
Transthyretin (TTR) –A transport protein made in the liver that carries the thyroid hormone T4 (thyroxine) and binds retinol binding protein. TTR found in CSF (cerebrospinal fluid) and blood serum. Research proposes that TTR initiates the growth of tumours including cancerous types.
Inorganic Compounds:
Sodium (Na) – Essential electrolyte for homeostasis of: blood pressure, neurotransmission, muscle function and maintenance of osmotic pressure within cells. Low sodium levels observed in cancer diagnostic testing.
Potassium (K) – Essential electrolyte for homeostasis of: the cardiovascular system, bone density, nerve and muscle function as well as maintenance of osmotic pressure within cells. Increased levels of K inside cancer cells suppresses the activity of the immune system.
Calcium – Essential electrolyte for: formation of bone, blood coagulation, regulation of the cardiovascular system, nerve transmission and hormone release. High levels of calcium in blood or hypercalcaemia can be an indication of cancer as cancer cells can invade bone and cause this connective tissue to release calcium into the bloodstream.
Radhika et al (2016)
DUSP1 – Protein coding gene initiated by response to damage to fibroblasts e.g. heat, oxidative stress reduces cell proliferation.
miR-31: MicroRNA-31 – Tumour suppressor inhibiting some stages of metastasis e.g. invasion and colonisation.
M2BP: (Mac-2 Binding Protein) – Cell adhesion protein that helps to regulate the immune system. Increased level of the protein associated with some cancers e.g. lung and prostate cancers.
MRP14 (Migration Inhibitory Factor-Related Protein 14) – S100 Calcium binding protein identified in stimulated neutrophils during inflammation. Inhibits macrophage migration.
CD59 – A gene that is coded for a glycoprotein that inhibits membrane attack complex, whereby cells self-destruct. Its overexpression reported with tumour progression and motility of tumour cells.
Profilin1 (PFN1) – Uses ATP (adenosine triphosphate) cellular energy to change the composition of actin.
Catalase – Antioxidant enzyme that protects cells from free radicals and breaks down hydrogen peroxide to non-toxic water and hydrogen molecules. Also reported to protect cancer cells for oxidative damage.
Khurshid et al (2018)
Proteomics:
CD59 – A gene that is coded for a glycoprotein that inhibits membrane attack complex, whereby cells self-destruct. Its overexpression reported with tumour progression and motility of tumour cells.
Profilin – Protein regulator of cellular actin regeneration and repair through direct binding with actin. The increase of Profilin levels is reported to be a tumour suppressor, whilst low levels are thought to allow cancer cell invasion of tissues.
MRP14 (Migration Inhibitory Factor-Related Protein 14) – S100 Calcium binding protein identified in stimulated neutrophils during inflammation. Inhibits macrophage migration.
M2BP (Mac-2 Binding Protein) – Cell adhesion protein that helps to regulate the immune system. Increased level of the protein associated with some cancers e.g. lung and prostate cancers.
CD44 – Glycoprotein on the surface of cells involved in numerous cell processes including cell mediation. Also, a cell lymphocyte receiving receptor. Research proposes increased expression in early cancer cells.
IgA (Immunoglobulin A) – Protein antibody found in saliva, tears and moist mucous membranes responsible for immune response to antigens, including allergic reactions. Low levels of IgA associated with cancer development.
Insulin growth factor (IGF) – Protein and hormone that initiates growth and helps regulate blood glucose. Tumour suppressing capabilities for all stages of carcinogenesis.
Inhibitors of Apoptosis:
SCC-Ag (Squamous Cell Carcinoma Antigen) – Biomarker from fragments of squamous cell carcinoma linked antigen. Clinically applied to diagnostics for cervical and lung cancers.
Carcinoembryonic Antigen (CEA) – Protein expressed in healthy adults at low levels with increases found clinically in adults with benign and malignant tumours.
Carcinoantigen (CA19-9) – Tumour antigen, clinically assessed in blood to diagnose pancreatic cancer.
CA128 – Protein tumour marker.
CA125 (Cancer Antigen 125) – Derived from mucin glycoproteins, tumour marker clinically used for diagnostic assessment of ovarian cancer.
Reactive nitrogen species (RNS) – Group of antimicrobials made from superoxide and nitric oxide. These cause oxidative stress in their metabolism, which is a contributing variable of oral cancer.
DNA damage marker:
8-OHdG: 8-hydroxy-2′-deoxyguanosine – Oxidised product of deoxyguanosine commonly detected in urine for assessment of oxidative stress. An inconclusive biomarker for carcinogenesis.
intermediate filament protein:
Cyfra 21-1 – Protein fragment a soluble cytokeratin 19/CK19 and epithelial marker.
Lactate dehydrogenase – (LDH) –Speed up the conversion of pyruvate to lactate and vice versa. Cancer patients typically have high levels of LDH.
Immunoglobulin and metalloproteinase:
MMP-2 (Matrix Metalloproteinase2 / Gelatinase A) – Proteolytic enzyme, linked cancer cell tissue invasion and metastasis.
MMP-11 (Matrix Metalloproteinase 11/ Stromelysin-3) – Proteolytic enzyme for protein coding, specifically the breakdown of tissues during remodelling.
Genomics:
P53 gene codon 63 – Tumour suppressor.
Transcriptomics:
mRNA IL-8: Interleukin-8 (IL-8) mRNA –Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making Interleukin-8.
mRNA IL-1-b: Interleukin 1 Beta mRNA – Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making Interleukin 1 Beta.
mRNA S100P: S100 Calcium Binding Protein P mRNA – Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making S100 Calcium Binding Protein P.
mRNA H3F3A: H3 histone family 3A mRNA – Messenger ribonucleic acid from cell nucleus DNA and carries genetic material for making H3 histone family 3A.
mRNA OAZ1: Ornithine Decarboxylase Antizyme 1 mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Ornithine Decarboxylase Antizyme 1.
mRNA DUSP1: Dual Specificity Phosphatase 1 mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Dual Specificity Phosphatase 1.
mRNA SAT: Spermidine/Spermine N1-acetyltransferase mRNA – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Spermidine/Spermine N1-acetyltransferase.
Metabolomics:
Caverdine – Found on soya beans is a compound and liquid with a bad odour, which has protective functions in phosphate deficiency and acid-base balance of pH in the body. Research is inconclusive as some suggest that Caverdine promotes tumour growth, whilst others state that Caverdine can halt progression of cancer cells.
Alanine – Amino acid for protein synthesis e.g. muscle, humoral (immune) system and nervous system. Alanine also regulates blood glucose and metabolises vitamin B6 (Pyridoxine) and Tryptophan. Suggested biomarker inferring cancer cell metabolism.
Serine – Amino acid for protein synthesis e.g. of muscle tissues, enzymes. Research has suggested the supportive role of Serine in cancer cell proliferation.
Glutamine – Amino acid for protein synthesis and the humoral (immune) system. Inconclusive effect on cancer cells some state inhibition of cancer cell growth, whilst others postulate that Glutamine initiates cancer cell growth.
Piperidine – A liquid compound that is colourless, with a bad odour. Synthesises other compounds like enamines from ketones. Tumour suppressor for inhibiting cancer cell growth.
Taurine – Taurine is a non-proteinogenic (not protein placed during gene translation) amino acid found in the heart, brain, retina, organs and muscles. It also inhibits cancer cell proliferation, initiates cell apoptosis and assists nerve cell growth.
Choline – Important for neurotransmission, cell growth and metabolism. Deficiency linked to cancer development.
Pyrroline hydroxycarboxylic acid – Metabolite.
Beta-alanine – A beta amino acid, supporting the production of Carnosine, which reduces protein damage in tissues e.g. the brain, heart and muscles throughout the body. Research proposes suppression of cancer cell proliferation and migration and increased effectiveness of cancer drug Doxorubicin.
Alpha-aminobutyric acid – A non-proteinogenic (not protein placed during gene translation) amino acid, responsible for cell metabolism. Research has also described its role in cancer diagnostics as improving identification of cancer cell binding sites for antibodies.
Betaine – A compound found in beetroot, some seafood and wheat that regulates water balance within cells, metabolises choline and assists cell metabolism transcription via DNA methylation.
Tyrosine – Amino acid for protein synthesis and manufacturing chemical for brain functioning. Research suggests that Tyrosine Kinases can also activate and inhibit cell functions and can support cell mutations leading to cancer development.
Leucine – Amino acid supplying energy to muscles, supporting muscle growth repair of bones and skin. Research proposes low levels prevent cancer cell proliferation and increase cancer cell death.
Isoleucine – Required for protein synthesis, immunity, helps regulate blood sugar levels and muscle recovery. Low levels linked to reduced number of cancer cells.
Histidine – Homeostatic properties for acid-base balance body maintained around pH 7 for optimum functioning. Supports the efficacy of cancer drugs like methotrexate.
Tryptophan- Homeostatic properties for nitrogen and makes niacin required for the production of the neurotransmitter serotonin. Research suggests that tumour cells ingest Tryptophan to avoid cell by the immune system. Linked to progressive stages of cancer.
Glutamic acid- Amino acid for protein synthesis and neurotransmitter excitation. Research suggests that Glutamic acid improves the conjugation (direct contact gene sharing) of cancer drugs.
Threonine – Amino acid obtained from a diet including beans, dairy and meat that required protein synthesis. Inconclusive data on effects as a tumour suppressor or promoter of cancer cell growth.
Carnitine – Group of compounds that regulate energy and lipid metabolism. Tumour suppressing ability.
Pipercolic acid – Product of Lysine metabolism that modulates gene expression, mitochondrial activity and stages of cell cycles such as proliferation and apoptosis.
Lactic acid – waste product of anaerobic respiration in the absence of oxygen. High levels in the body can be fatal as blood flow is lowered. Commonly produced by cancer cells.
Phenylalanine – Refers to the group of amino acids found in protein like dairy products, fish, meat and eggs. Used in the body to manufacture proteins and protein required molecules.
Valine – Amino acid for protein production and increases the release of growth hormone, energy to cells and muscle recovery and rejuvenation.
Streptococcus mitis – Gram negative, facultative anaerobic bacteria. Can colonise hard tissues like enamel and mucosa.
P. Gingivalis – Gram negative, proteolytic, anaerobic bacteria. Involved in many conditions including periodontal disease, invades gingival epithelium.
P. melaninogenica – Gram negative, anaerobic bacteria that is ‘haemolytic’ kills red blood cells and creates biofilm to spread.
Santosh et al (2016)
L-phenylalanine – A Phenylalanine amino acid found in protein like dairy products, fish, meat and eggs. Used in the body to manufacture proteins and protein required molecules.
Sphinganine – A sphingolipid or bioactive messenger regulating cell cycles from cell differentiation to cell death.
Phytosphingosine – A fat or lipid found in the outer layer of skin or stratum corneum. Known to induce cancer cell death.
S-carboxymethyl-L-cysteine – Drug used to lower the viscosity of sputum for patient with respiratory difficulties. A mucolytic. Also naturally occurring in vegetables such as onion or garlic.
Proteomic:
IL-1-b: Interleukin 1 Beta – Protein mediator made by many cells including white blood cells is a proinflammatory cytokine for monocytes.
IL-8: Interleukin 8 – Chemokine or small cytokine that mediates white blood cell migration for repair. IL8 activates neutrophils for phagocytosis.
M2BP
mRNA:
IL-8 – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Interleukin 8.
S100P – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making S100 Calcium Binding Protein P.
SAT1 – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making Spermidine/Spermine N1-acetyltransferase 1.
IL-1b – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making interleukin 1 Beta.
IIL-1b – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making interleukin 1 Beta.
IL-1b – Messenger nucleic acid from cell nucleus DNA and carries genetic material for making interleukin 1B
The 10 Papers reviewed because of course you want more
1.Cristaldi, M., Mauceri, R., Di Fede, O., Giuliana, G., Campisi, G. and Panzarella, V., 2019. Salivary Biomarkers for Oral Squamous Cell Carcinoma Diagnosis and Follow-Up: Current Status and Perspectives. Frontiers in Physiology, [online] 10, pp.1-12. Available at: <https://www.frontiersin.org/articles/10.3389/fphys.2019.01476/full> [Accessed 3 May 2020].
●2.Aro, K., Kaczor-Urbanowicz, K. and Carreras-Presas, C., 2019. Salivaomics in oral cancer. Current Opinion in Otolaryngology & Head and Neck Surgery, [online] 27(2), pp.91-97. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/30507690> [Accessed 3 May 2020].
●3.Gualtero, D. and Suarez Castillo, A., 2016. Biomarkers in saliva for the detection of oral squamous cell carcinoma and their potential use for early diagnosis: a systematic review. Acta Odontologica Scandinavica, [online] 74(3), pp.170-177. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/26577643> [Accessed 3 May 2020].
●4.Saxena, S., Sankhla, B., Sundaragiri, K. and Bhargava, A., 2017. A Review of Salivary Biomarker: A Tool for Early Oral Cancer Diagnosis. Advanced Biomedical Research, [online] 6(1), pp.90-96. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/28828341> [Accessed 3 May 2020].
●5.Chattopadhyay, I. and Panda, M., 2019. Recent trends of saliva omics biomarkers for the diagnosis and treatment of oral cancer. Journal of Oral Biosciences, [online] 61(2), pp.84-94. Available at: <https://www.sciencedirect.com/science/article/abs/pii/S1349007918301609> [Accessed 3 May 2020].
●6.Hema Shree, K., Ramani, P., Sherlin, H., Sukumaran, G., Jeyaraj, G., Don, K., Santhanam, A., Ramasubramanian, A. and Sundar, R., 2019. Saliva as a Diagnostic Tool in Oral Squamous Cell Carcinoma – a Systematic Review with Meta Analysis. Pathology & Oncology Research, [online] 25(2), pp.447-453. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/30712193> [Accessed 3 May 2020].
●7.Stuani, V., Rubira, C., Sant’Ana, A. and Santos, P., 2016. Salivary biomarkers as tools for oral squamous cell carcinoma diagnosis: A systematic review. Head & Neck, [online] 39(4), pp.797-811. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/27898189> [Accessed 3 May 2020].
●9.Khurshid, Z., Zafar, M., Khan, R., Najeeb, S., Slowey, P. and Rehman, I., 2018. Role of Salivary Biomarkers in Oral Cancer Detection. Advances in Clinical Chemistry, [online] 10(1476), pp.23-70. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/30144841> [Accessed 3 May 2020].
●10.Santosh, A., Jones, T. and Harvey, J., 2016. A review on oral cancer biomarkers: Understanding the past and learning from the present. Journal of Cancer Research and Therapeutics, [online] 12(2), pp.486-492. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/27461598> [Accessed 3 May 2020].
Helen glided a finger across the pages of her local paper, with a biscuit in her other hand. She took a bite and pondered whether she would actually go through with it this time. Libby her cat stroked her anxiety away by brushing her right leg and nuzzling into her Mum. Helen indecisively sighed then stuffed the rest of the biscuit into her mouth. Scooping Libby up to cradle her like an infant, Helen read then quietly recited the same words:
First ever Beginners’ Dance Class with Anyas Samuels. Thursday the 18th of April 2021
Helen was a ball of energy on the day, despite all her preparation in the weeks leading up to the event. She couldn’t believe Anyas Samuels, thee Anyas Samuels would be front and centre before her inhaling and exhaling the same air. She didn’t feel worthy, although her boyfriend Imran told her that she was being rather dramatic. Imran nodded nonchalantly and stated matter-of-factly,
‘Didn’t she lose to Renelle what’s her name on that dance programme? What’s it called again…Quick Shoes?’
Imran tutted with temporary frustration at his poor recall of a television show he was forced to endure. Twice a week. Simply for the love of the slightly obsessed Helen. He momentarily opened his mouth to ask his hun a question but decided otherwise. Imran couldn’t help but wonder why quick-learning Helen would doubt her ability to dance, whilst spending so many hours imitating dance choreography on the television.
Despite, her ease and fluidity at home Helen would always shy away from any overzealous actions on the dance floor or any other floor. Not even her favourite songs could muster a move in social settings. Not family functions, work parties or even at the multi-functional restaurant and clubs creeping into the area.
Imran decided to tag along to the class for moral support. He figured he should lend some moral support to encourage Helen’s breakthrough. Imran had acquired a sleep debt whilst he waited with Quick Shoes fanatics to buy his love tickets to the coveted dance class of the season. He hoped to distract Helen from her typical birthday wallow about ageing and what to her scrupulous eyes only, were clear signs for cosmetic surgery…
On the eighth floor the elevator doors sprung open with new vigour, Omar hurried out to stretch his legs and inhale some fresh air. As he looked around it became apparent that this kingdom was distinctively different.
Then he realized why; the tall and sickly thin green trees were blades of grass and the unattended sporadic pools were merely puddles despite their frightening depth. He tested this with a pebble, which was probably grit from the soil. The glaring size contrast wasn’t the only cause for concern, in this new world there was more sheep but on this land the sheep did not bleat. They spoke and stood upright just like him on their hind legs, they cycled, wore clothes, ate wraps the vegetable kind of course and even took lambs with rucksacks to the school bus. It wasn’t just the concept of lambs going to school that caught Omar’s eye, he marginally avoided becoming a pancake five times in succession to observe giants living alongside the sheep. The Prince could see how the folk tales of Jicotea elders might have been real encounters after all and he suspected that they probably came from this land. A big town sign referred to kingdom as ShRATI with a sheep symbol. Omar looked at me and muttered,
‘Whatever they feed the sheep here remind me to ban it when we get back to Jicotea.’
The bzzzzz!!! of a monstrous fly startled the Prince. He ran with me struggling to hold onto the cloth of the robe pocket for dear life, as it untied and swung with his every stride. The fly’s legs smacked in the likeness of a noisy eater with each movement, large spheres scanned the cobbles and shrubs in search of Omar who lay mechanically rigid. I could hear his short sharp inhales, the sounds that told me the Prince was trying to be as still as he could to avoid the prospect, which terrified him most. He wouldn’t have to wait for long to find out, less than a minute later the fly moved on and Omar anxiously rose from the ground, sweeping the area to ensure no other predators had him in their sights. The coast was…red. ShRATI was remarkably red and his royal highness joked that the town probably resembled a tomato from space: rooftops, fences, entire buildings (save for windows), a wave of ultisol trucks laying new soil for front gardens, red water pulsed from the fountains and the giants and sheep all attempted to outdo each other in their own uniforms of the same colour. As the Prince’s eyes became used to the view he concluded that the one colour town was rather bland until he spotted something…someone quite unique. A short distance away hunched the distressed Mook in blue jeans and a deep green shirt; his attire also gained much disapproving attention from passers-by. This giant was taller and slimmer than his peers that were quite rounded and they made it clear that they did not like this not one bit as they chanted,
‘Mook more like meek, he’s incredibly weak.’ It was painful for Omar to watch them throw a fly swarmed bin over the giant’s head and the action brought with it ten times the sympathy for the Prince to realise that he was far too small to assist Mook. The young ostracised giant struggled under the weight of removing the putrid bin but time did not pause to observe Mook as he wiggled and pulled. Soon the bright shades of the skyline were muted then no more. Mook stopped fighting the bin and flopped forward with exhaustion, the motion was quick and the lithe giant felt his torso upwards pop!!! Straight out. Lying back on the grass to catch his breath, Mook’s eyes adjusted to the darkness and the tiny specks of enchantment that inspired new ideas. Feeling more at peace he stole a casual glimpse of his pocket watch and muttered to himself in a pitch that wasn’t his own, Omar laughed seeing himself in the giant. I used my tail to cover the Prince’s mouth like humans do to unequivocally silence each other but the quick rise and suspicious scan informed us that Mook certainly heard the Prince, though he could not see him. Mook’s eyes flashed with terror as he rechecked his watch and took off running through the town; he momentarily transitioned into a moving colourless outline as he frantically, thundered through the town. I quickly turned to the Prince to bring this transformation to his attention but taking his own precious time to turn was just too long and he missed Mook’s new disappearing act. The Prince nonchalantly shrugged and suggested,
‘Maybe he has curfew’. I poked Omar with my tail and tried to catch up with the giant. I figured the longer we were amazed with every single event that took place, the greater the length of time that we would spend stuck in ShRATI and they did not make lamb stew. What?!! I was forced to look at sheep the entire day.
Arriving at Mook’s home we were pleasantly surprised to see that there were no cobwebs or scattered dishes and other unknown debris littered around. I guess those tales of giants, as messy beasts might have been just that. In fact despite showing up a considerable amount of time after Mook we were still able to witness his awkward telling off. He was indeed banished to his room for missing curfew and we’ll whisper the next reason…smelling badly.
Mook cleaned up and proceeded to sit glumly at his workspace. I suggested that we give the poor guy some alone time to get over his upset but Omar’s frown and gritted teeth told me that I should hop into his pocket to watch the boo hoo scene. I breathed a HUGE sigh of relief as Mook’s eyes lit up; he wiped his face and whipped out his sketchbook. Let’s briefly discuss the dirty handkerchief he unknowingly threw near the Prince…don’t worry we’ll skip a description of what was on it. Happily dancing to a rhythm only he could hear, Mook mixed colours and used various material to make the different fashion pieces from the sketches of his book. It was incredibly late when he was done and Omar was half asleep I had to nudge him awake to show him what the young giant had achieved. Mook put the piece on and made admiring comments towards himself in the mirror, clearly feeling rather suave. This made Omar completely forget where we were and loudly (just like his father) burst out laughing, instantly giving our location away. Despite, being so tall in general and a giant too Mook quickly turned to spot the Prince and I quickly retook my place in his robe pocket. Drawing closer to the window ledge with annoyance then amazement the giant leaned down to put us on eye level. You might want to cover your ears, as this was when he screamed,
I had a romantic dream (not a blue movie) just a cute girl meets boy kind of party. I was the girl as sometimes my dreams can be unpredictable and the boy was actually attractive, witty and kind. The latter is very important to me, as a pretty face with an ugly personality transforms into a beast on my scale. I remember thinking okay let’s have this in real life then. As in where in the world do they make this guy?!! I want to meet him. Yes, I said this whilst still aware that it was just a dream. Sad! Yes you can laugh too.
Typically I don’t have dreams like this. I’m an ideas person in real life. I dream of travel, opportunities, new devices and the like but alas I have no welding credentials.
A few days passed and no sign of said man….welp! I concluded the dream should be laid to rest too.
I was on the train reading and I looked up because I felt eyes but suspected everything else but who I saw. To my astonishment there he was in front of me, literally the man of my dreams…well singular but he was in my dream, then somehow also in front of me in real life. Anyway, he was sat across from me but one seat over, yes I still remember that too … sheesh! Pahahaha He pulled out a book and started “reading” too lol. C’mon that’s cute, just a bit of imitation you know what they say. Flatter me! Flatter me! Ha!
Still pretending not to notice him I said “Nah!!! It can’t be the same guy from my dream. The guy from my dream had a bald head.” This mini speech took place in my head of course. Suddenly, I swear my hands started to sweat and remembered all those eyes rolls I gave to super fans passing out. The hypocrisy. I felt like I might faint my darn self. It was all very Twilight Zone-ish the theme song came to mind. This couldn’t be the man from my dream. I told myself to stop being silly, besides the Mr on the train had a hat on so I couldn’t tell.
He looked at me like he knew me. “Noooo!!!” Maybe he was just slick like that I thought *eye roll* again in my head. I kept thinking of something to say in my head. He was looking right at me whilst I acted like the book in my hand was so incredibly fascinating. When I blatantly looked back at him, a few times I thought he wanted to say something but like me cluck! cluck! his pointless wings flapped too loudly. I gave up thinking. I couldn’t do it either I just felt too shy pahahaha. I don’t know what happened to all that spiel in the beginning, where I said I wanted to see him in real life yadda yadda. Out the window everything went, my resolve just evaporated. Poof! Gone, without a warning. I know I asked to meet him but gosh I did not imagine it would be so soon.
The “dream guy” sat on the edge of his seat feet pointing towards me. The Psychology Articles came to mind, specifically the body language related sections of my filing system. Didn’t feet point towards the person of interest?! He fidgeted some more whilst I pretended not to see him lol he leaned over towards me. I was impressed that was something obvious…well I don’t really know but I swear I was like finally! Finally!!! *again in my head people*. Outwardly, I had not moved a muscle. I figured any sudden moves would see him second guessing. I tell you I was like how many blinks can I skip. I certainly wasn’t going to make the first move I’m a bit…okay a whole cooked chicken too so not a peep he would get from me. Pathetically immobilised.
Just as he stretched his left foot towards me (yes I noticed EVERYTHING! Pahahaha) and took his hat off to reveal that beautiful bald head I realised the train had reached my stop. Had it not been for the fact I had booked a class, I would have stayed one stop longer to entertain the situation and hear what he wanted to tell me. He looked disappointed as he slunk back in his seat to let me off the train or maybe that’s just how I felt. He looked at me, I looked at him. Who’s going to tell him it wasn’t his bald head. #GUTTED.
Have you ever met someone from your dreams? That was the only dream I’ve had of that nature to date. Also the only celebrities I met in a dream were Redman and Method Man, yep no crooners. Legends. If they ever get round to the project they informed of in my dream, I’ll share the dream.
Teherah_Whatthe 