Antineoplastic resistance, synonymous with chemotherapy resistance, is the ability of cancer cells to survive and grow despite different anti-cancer therapies, i.e. their multiple drug resistance. There are two general causes of antineoplastic therapy failure:

Inherent resistance, such as genetic characteristics, giving cancer cells their resistance from the beginning, which is rooted in the concept of cancer cell heterogeneity and acquired resistance after drug exposure.

Glyceraldehyde 3-phosphate dehydrogenase (abbreviated as GAPDH or less commonly as G3PDH) () is an enzyme of ~37kDa that catalyzes the sixth step of glycolysis and thus serves to break down glucose for energy and carbon molecules. In addition to this long established metabolic function, GAPDH has recently been implicated in several non-metabolic processes, including transcription activation, initiation of apoptosis, ER to Golgi vesicle shuttling, and fast axonal, or axoplasmic transport. In sperm, a testis-specific isoenzyme GAPDHS is expressed.

Antineoplastic resistance, often used interchangeably with chemotherapy resistance, is the multiple drug resistance of neoplastic (cancerous) cells, or the ability of cancer cells to survive and grow despite anti-cancer therapies.

There are two general causes of antineoplastic therapy failure: Inherent genetic characteristics, giving cancer cells their resistance, which is rooted in the concept of cancer cell heterogeneity and acquired resistance after drug exposure. Altered membrane transport, enhanced DNA repair, apoptotic pathway defects, alteration of target molecules, protein and pathway mechanisms, such as enzymatic deactivation.

Since cancer is a genetic disease, two genomic events underlie acquired drug resistance: Genome alterations (e.g. gene amplification and deletion) and epigenetic modifications.

Cancer cells are constantly using a variety of tools, involving genes, proteins and altered pathways, to ensure their survival against antineoplastic drugs.

GAPDH is overexpressed in multiple human cancers, such as cutaneous melanoma, and its expression is positively correlated with tumor progression. Its glycolytic and antiapoptotic functions contribute to proliferation and protection of tumor cells, promoting tumorigenesis. Notably, GAPDH protects against telomere shortening induced by chemotherapeutic drugs that stimulate the sphingolipid ceramide. Meanwhile, conditions like oxidative stress impair GAPDH function, leading to cellular aging and death. Moreover, depletion of GAPDH has managed to induce senescence in tumor cells, thus presenting a novel therapeutic strategy for controlling tumor growth.

No sexual predilection is observed because the deficiency of glycogen synthetase activity is inherited as an autosomal recessive trait.

The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency. Major long-term concerns include growth delay, osteopenia, and neurologic damage resulting in developmental delay, intellectual deficits, and personality changes.

Coconut Cadang Cadang Viroid (CCCVd) can be confused with another viroid called Coconut Tinangaja Viroid (CTiVd). That is because both viroids have 64% of their sequence of nucleotides in common. They both affect coconut palm, and infected plants have similar symptoms: spots on the leaves reduced top, yellow palms and even death.

There are few differences between both viroids in the effects caused on fruit: CTiVd causes small nuts, while CCCVd causes round and reduced nuts. Moreover, CTiVd has 254 nucleotides of length, while CCCVd has 246.

Dialysis disequilibrium syndrome, commonly abbreviated DDS, is the occurrence of neurologic signs and symptoms, attributed to cerebral edema, during or following shortly after intermittent hemodialysis.

Classically, DDS arises in individuals starting hemodialysis due to chronic renal failure and is associated, in particular, with "aggressive" (high solute removal) dialysis. However, it may also arise in fast onset, i.e. acute, renal failure in certain conditions.

Friedreich's ataxia is the most prevalent inherited ataxia, affecting about 1 in 50,000 people in the United States. Males and females are affected equally. The estimated carrier prevalence is 1:110.

A 1984 Canadian study was able to trace 40 cases of classical Friedreich's disease from 14 French-Canadian kindreds previously thought to be unrelated to one common ancestral couple arriving in New France in 1634: Jean Guyon and Mathurine Robin.

The cause of DDS is currently not well understood. There are two theories to explain it; the first theory postulates that urea transport from the brain cells is slowed in chronic renal failure, leading to a large urea concentration gradient, which results in reverse osmosis. The second theory postulates that organic compounds are increased in uremia to protect the brain and result in injury by, like in the first theory, reverse osmosis. More recent studies on rats noted that brain concentrations of organic osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus attributed to osmotic effects related to a high urea gradient between plasma and brain.

Coconut cadang-cadang disease has no treatment yet. However, chemotherapy with antibiotics has been tried with tetracycline solutions; antibiotics failed trying to alter progress of the disease since they had no significant effect on any of the studied parameters. When the treated plants were at the early stage, tetracycline injections failed to prevent the progression of the palms to more advanced stages, nor did they affect significantly the mean number of spathes or nuts. Penicillin treatment had no apparent improvement either.

Control strategies are elimination of reservoir species, vector control, mild strain protection and breeding for host resistance. Eradication of diseased plants is usually performed to minimize spread but is of dubious efficacy due to the difficulties of early diagnosis as the virus etiology remains unknown and the one discovered are the three main stages in the disease development.

Somatic mutations in the PIK3CA have been identified as a cause of CLOVES syndrome. PIK3CA is a protein involved in the PI3K-AKT signalling pathway. Mutations in other parts of this pathway cause other overgrowth syndromes including proteus syndrome and hemimegaencephaly.

The pathogenesis of this disease is unclear. Arteriosclerosis obliterans has been postulated as the cause, along with errors of the clotting and fibrinolytic pathways such as antiphospholipid syndrome.

CLOVES syndrome is an extremely rare overgrowth syndrome, with complex vascular anomalies. CLOVES syndrome affects people with various symptoms, ranging from mild fatty soft-tissue tumors to vascular malformations encompassing the spine or internal organs. CLOVES syndrome is closely linked to other overgrowth disorders like proteus syndrome, Klippel–Trénaunay syndrome, Sturge–Weber syndrome, and hemihypertrophy, to name a few.

'CLOVES' is an acronym for:

- C is for congenital.

- L is for lipomatous, which means pertaining to or resembling a benign tumor made up of mature fat cells. Most CLOVES patients present with a soft fatty mass at birth, often visible on one or both sides of the back, legs and/or abdomen.

- O is for overgrowth, because there is an abnormal increase in the size of the body or a body part that is often noted at birth. Patients with CLOVES may have affected areas of their bodies that grow faster than in other people. Overgrowth of extremities (usually arms or legs) is seen, with large wide hands or feet, large fingers or toes, wide space between fingers, and asymmetry of body parts.

- V is for vascular malformations, which are blood vessel abnormalies. Patients with CLOVES have different venous, capillary, and lymphatic channels - typically capillary, venous and lymphatic malformations are known as "slow flow" lesions. Some patients with CLOVES have combined lesions (which are fast flow) and some have aggressive vascular malformation known as arteriovenous malformations (AVM). The effect of a vascular malformation varies per patient based on the type, size, and location of the malformation, and symptoms can vary.

- E is for Epidermal naevi, which are sharply-circumscribed chronic lesions of the skin, and benign. These are often flesh-colored, raised or warty.

- S is for Spinal/Skeletal Anomalies or scoliosis. Some patients with CLOVES have tethered spinal cord, vascular malformations in or around their spines, and other spinal differences. High-flow aggressive spinal lesions (like AVM) can cause serious neurological deficits/paralysis.

The syndrome was first recognised by Saap and colleagues who recognised the spectrum of symptoms from a set of seven patients. In this initial description the syndrome is named CLOVE syndrome. It is believed that the first description of a case of CLOVES syndrome was written by Hermann Friedberg, a German physician, in 1867.

Asphyxiating thoracic dysplasia or Jeune syndrome is a ciliopathy.It is also known as "Jeune syndrome".

It was described in 1955.

Medulloepithelioma carries a dismal prognosis with a median survival of 5 months.

Friedreich's ataxia is an autosomal recessive inherited disease that causes progressive damage to the nervous system. It manifests in initial symptoms of poor coordination such as gait disturbance; it can also lead to scoliosis, heart disease and diabetes, but does not affect cognitive function. The disease is progressive, and ultimately a wheelchair is required for mobility. Its incidence in the general population is roughly 1 in 50,000.

The particular genetic mutation (expansion of an intronic GAA triplet repeat in the FXN gene) leads to reduced expression of the mitochondrial protein frataxin. Over time this deficiency causes the aforementioned damage, as well as frequent fatigue due to effects on cellular metabolism.

The ataxia of Friedreich's ataxia results from the degeneration of nervous tissue in the spinal cord, in particular sensory neurons essential (through connections with the cerebellum) for directing muscle movement of the arms and legs. The spinal cord becomes thinner and nerve cells lose some of their myelin sheath (the insulating covering on some nerve cells that helps conduct nerve impulses).

The condition is named after the German physician Nikolaus Friedreich, who first described it in the 1860s.

A large number of conditions may cause symptoms and signs similar to diabetic myonecrosis and include: deep vein thrombosis, thrombophlebitis, cellulitis, fasciitis, abscess, haematoma, myositis, pseudothrombophlebitis (ruptured synovial cyst), pyomyositis, parasitic myositis, osteomyelitis, calcific myonecrosis, myositis ossificans, diabetic myotrophy, muscle strain or rupture, bursitis, vasculitis, arterial occlusion, haemangioma, lymphoedema, sarcoidosis, tuberculosis, cat-scratch disease, amyloidosis, as well as tumours of lipoma, chondroma, fibroma, leiomyoma and sarcoma.

More than 10,000 cases of potential calcium channel blocker toxicity occurred in the United States in 2010. When death occurs in medicine overdose, heart medications are the cause more than 10% of time. The three most common types of heart medications that result in this outcome are calcium channel blockers along with beta blockers and digoxin.

Onset is between 3 and 15 years of age with a mean of around 8. Both sexes are equally affected. The disorder accounts for about 2–7% of benign childhood focal seizures.

Jeune syndrome is a rare genetic disorder that affects the way a child’s cartilage and bones develop. It begins before the child is born. Jeune syndrome affects the child's rib cage, pelvis, arms and legs.

Usually, problems with the rib cage cause the most serious health problems for children with Jeune syndrome. Their rib cages (thorax) are smaller and narrower than usual. This can keep the child's lungs from developing fully or expanding when the child inhales. The child may breathe rapidly and shallowly. They may have trouble breathing when they have an upper or lower respiratory infection, like pneumonia.

Breathing trouble can range from mild to severe. In some children, it is not noticeable, aside from fast breathing. In most children, breathing problems are serious. About 60% to 70% of children with this condition die from respiratory failure as babies or young children.

Children with Jeune syndrome who survive often develop problems with their kidneys, another serious feature of Jeune syndrome. Over time they may experience renal failure.

As a result, few children with Jeune syndrome live into their teen years.

Children with Jeune syndrome have a form of dwarfism. They are short in stature, and their arms and legs are shorter than most people’s.

Another name for Jeune syndrome is asphyxiating thoracic dystrophy. This diagnosis is grouped with other chest problems called thoracic insufficiency syndrome (TIS).

It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.

The prognosis of ICOE-G is unclear, although available data indicate that remission occurs in 50–60% of patients within 2–4 years of onset. Seizures show a dramatically good response to carbamazepine in more than 90% of patients. However, 40–50% of patients may continue to have visual seizures and infrequent secondarily generalized convulsions, particularly if they have not been appropriately treated with antiepileptic drugs.

Sick sinus syndrome is a relatively uncommon syndrome in the young and middle age population. Sick sinus syndrome is more common in elderly adults, where the cause is often a non-specific, scar-like degeneration of the cardiac conduction system. Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

Malignant ectomesenchymoma is a rare, fast-growing tumor of the nervous system or soft tissue that occurs in children and young adults. Malignant ectomesenchymomas may form in the head and neck, abdomen, perineum, scrotum, or limbs. Also called ectomesenchymoma.