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Testicular Cancer

The term ” testicular cancer “includes several types of tumors germ testis. It is a cancer rare (about 1% of all cancers) but in all countries with a cancer registry and / or testicular tumors , this cancer is increasing for several decades and is also the cancer most common cancer in men 15 to 35 years. Both testes are rarely affected simultaneously (1 to 2% of cases), and after recovery from testicular cancer, the risk of developing cancer in the other testicle is 2 to 5% in 25 years.

The chemotherapy by salts of platinum since the 1970s has dramatically changed the prognosis of this disease, with almost 80% of these cancers are now cured (all stages combined). The effectiveness of treatment depends on the type of cancer and quality of care, it justifies refer patients to specialized centers. The futurists in epidemiology , in Canada believe that “It is quite likely that the incidence of testicular cancer continues to increase (we do not know why) and that the incidence of mesothelioma and mortality associated with it does growing.
Types Of Testicular Cancer:  We distinguish two main types histopathological :
Seminomas (50% of cases) that might flow from an uncontrolled proliferation of cells in the germinal epithelium of the tubule . They have an appearance hypoechoic and hypovascular ultrasound scrotum ). They are radio-sensitive and their prognosis is good in 95% of cases, but requires monitoring of the patient. A leydigome is a seminoma-induced proliferation of Leydig cells . The spermatocytic seminoma represents less than 1% of testicular cancer and affects the elderly, with a very good prognosis if treated. Non-Seminomatous cancer , or tumors Germ cell (NSGT) whose prognosis is generally poorer. They present a heterogeneous appearance and vascular ultrasound.
  • The carcinoma embryonic.

  • The chorio-carcinoma.

  • The teratomas .

Testicular cancer is rare (about 1% of cancers, 2% in children), but its impact as that of prostate cancer increased steadily since the 1900s, and most significantly in countries with white skin from the years 1950 (increase by a factor of 3 to 5 years from 1950 to 2000). Data is lacking for many developing countries, but this cancer appears more common among black populations in Africa and among Asians than among the white-skinned (the difference could be genetic and / or related to the environment, food or certain cultural traits). He became the tumor most common in young men, at least in rich countries to dominant white population.
In Europe:  In all countries where it is followed by a record cancer, except for reasons unexplained in Finland, an increased incidence of cancer was confirmed in early 1990 in Europe. In Europe, Denmark seems the most affected (4 times more than the nearby Finland to be among the least affected, and where the quality of the sperm looks best). In Europe, it has a west-east gradient in regions Baltic and North-South gradient in Western Europe. The record is Norwegian (prevalence increasing and two times higher than in Sweden, she even more affected than Finland (Swedish-Norwegian Study (ongoing from June 2008 to June 2015) aims to investigate possible genetic factors). Its incidence has doubled in many countries, including in France from 1970 to 2000 in all regions where epidemiological monitoring was. The French urologists B. Boillot and R. Moalic estimate that the number of testicular tumors pre- pubertal increases in France for several decades (like those of adults). The impact of these two cancers (pre-and post-pubertal) combined increases of 3.4% per year for 30 years (while the incidence of tumors Non seminomatous decreased in adults over 55 years);
The steady growth and documented since the 1950s the incidence of testicular cancer (TC) in developed countries experienced a temporary exception: The incidence appears to have been much slower for men born during the Second World War or just before or just after, a Norwegian study found published in 2005. This retrospective study has shown – not to draw any definitive conclusions – that, given the available data, the average weight of the mother at delivery was (between 1935 and 1955) correlated with the average risk of testicular cancer for future boys born at the same time. One explanation could be that insulin levels increased with maternal weight, which reduces the rate of hormone-binding globulin , and consequently makes it more bioavailable estrogen to placental transfer. They were then in the male fetus to endocrine disruptor action.
Maternal weight might increase the risk of testicular cancer or hormonal disorders in children and males exposed in utero to an abnormally high dose of estrogen during the first trimester of pregnancy.
Many clues suggest, therefore, for environmental causes. 2002 new cases were registered in 2005 and its incidence has increased by 2.5% over the period 1980-2005 and especially for childhood cancer, exposure to endocrine disruptors or carcinogens in utero . In this case the cancer is one of the testicular dysgenesis syndrome
Incidence: It occurs most often between 20 and 40, but there are three peaks in frequency of testicular cancer:
In the first years of life (before age 5) and puberty . In France, 1-2% of solid tumors of early childhood cancers are testicular The young child is 5% of testicular cancer if it does not include the period known as adolescence in childhood, and 0.5 % if we include this period. These tumors are increasing a little slower than in adults, but significantly (+ 1.3% per year), which is an index of common cause, probably one or more point (s) cancer (s) Development testes. Unlike testicular tumors in adults who require surgical removal of the testicle (orchiectomy) 29 to 48% of prepubertal testicular tumors are malignant and allow a less conservative surgery . A risk factor is associated with cryptorchidism (this risk is associated with cancer in adults than that of the prepubescent child); after puberty , are the most frequent cases (maximum frequency between 25 and 35). after 60 years (more rarely)

Risk factors: Some are clearly identified (but not explained). They are:

  • the cryptorchidism , which would increase the risk of developing testicular cancer by 3.6 to 5.2 according to studies, the gold cryptorchidism and hypospadias are significantly more frequent in Europe and the USA: + 65 to 77% during recent decades in the United Kingdom , for cryptorchidism, and shypospadias doubling in 10 years (1970 to 1980) United States.
  • A study on the risk factors for 131 cases of testicular cancer (in men under 40 years) confirmed a risk (here multiplied by 5) in case of cryptorchidism at birth, but she has identified two new risk factors: six mothers of patients had received hormone treatment during pregnancy (cons one for mothers dy control group), eight mothers and two mothers of patients against the control group had reported nausea as excessive complication of pregnancy. The authors believe that these three factors reflect the fact that a relative excess of certain hormones (estrogen in particular) at the time of testicular differentiation could promote carcinogenesis future of these cells;
  • the contralateral cancers ;
  • the Klinefelter syndrome , which is characterized by multiple chromosomal abnormalities resulted in a morphology eunuchoid , gynecomastia and small testes in adults or adolescents;
  • the testicular atrophy or mumps orchitis (rare complication of mumps).
  • family history (risk 6 to 10 times higher for a brother with this same cancer). Family history of cancer are also a risk factor;
  • Infertility;
  • smoking ;
  • heavy weight of the mother during pregnancy;
  • exposure in utero to diethylstilbestrol or other endocrine disrupters or hormone treatment of the mother;
  • exposure to certain cosmetics is also a risk factor recently suggested (endocrine-disrupting effect) …

Symptoms:

  • The discovery mode is the most frequently increase the volume of a stock because of an intra-testicular mass. The mass is usually painless.
  • Sometimes the diagnosis is made ​​on an abdominal mass or a sign in relation to metastasis brain ( seizures , impaired consciousness, and headache ).
  • Secretion of Beta HCG by the injury may cause swelling of mammary glands ( gynecomastia ) is also present in humans.

Diagnosis: The diagnosis of cancer is increased after removal of the testicle essential. We distinguish among different types of testicular cancer and seminomas pure other tumors. Seminomas have a better prognosis. The presence of metastases at diagnosis decreases the chances of recovery. The biopsy of intra-testicular mass is not used in the diagnostic procedure; Upon discovery of a mass testis , the first review is proposed ultrasound of the testicles. If it confirms the suspicious nature of the injury, the testicle may be necessary. This surgical procedure, known as orchiectomy , is practiced through groin . It aims to prevent the spread of cancer cells and metastasis. When the diagnosis of cancer is confirmed, a staging is required to search for possible metastatic lymph node or visceral. The assessment will include a scan of the thorax , abdomen and pelvis and in some cases a CT or MRI brain. The measurement of tumor markers such as HCG , AFP and LDH are also part of the staging of the disease.

Treatment: It is based on surgery chemotherapy and radiotherapy and is now well codified, with the aim of healing with the least possible sequelae. If the use of cisplatin in the 1970s has transformed the prognosis of testicular cancer, it remains a serious illness warranting extreme rigor in its management. The best results in terms of healing are provided by specialized medical teams. The therapeutic strategy is defined in terms of initial assessment and disease progression during treatment (change of tumor markers, residual masses). The goal of treatment, side effects in the short and long term and the importance of monitoring should be clearly explained to the patient to ensure its full cooperation.

Chemotherapy: Different protocols (i.e., the combination of different drugs given in precise doses, according to a particular chronology) have shown for years to be effective in the treatment of this cancer. Treatments equally effective, but side effects increasingly appeared reduced. The protocols are designated by the initials of the products used: BEP = Bleomycin, Etoposide, Cisplatin (P for platinum).

Radiotherapy: Irradiation is used to treat advanced seminomas, in one session of radiation a day for several weeks. These rays are the lymphatic channels from the groin area and leading to the lymph nodes along the aorta . The patient should be monitored over time because there is an increased risk of second cancer induced by radiotherapy. And it seems that although the post-operative radiation increases the risk of second cancer as non-seminomatous cancers (usually not treated with radiation) are less followed by a second cancer.

Surgery: The removal of the testicle, The removal of the affected testicle ( orchiectomy ) is the first time of treatment. It can be done under general anesthesia, spinal anesthesia or regional anesthesia (block ilio-face) by an inguinal incision (at the groin) and not through the scrotum . Prosthesis in silicone for aesthetic purposes may be raised if the patient wants. The stage of cancer is explained by analyzing pathological testis removed and thoraco-abdominopelvic. Falling rates of markers to confirm the absence of any remaining tumor. Depending on the type and stage of cancer, further treatment may be proposed (radiotherapy or chemotherapy) or para-aortic dissection, or simple monitoring.

Lymph Node Dissection: This is – after an initial chemotherapy – or purpose of diagnosis (without tumor markers) to remove (by a midline incision in the abdomen), abdominal lymph nodes along the aorta, which arrive in the lymph from the testicles.

The Removal Of Residual Masses: If lymph node or visceral metastases are detected at diagnosis, the patient is often treated by three or four courses of chemotherapy and a new scan is performed four weeks after the last treatment. If the scanner finds residual masses, removal of these residual masses is generally performed by a surgeon.

 
 
 
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