In histopathology, nuclear moulding, also nuclear molding, is conformity of adjacent cell nuclei to one another.

It is a feature of small cell carcinomas and particularly useful for differentiation of small cell and non-small cell carcinomas, i.e. adenocarcinoma and squamous carcinoma.

Cancer is a stochastic effect of radiation, meaning that it only has a probability of occurrence, as opposed to deterministic effects which always happen over a certain dose threshold. The consensus of the nuclear industry, nuclear regulators, and governments, is that the incidence of cancers due to ionizing radiation can be modeled as increasing linearly with effective radiation dose at a rate of 5.5% per sievert. Individual studies, alternate models, and earlier versions of the industry consensus have produced other risk estimates scattered around this consensus model. There is general agreement that the risk is much higher for infants and fetuses than adults, higher for the middle-aged than for seniors, and higher for women than for men, though there is no quantitative consensus about this. This model is widely accepted for external radiation, but its application to internal contamination is disputed. For example, the model fails to account for the low rates of cancer in early workers at Los Alamos National Laboratory who were exposed to plutonium dust, and the high rates of thyroid cancer in children following the Chernobyl accident, both of which were internal exposure events. The European Committee on Radiation Risk calls the ICRP model "fatally flawed" when it comes to internal exposure.

Radiation can cause cancer in most parts of the body, in all animals, and at any age, although radiation-induced solid tumors usually take 10–15 years, and can take up to 40 years, to become clinically manifest, and radiation-induced leukemias typically require 2–10 years to appear. Some people, such as those with nevoid basal cell carcinoma syndrome or retinoblastoma, are more susceptible than average to developing cancer from radiation exposure. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect.

Radiation exposure can cause cancer in any living tissue, but high-dose whole-body external exposure is most closely associated with leukemia, reflecting the high radiosensitivity of bone marrow. Internal exposures tend to cause cancer in the organs where the radioactive material concentrates, so that radon predominantly causes lung cancer, iodine-131 is most likely to cause thyroid cancer, etc.

Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies. Clear evidence establishes ultraviolet radiation, especially the non-ionizing medium wave UVB, as the cause of most non-melanoma skin cancers, which are the most common forms of cancer in the world.

Skin cancer may occur following ionizing radiation exposure following a latent period averaging 20 to 40 years. A Chronic radiation keratosis is a precancerous keratotic skin lesion that may arise on the skin many years after exposure to ionizing radiation. Various malignancies may develop, most frequency basal-cell carcinoma followed by squamous-cell carcinoma. Elevated risk is confined to the site of radiation exposure. Several studies have also suggested the possibility of a causal relationship between melanoma and ionizing radiation exposure. The degree of carcinogenic risk arising from low levels of exposure is more contentious, but the available evidence points to an increased risk that is approximately proportional to the dose received. Radiologists and radiographers are among the earliest occupational groups exposed to radiation. It was the observation of the earliest radiologists that led to the recognition of radiation-induced skin cancer—the first solid cancer linked to radiation—in 1902. While the incidence of skin cancer secondary to medical ionizing radiation was higher in the past, there is also some evidence that risks of certain cancers, notably skin cancer, may be increased among more recent medical radiation workers, and this may be related to specific or changing radiologic practices. Available evidence indicates that the excess risk of skin cancer lasts for 45 years or more following irradiation.

As there is no known cure, few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis, such as heart attack or stroke.

Mental development is not adversely affected; in fact, intelligence tends to be average to above average. With respect to the features of aging that progeria appears to manifest, the development of symptoms is comparable to aging at a rate eight to ten times faster than normal. With respect to features of aging that progeria does not exhibit, patients show no neurodegeneration or cancer predisposition. They also do not develop conditions that are commonly associated with aging, such as cataracts (caused by UV exposure) and osteoarthritis.

Although there may not be any successful treatments for progeria itself, there are treatments for the problems it causes, such as arthritic, respiratory, and cardiovascular problems. Sufferers of progeria have normal reproductive development and there are known cases of women with progeria who had delivered healthy offspring.

Hyalinizing clear cell carcinoma, abbreviated HCCC, is a rare malignant salivary gland tumour, with a good prognosis, that is usually found on the tongue or palate.

Laminopathies ("" + "") are a group of rare genetic disorders caused by mutations in genes encoding proteins of the nuclear lamina. They are included in the more generic term "nuclear envelopathies" that was coined in 2000 for diseases associated with defects of the nuclear envelope. Since the first reports of laminopathies in the late 1990s, increased research efforts have started to uncover the vital role of nuclear envelope proteins in cell and tissue integrity in animals.

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.

Dysmelia can be caused by

- inheritance of abnormal genes, e.g. polydactyly, ectrodactyly or brachydactyly, symptoms of deformed limbs then often occur in combination with other symptoms (syndromes)

- external causes during pregnancy (thus not inherited), e.g. via amniotic band syndrome

- teratogenic drugs (e.g. thalidomide, which causes phocomelia) or environmental chemicals

- ionizing radiation (nuclear weapons, radioiodine, radiation therapy)

- infections

- metabolic imbalance

Monoblasts are normally found in bone marrow and do not appear in the normal peripheral blood. They mature into monocytes which, in turn, develop into macrophages.

A solid pseudopapillary tumour (also known as solid pseudopapillary neoplasm or, more formally, solid pseudopapillary tumour/neoplasm of the pancreas) is a low-grade malignant neoplasm of the pancreas of architecture that typically afflicts young women.

In urologic pathology, PUNLMP, short for papillary urothelial neoplasm of low malignant potential, is an exophytic (outward growing), (microscopically) nipple-shaped (or papillary) pre-malignant growth of the lining of the upper genitourinary tract (the urothelium), which includes the renal pelvis, ureters, urinary bladder and part of the urethra.

"PUNLMP" is pronounced "pun"-"lump", like the words "pun" and "lump".

As their name suggests, PUNLMPs are neoplasms, i.e. clonal cellular proliferations, that are thought to have a low probability of developing into urothelial cancer, i.e. a malignancy such as bladder cancer.

PUNLMPs can lead to blood in the urine (hematuria) or may be asymptomatic.

Laminopathies and other nuclear envelopathies have a large variety of clinical symptoms including skeletal and/or cardiac muscular dystrophy, lipodystrophy and diabetes, dysplasia, dermo- or neuropathy, leukodystrophy, and progeria (premature aging). Most of these symptoms develop after birth, typically during childhood or adolescence. Some laminopathies however may lead to an early death, and mutations of lamin B (LMNB1 gene) may be lethal before or at birth.

Pelger–Huët anomaly (pronunciation: [pel′gər hyo̅o̅′ət]) is a blood laminopathy associated with the lamin B receptor.

It is characterized by a white blood cell type known as a neutrophil whose nucleus is hyposegmented.

It is a genetic disorder with an autosomal dominant inheritance pattern. Heterozygotes are clinically normal, although their neutrophils may be mistaken for immature cells which may cause mistreatment in a clinical setting. Homozygotes tend to have neutrophils with rounded nuclei that do have some functional problems.

A typical monoblast is about 12 to 20 µm in diameter, has a nuclear to cytoplasm ratio of 4:1 to 3:1, and, like most myeloid blasts, has a round to oval nucleus with fine chromatin structure. One to four nucleoli are usually visible. The nucleus can be central or eccentric and it can show evidence of indentation or folding. The cytoplasm is agranular, stains moderately to lightly basophilic, and often has an intensely stained periphery and a prominent perinuclear zone.

Smooth muscle tumor of uncertain malignant potential, abbreviated STUMP, is an uncommon tumor of the uterine smooth muscle that may behave like a benign tumor or a cancerous tumor.

This tumor should not be confused with the prostatic stromal tumor of uncertain malignant potential which may be abbreviated the same way ("STUMP").

The Bell criteria were developed to help categorize them and differentiate them from their main differential diagnoses, leiomyosarcoma and uterine leiomyoma.

Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. How it is handled depends primarily on the type of leukemia. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester.

In pathology, Anitschkow (or Anichkov) cells are often cells associated with rheumatic heart disease. Anitschkow cells are enlarged macrophages found within granulomas (called Aschoff bodies) associated with the disease.

The cells are also called caterpillar cells, as they have an ovoid nucleus and chromatin that is condensed toward the center of the nucleus in a wavy rod-like pattern that to some resembles a caterpillar. Larger Anitschkow cells may coalesce to form multinucleated Aschoff giant cells. Anitschkow cells were named after the Russian pathologist Nikolai Nikolajewitsch Anitschkow.

Squamous epithelial cells with nuclear changes resembling Anitschkow cells have also been observed in recurrent aphthous stomatitis, iron deficiency anemia, children receiving chemotherapy, as well as in healthy individuals.

Dysmelia can refer to

- missing (aplasia) limbs: amelia, oligodactyly, congenital amputation e.g. Tibial or Radial aplasia

- malformation of limbs: shortening (micromelia, rhizomelia or mesomelia), ectrodactyly, phocomelia, meromelia, syndactyly, brachydactyly, club foot

- too many limbs: polymelia, polydactyly, polysyndactyly

- others: Tetraamelia, hemimelia, Symbrachydactyly

In veterinary practice, nuclear sclerosis is a consistent finding in dogs greater than six years old. Nuclear sclerosis appears as a bilateral bluish-grey haziness at the nucleus, or center of the lens, caused by an increase in the refractive index of that part of the lens due to its increased density. It is often confused with cataracts. The condition is differentiated from a cataract by its appearance and by shining a penlight into the eye. With nuclear sclerosis, a reflection from the tapetum will be seen, while a cataract will block reflection.

There is no treatment for this condition currently.

HCCC consist of cells with abundant clear cytoplasm, arranged in cords, trabeculae or clusters in a hyalinized stroma. Nuclear pleomorphism is usually minimal and mitoses are infrequently seen.

Owing to their glycogen content, which explains the "clear" appearance under the microscope, tumour cells stain with PAS. Immunostains for S100 and smooth muscle actin (SMA) are typically negative, but positive for cytokeratins and epithelial membrane antigen (EMA).

HCCCs typically have a recurrent chromosomal translocation, t(12;22), involving the genes EWSR1 and ATF1. The same translocation is seen in clear cell sarcoma.

The histologic differential diagnosis includes mucoepidermoid carcinoma (clear cell variant), acinic cell carcinoma (clear cell variant), epithelial-myoepithelial carcinoma and metastatic clear cell carcinoma.

Restrictive dermopathy (RD) is caused either by the loss of the gene ZMPSTE24, which encodes a protein responsible for the cleavage of farnesylated prelamin A into mature non-farnesylated lamin, or by a mutation in the LMNA gene. This results in the accumulation of farnesyl-prelamin A at the nuclear membrane. Mechanistically, restrictive dermopathy is somewhat similar to Hutchinson–Gilford progeria syndrome (HGPS), a disease where the last step in lamin processing is hindered by a mutation that causes the loss of the ZMPSTE24 cleavage site in the lamin A gene.

Serous tumours are part of the surface epithelial-stromal tumour group of ovarian neoplasms, which derive from Mullerian epithelium.

They are common neoplasms with a strong tendency to bilaterality, and they account for 50% of all ovarian tumours.

Sixty percent are benign (cystadenoma), 10% are borderline and 30% are malignant (cystadenocarcinoma).

Is a benign dominantly inherited defect of terminal neutrophil differentiation as a result of mutations in the lamin B receptor gene. The characteristic leukocyte appearance was first reported in 1928 by Karel Pelger (1885-1931), a Dutch Hematologist, who described leukocytes with dumbbell-shaped bilobed nuclei, a reduced number of nuclear segments, and coarse clumping of the nuclear chromatin. In 1931, Gauthier Jean Huet (1879-1970), a Dutch Pediatrician, identified it as an inherited disorder.

It is a genetic disorder with an autosomal dominant inheritance pattern. Heterozygotes are clinically normal, although their neutrophils may be mistaken for immature cells, which may cause mistreatment in a clinical setting. Homozygotes tend to have neutrophils with rounded nuclei that do have some functional problems. Homozygous individuals inconsistently have skeletal anomalies such as post-axial polydactyly, short metacarpals, short upper limbs, short stature, or hyperkyphosis.

Identifying Pelger–Huët anomaly is important to differentiate from bandemia with a left-shifted peripheral blood smear and neutrophilic band forms and from an increase in young neutrophilic forms that can be observed in association with infection.

Most affected people have a stable clinical course but are often transfusion dependent.