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What is genetic testing?

Even when people have one copy of a dominant cancer-predisposing mutation, two copies of a recessive mutation, or, for males, one copy of an X-linked recessive mutation, they may not develop cancer. Some mutations are “incompletely penetrant,” which means that only some people will show the effects of these mutations. Mutations can also “vary in their expressivity,” which means that the severity of the symptoms may vary from person to person.

What genetic tests are available for cancer risk?

More than 50 hereditary cancer syndromes have been described. The majority of these are caused by highly penetrant mutations that are inherited in a dominant fashion. The list below includes some of the more common inherited cancer syndromes for which genetic testing is available, the gene(s) that are mutated in each syndrome, and the cancer types most often associated with these syndromes.

Hereditary breast cancer and ovarian cancer syndrome

Genes: BRCA1, BRCA2
Related cancer types: Female breast, ovarian, and other cancers, including prostate, pancreatic, and male breast cancer

Li-Fraumeni syndrome

Gene: TP53
Related cancer types: Breast cancer, soft tissue sarcoma, osteosarcoma (bone cancer), leukemia, brain tumors, adrenocortical carcinoma (cancer of the adrenal glands), and other cancers

Cowden syndrome (PTEN hamartoma tumor syndrome)

Gene: PTEN
Related cancer types: Breast, thyroid, endometrial (uterine lining), and other cancers

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

Genes: MSH2, MLH1, MSH6, PMS2, EPCAM
Related cancer types: Colorectal, endometrial, ovarian, renal pelvis, pancreatic, small intestine, liver and biliary tract, stomach, brain, and breast cancers

Familial adenomatous polyposis

Gene: APC
Related cancer types: Colorectal cancer, multiple non-malignant colon polyps, and both non-cancerous (benign) and cancerous tumors in the small intestine, brain, stomach, bone, skin, and other tissues

Retinoblastoma

Gene: RB1
Related cancer types: Eye cancer (cancer of the retina), pinealoma (cancer of the pineal gland), osteosarcoma, melanoma, and soft tissue sarcoma

Multiple endocrine neoplasia type 1 (Wermer syndrome)

Gene: MEN1
Related cancer types: Pancreatic endocrine tumors and (usually benign) parathyroid and pituitary gland tumors

Multiple endocrine neoplasia type 2

Gene: RET
Related cancer types: Medullary thyroid cancer and pheochromocytoma (benign adrenal gland tumor)

Von Hippel-Lindau syndrome

Gene: VHL
Related cancer types: Kidney cancer and multiple noncancerous tumors, including pheochromocytoma

Who should consider genetic testing for cancer risk?

Many experts recommend that genetic testing for cancer risk should be strongly considered when all three of the following criteria are met:

The person being tested has a personal or family history that suggests an inherited cancer risk condition
The test results can be adequately interpreted (that is, they can clearly tell whether a specific genetic change is present or absent)
The results provide information that will help guide a person’s future medical care

The features of a person’s personal or family medical history that, particularly in combination, may suggest a hereditary cancer syndrome include:

Cancer that was diagnosed at an unusually young age
Several different types of cancer that have occurred independently in the same person
Cancer that has developed in both organs in a set of paired organs, such as both kidneys or both breasts
Several close blood relatives that have the same type of cancer (for example, a mother, daughter, and sisters with breast cancer)
Unusual cases of a specific cancer type (for example, breast cancer in a man)
The presence of birth defects, such as certain noncancerous (benign) skin growths or skeletal abnormalities, that are known to be associated with inherited cancer syndromes
Being a member of a racial/ethnic group that is known to have an increased chance of having a certain hereditary cancer syndrome and having one or more of the above features as well

It is strongly recommended that a person who is considering genetic testing speak with a professional trained in genetics before deciding whether to be tested. These professionals can include doctors, genetic counselors, and other health care providers (such as nurses, psychologists, or social workers). Genetic counseling can help people consider the risks, benefits, and limitations of genetic testing in their particular situation. Sometimes the genetic professional finds that testing is not needed.

Genetic counseling includes a detailed review of the individual’s personal and family medical history related to possible cancer risk. Counseling also includes discussions about such issues as:

Whether genetic testing is appropriate, which specific test(s) might be used, and the technical accuracy of the test(s)
The medical implications of a positive or a negative test result (see below)
The possibility that a test result might not be informative—that is, that the information may not be useful in making health care decisions (see below)
The psychological risks and benefits of learning one’s genetic test results
The risk of passing a genetic mutation (if one is present in a parent) to children

Learning about these issues is a key part of the informed consent process. Written informed consent is strongly recommended before a genetic test is ordered. People give their consent by signing a form saying that they have been told about, and understand, the purpose of the test, its medical implications, the risks and benefits of the test, possible alternatives to the test, and their privacy rights.

Unlike most other medical tests, genetic tests can reveal information not only about the person being tested but also about that person’s relatives. The presence of a harmful genetic mutation in one family member makes it more likely that other blood relatives may also carry the same mutation. Family relationships can be affected when one member of a family discloses genetic test results that may have implications for other family members. Family members may have very different opinions about how useful it is to learn whether they do or do not have a disease-related genetic mutation. Health discussions may get complicated when some family members know their genetic status while other family members do not choose to know their test results. A conversation with genetics professionals may help family members better understand the complicated choices they may face.

How is genetic testing done?

Genetic tests are usually requested by a person’s doctor or other health care provider. Although it may be possible to obtain some genetic tests without a health care provider’s order, this approach is not recommended because it does not give the patient the valuable opportunity to discuss this complicated decision with a knowledgeable professional.

Testing is done on a small sample of body fluid or tissue—usually blood, but sometimes saliva, cells from inside the cheek, skin cells, or amniotic fluid (the fluid surrounding a developing fetus).

The sample is then sent to a laboratory that specializes in genetic testing. The laboratory returns the test results to the doctor or genetic counselor who requested the test. In some cases, the laboratory may send the results to the patient directly. It usually takes several weeks or longer to get the test results. Genetic counseling is recommended both before and after genetic testing to make sure that patients have accurate information about what a particular genetic test means for their health and care.

What do the results of genetic testing mean?

Genetic testing can have several possible results: positive, negative, true negative, uninformative negative, false negative, variant of unknown significance, or benign polymorphism. These results are described below.

A “positive test result” means that the laboratory found a specific genetic alteration (or mutation) that is associated with a hereditary cancer syndrome. A positive result may:

Confirm the diagnosis of a hereditary cancer syndrome
Indicate an increased risk of developing certain cancer(s) in the future
Show that someone carries a particular genetic change that does not increase their own risk of cancer but that may increase the risk in their children if they also inherit an altered copy from their other parent (that is, if the child inherits two copies of the abnormal gene, one from their mother and one from their father).
Suggest a need for further testing
Provide important information that can help other family members make decisions about their own health care.

Also, people who have a positive test result that indicates that they have an increased risk of developing cancer in the future may be able to take steps to lower their risk of developing cancer or to find cancer earlier, including:

Being checked at a younger age or more often for signs of cancer
Reducing their cancer risk by taking medications or having surgery to remove “at-risk” tissue (These approaches to risk reduction are options for only a few inherited cancer syndromes.)
Changing personal behaviors (like quitting smoking, getting more exercise, and eating a healthier diet) to reduce the risk of certain cancers

A positive result on a prenatal genetic test for cancer risk may influence a decision about whether to continue a pregnancy. The results of pre-implantation testing (performed on embryos created by in vitro fertilization) can guide a doctor in deciding which embryo (or embryos) to implant in a woman’s uterus.

Finally, in patients who have already been diagnosed with cancer, a positive result for a mutation associated with certain hereditary cancer syndromes can influence how the cancer is treated. For example, some hereditary cancer disorders interfere with the body’s ability to repair damage that occurs to cellular DNA. If someone with one of these conditions receives a standard dose of radiation or chemotherapy to treat their cancer, they may experience severe, potentially life-threatening treatment side effects. Knowing about the genetic disorder before treatment begins allows doctors to modify the treatment and reduce the severity of the side effects.

A “negative test result” means that the laboratory did not find the specific alteration that the test was designed to detect. This result is most useful when working with a family in which the specific, disease-causing genetic alteration is already known to be present. In such a case, a negative result can show that the tested family member has not inherited the mutation that is present in their family and that this person therefore does not have the inherited cancer syndrome tested for, does not have an increased genetic risk of developing cancer, or is not a carrier of a mutation that increases cancer risk. Such a test result is called a “true negative.” A true negative result does not mean that there is no cancer risk, but rather that the risk is probably the same as the cancer risk in the general population.

When a person has a strong family history of cancer but the family has not been found to have a known mutation associated with a hereditary cancer syndrome, a negative test result is classified as an “uninformative negative” (that is, does not provide useful information). It is not possible to tell whether someone has a harmful gene mutation that was not detected by the particular test used (a “false negative”) or whether the person truly has no cancer-predisposing genetic alterations in that gene. It is also possible for a person to have a mutation in a gene other than the gene that was tested.

If genetic testing shows a change that has not been previously associated with cancer in other people, the person’s test result may report “variant of unknown significance,” or VUS. This result may be interpreted as “ambiguous” (uncertain), which is to say that the information does not help in making health care decisions.

If the test reveals a genetic change that is common in the general population among people without cancer, the change is called a polymorphism. Everyone has commonly occurring genetic variations (polymorphisms) that are not associated with any increased risk of disease.

Who can help people understand their test results?

A genetic counselor, doctor, or other health care professional trained in genetics can help an individual or family understand their test results. Such counseling may include discussing recommendations for preventive care and screening with the patient, referring the patient to support groups and other information resources, and providing emotional support to the person receiving the results.

Email motherhealth@gmail.com for a DNA test for early cancer detection.

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How to stop sugar cravings or other forms of addiction?

Eat protein-rich foods and good carbs and stay away from seeing the delicious chocolate cake treat in front of you. Do not go food shopping when you are hungry. Eat your fish first before you have a small bite of dessert. Feel the dessert in your mouth and then tell your brain that you are now satisfied with a small bite and will eat again tomorrow. Portion control and exercise will help you.

Fiber is your friend. Eat fiber-rich whole foods such as spinach, kale, and other greens. Eat the skin of sweet potatoes and other root crops.

When we are under stress and lack sleep, we grab that chocolate ice cream for the magnesium in chocolates relaxes us. But you can also find magnesium in whole foods such as nuts and seeds.

Our senses and brain especially our sense of sight can entice us to try a bite of that ice cream cake in front of us. Store healthy foods in your fridge.

How can we control our genes responsible for addiction and our brain from giving in to our addiction (sugar, alcohol, other addictions)?

Addiction

Addiction is a disorder of the brain’s reward system which arises through transcriptional and epigenetic mechanisms and occurs over time from chronically high levels of exposure to an addictive stimulus (e.g., morphine, cocaine, sexual intercourse, gambling, etc.).^[1]^[10]^[11] ΔFosB, a gene transcription factor, is a critical component and common factor in the development of virtually all forms of behavioral and drug addictions.^[10]^[11]^[12]^[13] Two decades of research into ΔFosB’s role in addiction have demonstrated that addiction arises, and the associated compulsive behavior intensifies or attenuates, along with the genetic overexpression of ΔFosB in the D1-type medium spiny neurons of the nucleus accumbens.^[1]^[10]^[11]^[12] Due to the causal relationship between ΔFosB expression and addictions, it is used preclinically as an addiction biomarker.^[1]^[10]^[12] ΔFosB expression in these neurons directly and positively regulates drug self-administrationand reward sensitization through positive reinforcement, while decreasing sensitivity to aversion.

Cognitive inhibition

Cognitive inhibition is the suppression of unwanted or irrelevant thoughts to protect working memory and attention resources.^[103]

Cognitive inhibition is most often measured through tests of directed ignoring, self-report on one’s intrusive thoughts, and negative priming tasks. As with interference control, personality psychologists have measured cognitive inhibition using the Rothbart Effortful Control scale and the Big Five Conscientiousness scale. The anterior cingulate, the prefrontal regions, and the association cortex seem to be involved in cognitive inhibition.^[103]

Behavioral inhibition

Behavioral Inhibition is the suppression of prepotent response.

Behavioral inhibition is usually measured using the Go/No Go task, Stop signal task, and reports of suppression of attentional orienting. Surveys that are theoretically relevant to behavioral inhibition include the Rothbart effortful control scale, and the Big Five Conscientiousness dimension.^[103] The rationale behind the use of behavioral measures like the Stop signal task is that “go” processes and “stop processes” are independent, and that, upon “go” and “stop” cues, they “race” against each other; if the go process wins the race, the prepotent response is executed, whereas if the stop processes wins the race, the response is withheld. In this context, impulsivity is conceptualized as a relatively slow stop process.^[107] The brain regions involved in behavioral inhibition appear to be the lateral and orbital prefrontal regions along with premotor processes.

Oculomotor Inhibition

Oculomotor Inhibition is the effortful suppression of reflexive saccade.^[103]

Oculomotor inhibition is tested using antisaccade and oculomotor tasks. Also, the Rothbart effortful control measure and the Big Five Conscientiousness dimension are thought to tap some of the effortful processes underlying the ability to suppress saccade. The frontal eye fields and the dorsolateral prefrontal cortex are involved in oculomotor inhibition.

Motivational inhibition

In response to punishment

Motivational inhibition and response in the face of punishment can be measured using tasks tapping inhibition of primary response, modified go/no go tasks, inhibition of competing response, and emotional Stroop tasks.^[103] Personality psychologists also use the Gray behavioral inhibition system measure, the Eysenck scale for neurotic introversion, and the Zuckerman Neuroticism-Anxiety scale.^[103] The Septal-hippocampal formation, cingulate, and motor systems seem to be the brain areas most involved in response to punishment.^[103]

In response to novelty

Response to novelty has been measured using the Kagan behavioral inhibition system measure and scales of neurotic introversion.^[103] The amygdaloid system is implicated in novelty response.^[103]

Automatic inhibition of attention

Recently inspected stimuli

Suppression of recently inspected stimuli for both attention and oculomotor saccade is usually measured using attentional and oculomotor inhibition of return tests. The superior colliculus and the midbrain, oculomotor pathway are involved in suppression of stimuli.

Glycoproteomics-based discovery of cancer and stem cell biomarkers

Glycoproteomics-based discovery of cancer and stem cell biomarkers Given the strong correlation of altered glycosylation patterns with malignancy, glycosylated proteins may be an information-rich s…

Source: Glycoproteomics-based discovery of cancer and stem cell biomarkers

How the flu virus infects our bodies, sugar’s role

The flu virus is a highly shifting virus that changes very fast.
Influenza virus has high ability to move from one organism to another.
Bird flu can make humans very sick but non-transmissable.
The swine flu, H1N1 influenza, can go from pigs to humans and from humans to humans. A pandemic case.

Sugar

During early stage of influenza virus, sugar is involved.

Connie’s comments: Avoid sugar and eat more whole foods (colored greens/veggies).

Email motherhealth@gmail.com for a DNA blood test to test for cancer early before it grows to stage 1.

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Glycoproteomics-based discovery of cancer and stem cell biomarkers

Given the strong correlation of altered glycosylation patterns with malignancy, glycosylated proteins may be an information-rich subset of the proteome from which cancer biomarkers can be discovered. We employ metabolic labeling with azidosugars as a means to tag specific classes of glycoproteins for enrichment from human tissue samples and subsequent identification by mass spectrometry. A challenge in this endeavor is defining sites of glycosylation on peptide digests derived from such complex samples. To facilitate this effort, we are creating isotopic labeling strategies and computational methods that enable the detection of glycosylated peptides independent of the mass of the pendant glycan. Collectively, these tools allow us to profile changes in protein glycosylation associated with human prostate cancer progression and embryoic stem cell differentiation.

Bacterial Toxins

Toxigenic bacteria, which include some species of Escherichia, Shigella, Vibrio, and Clostridium, release protein toxins that alter essential host processes, including endocytic pathways, cell signaling and cytoskeletal reorganization. These toxins are key virulence factors that damage host tissues, and aid the spread of bacteria and evasion of immune clearance. Many bacterial toxins have been shown to bind host glycans. Glycan receptor specificity is critical for the pathogenic process, as it determines host susceptibility, tissue tropism, and the nature and spectrum of the resultant pathology. With contributions from the CFG, knowledge of the molecular and structural bases for toxin-glycan interactions is providing a rational framework for design of specific toxin inhibitors with considerable potential as anti-infective therapeutic agents.

Cellular expression of GBP and ligands

HA is expressed on the surface of influenza virus infected cells before being budded out into progeny virions. H3N2 viruses infect the respiratory tract of humans and birds; in birds they may also infect the gut epithelia. Using MAA and SNA lectins, the upper respiratory tract appears to have more 2-6 linked sialic acid while 2-3 sialic acid appears more abundant in the lungs, but relationship between the different specificities of H3N2 HAs and the cell types infected remains unclear ^[3]. H3N2 viruses infect very few continuous cell lines. Madin-Darby canine kidney cells are most commonly used. Non-permissive cell lines may take up virus efficiently, replicate RNA and express HA on the cell surface but do not bud new virus particles ^[4].

Biosynthesis of ligands

Sialylated glycoproteins or glycolipids recognized by human influenza hemagglutinin H3 are synthesized by host cells. The H3 hemagglutinin shows considerable diversity in binding but with rare exceptions the sialic acid is attached 2-6 to the next sugar on structures that are mostly typical of N-linked glycans on proteins. The enzymes required for biosynthesis of the type 2 poly N-acetyllactosamine chains and modification with sialic acid or with sialic acid and fucose, have been defined ([1][poly N-acetyllactosamine extension biosynthesis]). The sialyltransferases that generate ligands for most H3 subtype hemagglutinins are ST6Gal1, ST6GalII, ST6GalNAc1, ST6GalNAcII, ST6GalNAcIV.

Biological roles of GBP-ligand interaction

Sialylated glycans on the surface of cells lining the respiratory tract serve to capture virus to initiate infection. Glycan array analyses have confirmed that human influenza viruses such as those carrying the H3 HA bind only to structures with NeuAcα2-6 and avian isolates bind only to structures containing NeuAcα2-3. The role of this GBP-glycan interaction in initiating endocytosis is still unclear, but in the low pH of the endosomal compartment, the HA undergoes a large conformational change ^[6] that brings about fusion of the viral membrane with the cell membrane so that viral nucleocapsids are released, enter the nucleus and initiate viral transcription and replication.

Capsid Virus GBPs

A significant number of non-enveloped capsid viruses use glycans as cell attachment receptors. In some cases, viruses exclusively engage glycan structures at the cell surface, while in other cases glycans serve as co-receptors, and viruses also bind to proteins. The carbohydrate structures recognized by capsid viruses are diverse, ranging from gangliosides and other glycolipids to protein-bound glycans. Changes in carbohydrate binding specificity among family members of the same virus can often lead to altered tropism and pathogenicity. Thus, the elucidation of parameters that guide the specificity of interactions with glycans are of critical importance for understanding the complex biology of capsid viruses. The three paradigms listed below represent virus families whose glycan binding properties have been successfully studied by CFG investigators.

Glycocalyx engineering toward probing cancer glycome evolution

While altered glycosylation patterns have long been identified as hallmarks of cancer, their functional significance with respect to tumor progression are not well understood. Two examples are overexpression of mucin glycoproteins¬ (densely glycosylated cell-surface molecules with unusual physical properties) and hypermodification of glycoproteins with the terminal sugar sialic acid. These glycosylation phenotypes are found on numerous cancer types with highly varied underlying driver mutations and their magnitude tends to correlate with tumor aggressiveness. To test hypotheses regarding the functional significance of cancer glycomes, we developed an approach to engineer the cell surface “glycocalyx” with chemically defined glycopolymers that emulate cancer-associated structures. Using living polymerization and chemoselective ligation chemistries, we synthesize glycopolymers functionalized with a biophysical probe on one end and a lipid capable of membrane insertion on the other. These biomimetic structures can be displayed on live cell membranes where they acquire functions analogous to natural mucin glycoproteins. With this glycocalyx engineering platform, we identified a role for hypersialylation in protection of tumor cells from innate immunosurveillance. Ongoing work focuses on the effects of mucin overexpression on cell adhesion and signaling.

In vivo imaging of glycans and other biomolecules

We have found bioorthogonal chemistry and other chemical approaches to be powerful allies in studies of glycobiology, a frontier area of biomedical science with limited experimental tools available for probing relationships of structure and function. Glycans decorate cell surfaces and secreted proteins and their structures change during dynamic physiological processes such as malignant transformation and stem cell differentiation. Yet, the precise biological functions of cell surface glycans, considered by many to be the “dark matter” of the cell, are largely unknown. Cancer-specific glycosylation patterns have been identified on tumor tissue ex vivo, prompting much excitement around their potential use as targets for molecular imaging and as disease biomarkers. To realize these possibilities, we developed a technique for glycan imaging that involves metabolic labeling with synthetic azidosugars followed by in vivo bioorthogonal reaction with optical or MRI contrast probes. We employ this chemical imaging platform to study glycomic changes associated with cancer, as well as during embryogenesis and microbial infection using zebrafish as a model organism.

Recently we pursued an analogous method for imaging bacterial peptidoglycan using azide- or alkyne-functionalized D-alanine analogs as metabolic labels. We are using this technique to probe spatiotemporal changes in peptidoglycan biosynthesis associated with infection by the intracellular pathogens such as Mycobacterium tuberculosis and Listeria monocytogenes. More broadly, we consider metabolic labeling with bioorthogonal “chemical reporters” as a general approach to interrogate biomolecules that might not be accessible to conventional genetic reporter strategies.

https://bertozzigroup.stanford.edu/research.htm

Bacterial Adhesins and Lectins

Infection by bacteria is generally initiated by the specific recognition of host epithelial surfaces by adhesins and lectins. These GBPs are therefore virulence factors that play a role in the first step of adhesion and invasion. The GBPs are called adhesins when they are part of organelles, such as fimbriae and flagella. They are referred to as lectins when they are soluble, and lectin-domain when attached to other proteins, which are often hydrolytic enzymes also involved in the infection process. The human targets for bacterial adhesins and lectins are mostly fucosylated human histo-blood group and/or sialylated epitopes. Defining the biological role of bacterial adhesins and lectins together with their structure and specificity is a prerequisite for the development of strategies for inhibiting their binding to human tissues.

C-type lectin

The C-type lectin family consists of proteins with diverse overall organization that contain structurally related carbohydrate-recognition domains. Although they generally share a common mechanism for interacting with sugars through a bound calcium ion, the spectrum of ligands bound by different members of the family is diverse and can include both endogenous mammalian oligosaccharides as well a sugar-containing structures on pathogenic micro-organisms. The biological functions of the C-type lectins are correspondingly diverse, but many of the best understood examples are membrane receptors found on the surface of cells of the immune system, which mediate interactions of these cells with each other and with viruses, bacteria, fungi and parasites, while other members of the family are soluble mediators of innate immunity. Outside the immune system, members of this group participate in clearance of circulating glycoproteins.

Galectins

Galectins are a family of glycan-binding proteins that are expressed in all multicellular organisms, in virtually every cell and tissue, and that vary considerably in function. There are 15 overall genes encoding galectins in different animals and 11 are expressed in humans.
All galectins share a consensus sequence of about 130 amino acids and a homologous carbohydrate recognition domain (CRD) that specifically binds many different types of glycans, including those containing b-galactosides and poly-N-acetyllactosamines, but also including blood group antigens, and sialic acid- or sulfate-containing structures found in O- and N-glycans.
The jellyroll-like conformation of the CRD, the hallmark of the galectin family, is composed of two anti-parallel b-sheets that establish a b-sandwich Differences in ligand specificity among this family are determined by specific amino acids in the CRDs, allowing recognition of different modifications of galactose-containing glycans, thus defining the affinity of a particular galectin for specific glycoprotein or glycolipid receptors in a certain tissue or cell type. Galectins are synthesized in the cytoplasm and secreted via a non-classical secretion pathway, so that galectins are found in a variety of intracellular compartments, as well as in the extracellular milieu of almost every cell and tissue type.
There are three structural subfamilies of galectins – the prototype, the chimeric, and the tandem repeat. The three paradigmatic galectins described below represent the three structural subfamilies. The prototypical galectin subfamily include galectins-1, -2, -7, -10, -13, and -14; the chimeric galectin subfamily has a single representative galectin-3; and the tandem repeat galectin subfamily includes galectins-4, -8, -9, and -12. Recognition of cell surface glycans by many of the galectins, which is associated with oligomerization and lattice formation of the receptors, induces signaling pathways that are being well defined in leukocytes and epithelial cells. In addition, galectins are important in innate immune responses and can directly recognize glycans on pathogens and provide protection independently of antibodies.

Both calreticulin and the cation-dependent mannose-6-phosphate receptor are glycan-binding proteins recognizing discrete and specific carbohydrates involved in intracellular trafficking of membrane and secretory glycoproteins. In the case of calreticulin, glycan binding is associated with the quality control apparatus ensuring that only properly folded proteins will exit the endoplasmic reticulum. In the case of the cation-dependent mannose-6-phosphate receptor, phosphorylated mannose residues are recognized, allowing lysosomal proteins to be properly targeted. These paradigms are important for understanding diseases of protein misfolding and many lysosomal storage disorders. The ficolins are a class of glycan-binding proteins with affinity for N-acetyl residues that have distinct fold from other known lectins yet mediate pathogen recognition. Polymorphisms in ficoloin genes may also have pathophysiological implications.

http://www.functionalglycomics.org/CFGparadigms/index.php/Welcome_to_the_CFG_Paradigm_Pages

Connie’s comments:

Bacteria, virus and other pathogens need an acidic environment and attaches themselves to sugar-rich carbohydrates to grow. Those with genes related to low immune system and poor metabolism of sugar and carbs are more affected.

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What genetic tests are available for cancer risk?

Cowden syndrome (PTEN hamartoma tumor syndrome)

Lynch syndrome (hereditary nonpolyposis colorectal cancer)

Multiple endocrine neoplasia type 1 (Wermer syndrome)

Who should consider genetic testing for cancer risk?

The features of a person’s personal or family medical history that, particularly in combination, may suggest a hereditary cancer syndrome include:

Genetic counseling includes a detailed review of the individual’s personal and family medical history related to possible cancer risk. Counseling also includes discussions about such issues as:

How is genetic testing done?

Who can help people understand their test results?

Thank you for your response. ✨

Addiction

Cognitive inhibition

Behavioral inhibition

Oculomotor Inhibition

Motivational inhibition

In response to punishment

In response to novelty

Automatic inhibition of attention

Recently inspected stimuli

Sugar

Thank you for your response. ✨

Glycoproteomics-based discovery of cancer and stem cell biomarkers

Bacterial Toxins

Cellular expression of GBP and ligands

Biosynthesis of ligands

Biological roles of GBP-ligand interaction

Capsid Virus GBPs

Glycocalyx engineering toward probing cancer glycome evolution

In vivo imaging of glycans and other biomolecules

Bacterial Adhesins and Lectins

C-type lectin

Galectins

Bacteria, virus and other pathogens need an acidic environment and attaches themselves to sugar-rich carbohydrates to grow. Those with genes related to low immune system and poor metabolism of sugar and carbs are more affected.

Eat whole foods rich in fiber , less sugar , to fight cancer profileration.