The cause of neuroblastoma is not well understood. The great majority of cases are sporadic and non-familial. About 1–2% of cases run in families and have been linked to specific gene mutations. Familial neuroblastoma in some cases is caused by rare germline mutations in the anaplastic lymphoma kinase (ALK) gene. Germline mutations in the PHOX2A or KIF1B gene have been implicated in familial neuroblastoma as well. Neuroblastoma is also a feature of neurofibromatosis type 1 and the Beckwith-Wiedemann syndrome.

MYCN oncogene amplification within the tumor is a common finding in neuroblastoma. The degree of amplification shows a bimodal distribution: either 3- to 10-fold, or 100- to 300-fold. The presence of this mutation is highly correlated to advanced stages of disease.

Duplicated segments of the LMO1 gene within neuroblastoma tumor cells have been shown to increase the risk of developing an aggressive form of the cancer.

Neuroblastoma has been linked to copy-number variation within the NBPF10 gene, which results in the 1q21.1 deletion syndrome or 1q21.1 duplication syndrome.

Several risk factors have been proposed and are the subject of ongoing research. Due to characteristic early onset many studies have focused on parental factors around conception and during gestation. Factors investigated have included occupation (i.e. exposure to chemicals in specific industries), smoking, alcohol consumption, use of medicinal drugs during pregnancy and birth factors; however, results have been inconclusive.

Other studies have examined possible links with atopy and exposure to infection early in life, use of hormones and fertility drugs, and maternal use of hair dye.

Based on a series of 493 neuroblastoma samples, it has been reported that overall genomic pattern, as tested by array-based karyotyping, is a predictor of outcome in neuroblastoma:

- Tumors presenting exclusively with whole chromosome copy number changes were associated with excellent survival.

- Tumors presenting with any kind of segmental chromosome copy number changes were associated with a high risk of relapse.

- Within tumors showing segmental alterations, additional independent predictors of decreased overall survival were N-myc amplification, 1p and 11q deletions, and 1q gain.

Earlier publications categorized neuroblastomas into three major subtypes based on cytogenetic profiles:

- Subtype 1: favorable neuroblastoma with near triploidy and a predominance of numerical gains and losses, mostly representing non-metastatic NB stages 1, 2 and 4S.

- Subtypes 2A and 2B: found in unfavorable widespread neuroblastoma, stages 3 and 4, with 11q loss and 17q gain without N-myc amplification (subtype 2A) or with N-myc amplification often together with 1p deletions and 17q gain (subtype 2B).

Virtual karyotyping can be performed on fresh or paraffin-embedded tumors to assess copy number at these loci. SNP array virtual karyotyping is preferred for tumor samples, including neuroblastomas, because they can detect copy neutral loss of heterozygosity (acquired uniparental disomy). Copy neutral LOH can be biologically equivalent to a deletion and has been detected at key loci in neuroblastoma. ArrayCGH, FISH, or conventional cytogenetics cannot detect copy neutral LOH.

Most ganglioneuromas are noncancerous, thus expected outcome is usually good. However, a ganglioneuroma may become cancerous and spread to other areas, or it may regrow after removal.

If the tumor has been present for a long time and has pressed on the spinal cord or caused other symptoms, it may have caused irreversible damage that cannot be corrected with the surgical removal of the tumor. Compression of the spinal cord may result in paralysis, especially if the cause is not detected promptly.

There are no known risk factors for ganglioneuromas. However, the tumors may be associated with some genetic problems, such as neurofibromatosis type 1.

Ganglioneuroblastoma is a variant of neuroblastoma that is surrounded by ganglion cells.

It can be difficult to diagnose.

Nodular ganglioneuroblastoma can be divided by prognosis.

Ectomesenchymoma is a rare, fast-growing tumor of the nervous system or soft tissue that occurs mainly in children, although cases have been reported in patients up to age 60. Ectomesenchymomas may form in the head and neck, abdomen, perineum, scrotum, or limbs. Also called malignant ectomesenchymoma.

Malignant ectomesenchymoma (MEM) is a rare tumor of soft tissues or the CNS, which is composed of both neuroectodermal elements [represented by ganglion cells and/or well-differentiated or poorly differentiated neuroblastic cells such as ganglioneuroma, ganglioneuroblastoma, neuroblastoma, peripheral primitive neuroectodermal tumors – PNET] and one or more mesenchymal neoplastic elements, usually rhabdomyosarcoma . The most accepted theory suggests that this tumor arises from remnants of migratory neural crest cells and thus from the ectomesenchyme.

There are no known risk factors that have been identified specific to the disease. The tumor appears to arise from the primitive cells of childhood, and is considered a childhood cancer.

Research has indicated that there is a chimeric relationship between desmoplastic small-round-cell tumor (DSRCT) and Wilms' tumor and Ewing's sarcoma. Together with neuroblastoma and non-Hodgkin's lymphoma, they form the small cell tumors.

DSRCT is associated with a unique chromosomal translocation t(11;22)(p13:q12) resulting in an EWS/WT1 transcript that is diagnostic of this tumor. This transcript codes for a protein that acts as a transcriptional activator that fails to suppress tumor growth.

The EWS/WT1 translocation product targets ENT4. ENT4 is also known as PMAT.

The prognosis for DSRCT remains poor. Prognosis depends upon the stage of the cancer. Because the disease can be misdiagnosed or remain undetected, tumors frequently grow large within the abdomen and metastasize or seed to other parts of the body.

There is no known organ or area of origin. DSRCT can metastasize through lymph nodes or the blood stream. Sites of metastasis include the spleen, diaphragm, liver, large and small intestine, lungs, central nervous system, bones, uterus, bladder, genitals, abdominal cavity, and the brain.

A multi-modality approach of high-dose chemotherapy, aggressive surgical resection, radiation, and stem cell rescue improves survival for some patients. Reports have indicated that patients will initially respond to first line chemotherapy and treatment but that relapse is common.

Some patients in remission or with inoperable tumor seem to benefit from long term low dose chemotherapy, turning DSRCT into a chronic disease.

The tumor largely affects children under 15 years of age and about 20% only are found in adults with nearly 60% involving males and 40% females (1). The most frequent locations are head and neck (orbit and nasopharynx), central nervous system, abdomen and retroperitoneum, pelvis, perineum, scrotum and prostate(1). Clinical symptoms are not specific and usually caused by local tumor compression and infiltration.

It is contained within the "neuroblastic tumors" group, which includes:

- Ganglioneuroma (benign)

- Ganglioneuroblastoma (intermediate).

- Neuroblastoma (aggressive)

Embryonal teratomas most commonly occur in the sacrococcygeal region: sacrococcygeal teratoma is the single most common tumor found in newly born humans.

Of teratomas on the skull sutures, approximately 50% are found in or adjacent to the orbit. Limbal dermoid is a choristoma, not a teratoma.

Teratoma qualifies as a rare disease, but is not extremely rare. Sacrococcygeal teratoma alone is diagnosed at birth in one out of 40,000 humans. Given the current human population and birth-rate, this equals five per day or 1800 per year. Add to that number sacrococcygeal teratomas diagnosed later in life, and teratomas in other locales, and the incidence approaches ten thousand new diagnoses of teratoma per year.

Smoking and alcohol abuse as the major risk factors. Viral causes has recently been taken under consideration as one of the risk factors. Viruses such as Epstein-Barr virus (EBV) (majorly involved in causing nasopharyngeal carcinoma) and human papilloma virus are included in this category. Chewing of betel nut ("Areca catechu") quid has been directly associated to cause oral cancers. It has also been stated under the FDA poisonous plant data base by the U.S Food and Drug Administration

An unbalanced diet, deficit in fruits and vegetables has shown to increase the risk of cancer.

In light of the ethical issues surrounding the source of human stem cells, teratomas are being looked at as an alternative source for research because they lack the potential to grow into functional human beings.

Tonsillar carcinoma can be either HPV related or HPV unrelated. It is shown that cases which are HPV positive have a better prognosis than those with HPV negative oropharyngeal cancer.

It has been observed that HPV18 is the most prevalent type in Small cell cervical cancer.

Like other types of cervical cancer it seems to be associated with high-risk (e.g. 16, 18, 31) HPV Infection.

Cigarette smoking, both active and passive, increases the risk of cervical cancer. Among HPV-infected women, current and former smokers have roughly two to three times the incidence of invasive cancer. Passive smoking is also associated with increased risk, but to a lesser extent.

Smoking has also been linked to the development of cervical cancer. Smoking can increase the risk in women a few different ways, which can be by direct and indirect methods of inducing cervical cancer. A direct way of contracting this cancer is a smoker has a higher chance of CIN3 occurring which has the potential of forming cervical cancer. When CIN3 lesions lead to cancer, most of them have the assistance of the HPV virus, but that is not always the case, which is why it can be considered a direct link to cervical cancer. Heavy smoking and long-term smoking seem to have more of a risk of getting the CIN3 lesions than lighter smoking or not smoking at all. Although smoking has been linked to cervical cancer, it aids in the development of HPV which is the leading cause of this type of cancer. Also, not only does it aid in the development of HPV, but also if the woman is already HPV-positive, she is at an even greater likelihood of contracting cervical cancer.

The differential diagnosis of serous carcinoma not otherwise specified includes:

- Ovarian serous carcinoma, a type of ovarian cancer.

- Uterine serous carcinoma, also known as "uterine papillary serous carcinoma", a type of uterine cancer.

- Fallopian tube serous carcinoma, a type of uterine tube cancer.

- Cervical serous carcinoma, a rare type of cervical cancer.

- Primary peritoneal serous carcinoma, a very rare cancer that arise from the peritoneum.

There has been the suggestion that the above diagnoses really represent one entity.

Long-term use of oral contraceptives is associated with increased risk of cervical cancer. Women who have used oral contraceptives for 5 to 9 years have about three times the incidence of invasive cancer, and those who used them for 10 years or longer have about four times the risk.

Cervical cancers can recur with symptoms of vaginal bleeding and/or discharge, pelvic pain, pain in the back and legs, leg swelling (edema), chronic cough and weight loss. It can recur in the vagina, pelvis, lymph nodes, lung, or liver. “If radiation was not given previously, recurrences that are confined to the pelvis may be treated with external beam radiation with chemotherapy and intracavitary or interstitial radiation therapy. If radiation therapy was already given, the only option is the removal of the vagina, uterus, and the bladder and/or rectum with the creation of an artificial bladder-a pelvic exenteration. The five-year survival rate after a pelvic exenteration is about 50 percent.” (womenscancercenter.com) Chemotherapy is useful in women with recurrent tumors which cannot be removed surgically or in women with metastatic diseases. Chances of survival of chemotherapy, if diagnosed in early stage, is grater than 50%.

Between 250,000 and 1 million American women are diagnosed with CIN annually. Women can develop CIN at any age, however women generally develop it between the ages of 25 to 35.

It used to be thought that cases of CIN progressed through these stages toward cancer in a linear fashion.

However most CIN spontaneously regress. Left untreated, about 70% of CIN-1 will regress within one year, and 90% will regress within two years. About 50% of CIN 2 will regress within 2 years without treatment.

Progression to cervical carcinoma in situ (CIS) occurs in approximately 11% of CIN1 and 22% of CIN2. Progression to invasive cancer occurs in approximately 1% of CIN1, 5% in CIN2 and at least 12% in CIN3.

Progression to cancer typically takes 15 (3 to 40) years. Also, evidence suggests that cancer can occur without first detectably progressing through these stages and that a high grade intraepithelial neoplasia can occur without first existing as a lower grade.

It is thought that the higher risk HPV infections, have the ability to inactivate tumor suppressor genes such as the p53 gene and the RB gene, thus allowing the infected cells to grow unchecked and accumulate successive mutations, eventually leading to cancer.

Treatment does not affect the chances of getting pregnant but does increase the risk of second trimester miscarriages.

Villoglandular adenocarcinoma of the cervix, also villoglandular papillary adenocarcinoma, papillary villoglandular adenocarcinoma and well-differentiated villoglandular adenocarcinoma, abbreviated VGA, is a rare type of cervical cancer that, in relation to other cervical cancers, is typically found in younger women and has a better prognosis.

A similar lesion, "villoglandular adenocarcinoma of the endometrium", may arise from the inner lining of the uterus, the endometrium.

Cytologic features of serous carcinoma are:

- Marked intragroup nuclear pleomorphism.

- Macronucleoli.

- "Knobby" group borders (in large groups).

- Hydropic vacuoles.

Symptoms of serous carcinoma may include:

- Discomfort/pain or bloating in abdomen

- Frequent urination

- Weight loss

The treatment is dependent on the stage. As the prognosis of this tumour is usually good, fertility sparing approaches (conization, cervicectomy) may be viable treatment options.

Studies have shown that obesity of the mother increases the risk of neural tube disorders such as iniencephaly by 1.7 fold while severe obesity increases the risk by over 3 fold.