Based on the site of origin and the usual stage of presentation, testicular cancer can be classified into a number of distinct neoplasms. Even though a variety of types of cells in the testicle can become cancerous, germline cell-derived tumors account for the great majority of testicular cancers.
The proportional distribution relies on age: whereas practically all cancers in young adult men are germ cell tumors, a substantial number of lymphomas and secondary carcinomas can be predicted in individuals above seventy years old. In other terms, as detailed in greater detail later in the text, germ cell carcinoma can affect people of all ages, although young males account for more than ninety percent of cases, and this subgroup is the focus of this chapter.
Seminomatous, Leydig, Sertoli, non-seminomatous, choriocarcinoma, embryonal, yolk-sac derivatives, and teratoma are the several types of testicular malignancies. Seminoma and non-seminomatous tumors are commonly lumped together as germ cell tumors, and they’re notable for being more chemotherapy-resistant than the other forms.
Seminoma is one of the most curable cancers, accounting for around a third of all testicle germ cell tumors and having a survival rate of ninety-eight percent to ninety-nine percent in early-stage illness. While the overall prevalence of testicles cancer is modest, accounting for approximately 1% to 2% of all male cancers, it continues to be a common malignancy among men aged 15 to 35.
Epidemiology
GCTs (germ cell cancers of the testicles) are the most prevalent mass malignancies in young men (age 15 to 45). It is ten times more frequent in northern European males and 5 times highly frequent in all White males than it is in the general population. Seminoma’s overall prevalence rises as people get older.
Anatomy
Pathophysiology
The germ cells epithelium of the seminiferous tubules gives rise to testicle seminoma. The proliferation of underdeveloped spermatogonia is assumed to be the cause of the disease. The pathogenesis of carcinoma-in-situ is most likely to be caused by stalled gonocyte development, which results in the retention of embryonic characteristics and enhanced genomic instability.
Acquisition of the short arm of chromosome 12, Isochromosome i(12p), probably involving KRAS2 and potentially NANOG, is linked to the transition from precursor lesion to invasive malignancy (pseudogenes). The specific mechanism has yet to be discovered. Seminoma, on the other hand, has a higher frequency of isozymes 7, 15, 19, and X.
Etiology
Seminoma has a cause that is unclear. The most recent notion is that atmospheric endocrine troublemakers have estrogen-mimicking and antiandrogenic effects, causing the gonocyte to develop slowly. During a brief period of intrauterine development, the illness most likely develops as carcinoma in situ. TDS (Testicular dysgenesis syndrome (is a generally established theoretical notion.
Testicular dysgenesis syndrome classifies germ cell cancers, hypospadias, poor spermatogenesis, and cryptorchism as a category based on studies that share several potential risks that are thought to start from fetal life. Over the last few decades, there has been an upsurge in the number of cases documented.
Approximately ten percent of all germ cell cancer patients have a personal background of cryptorchidism. When compared to a regular testicle, a person with an unruptured testicle seems to be at least four times more likely to develop cancer. This risk rises with age at the time of repair. Trisomy 21 patients are fifty times more likely to get testicular cancer.
Common inherited testicular cancer has been linked to recessive mutation inheritance. The HLA class II allele DRB1*0410 was associated with this connection in a Japanese population. It appeared to be linked to a homozygous allele of the GSTP1 gene, and the proliferation of (CAG)n repeats in a UK investigation.
Genetics
Prognostic Factors
The Testicular Cancer Society states: “The rate of survival is in excess of ninety-five percent. The survival probability is ninety-nine percent if identified early and the cancer is contained to the testicle.
The survival rate is ninety-six percent if cancer has spread to local lymph nodes, and maybe there is distant metastasis, the survival percentage is approximate 70%.”
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK448137/
https://www.ncbi.nlm.nih.gov/books/NBK563159/
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Based on the site of origin and the usual stage of presentation, testicular cancer can be classified into a number of distinct neoplasms. Even though a variety of types of cells in the testicle can become cancerous, germline cell-derived tumors account for the great majority of testicular cancers.
The proportional distribution relies on age: whereas practically all cancers in young adult men are germ cell tumors, a substantial number of lymphomas and secondary carcinomas can be predicted in individuals above seventy years old. In other terms, as detailed in greater detail later in the text, germ cell carcinoma can affect people of all ages, although young males account for more than ninety percent of cases, and this subgroup is the focus of this chapter.
Seminomatous, Leydig, Sertoli, non-seminomatous, choriocarcinoma, embryonal, yolk-sac derivatives, and teratoma are the several types of testicular malignancies. Seminoma and non-seminomatous tumors are commonly lumped together as germ cell tumors, and they’re notable for being more chemotherapy-resistant than the other forms.
Seminoma is one of the most curable cancers, accounting for around a third of all testicle germ cell tumors and having a survival rate of ninety-eight percent to ninety-nine percent in early-stage illness. While the overall prevalence of testicles cancer is modest, accounting for approximately 1% to 2% of all male cancers, it continues to be a common malignancy among men aged 15 to 35.
GCTs (germ cell cancers of the testicles) are the most prevalent mass malignancies in young men (age 15 to 45). It is ten times more frequent in northern European males and 5 times highly frequent in all White males than it is in the general population. Seminoma’s overall prevalence rises as people get older.
The germ cells epithelium of the seminiferous tubules gives rise to testicle seminoma. The proliferation of underdeveloped spermatogonia is assumed to be the cause of the disease. The pathogenesis of carcinoma-in-situ is most likely to be caused by stalled gonocyte development, which results in the retention of embryonic characteristics and enhanced genomic instability.
Acquisition of the short arm of chromosome 12, Isochromosome i(12p), probably involving KRAS2 and potentially NANOG, is linked to the transition from precursor lesion to invasive malignancy (pseudogenes). The specific mechanism has yet to be discovered. Seminoma, on the other hand, has a higher frequency of isozymes 7, 15, 19, and X.
Seminoma has a cause that is unclear. The most recent notion is that atmospheric endocrine troublemakers have estrogen-mimicking and antiandrogenic effects, causing the gonocyte to develop slowly. During a brief period of intrauterine development, the illness most likely develops as carcinoma in situ. TDS (Testicular dysgenesis syndrome (is a generally established theoretical notion.
Testicular dysgenesis syndrome classifies germ cell cancers, hypospadias, poor spermatogenesis, and cryptorchism as a category based on studies that share several potential risks that are thought to start from fetal life. Over the last few decades, there has been an upsurge in the number of cases documented.
Approximately ten percent of all germ cell cancer patients have a personal background of cryptorchidism. When compared to a regular testicle, a person with an unruptured testicle seems to be at least four times more likely to develop cancer. This risk rises with age at the time of repair. Trisomy 21 patients are fifty times more likely to get testicular cancer.
Common inherited testicular cancer has been linked to recessive mutation inheritance. The HLA class II allele DRB1*0410 was associated with this connection in a Japanese population. It appeared to be linked to a homozygous allele of the GSTP1 gene, and the proliferation of (CAG)n repeats in a UK investigation.
The Testicular Cancer Society states: “The rate of survival is in excess of ninety-five percent. The survival probability is ninety-nine percent if identified early and the cancer is contained to the testicle.
The survival rate is ninety-six percent if cancer has spread to local lymph nodes, and maybe there is distant metastasis, the survival percentage is approximate 70%.”
https://www.ncbi.nlm.nih.gov/books/NBK448137/
https://www.ncbi.nlm.nih.gov/books/NBK563159/
medtigo
Testicular Carcinoma : Seminoma
Updated :
June 17, 2022
Based on the site of origin and the usual stage of presentation, testicular cancer can be classified into a number of distinct neoplasms. Even though a variety of types of cells in the testicle can become cancerous, germline cell-derived tumors account for the great majority of testicular cancers.
The proportional distribution relies on age: whereas practically all cancers in young adult men are germ cell tumors, a substantial number of lymphomas and secondary carcinomas can be predicted in individuals above seventy years old. In other terms, as detailed in greater detail later in the text, germ cell carcinoma can affect people of all ages, although young males account for more than ninety percent of cases, and this subgroup is the focus of this chapter.
Seminomatous, Leydig, Sertoli, non-seminomatous, choriocarcinoma, embryonal, yolk-sac derivatives, and teratoma are the several types of testicular malignancies. Seminoma and non-seminomatous tumors are commonly lumped together as germ cell tumors, and they’re notable for being more chemotherapy-resistant than the other forms.
Seminoma is one of the most curable cancers, accounting for around a third of all testicle germ cell tumors and having a survival rate of ninety-eight percent to ninety-nine percent in early-stage illness. While the overall prevalence of testicles cancer is modest, accounting for approximately 1% to 2% of all male cancers, it continues to be a common malignancy among men aged 15 to 35.
GCTs (germ cell cancers of the testicles) are the most prevalent mass malignancies in young men (age 15 to 45). It is ten times more frequent in northern European males and 5 times highly frequent in all White males than it is in the general population. Seminoma’s overall prevalence rises as people get older.
The germ cells epithelium of the seminiferous tubules gives rise to testicle seminoma. The proliferation of underdeveloped spermatogonia is assumed to be the cause of the disease. The pathogenesis of carcinoma-in-situ is most likely to be caused by stalled gonocyte development, which results in the retention of embryonic characteristics and enhanced genomic instability.
Acquisition of the short arm of chromosome 12, Isochromosome i(12p), probably involving KRAS2 and potentially NANOG, is linked to the transition from precursor lesion to invasive malignancy (pseudogenes). The specific mechanism has yet to be discovered. Seminoma, on the other hand, has a higher frequency of isozymes 7, 15, 19, and X.
Seminoma has a cause that is unclear. The most recent notion is that atmospheric endocrine troublemakers have estrogen-mimicking and antiandrogenic effects, causing the gonocyte to develop slowly. During a brief period of intrauterine development, the illness most likely develops as carcinoma in situ. TDS (Testicular dysgenesis syndrome (is a generally established theoretical notion.
Testicular dysgenesis syndrome classifies germ cell cancers, hypospadias, poor spermatogenesis, and cryptorchism as a category based on studies that share several potential risks that are thought to start from fetal life. Over the last few decades, there has been an upsurge in the number of cases documented.
Approximately ten percent of all germ cell cancer patients have a personal background of cryptorchidism. When compared to a regular testicle, a person with an unruptured testicle seems to be at least four times more likely to develop cancer. This risk rises with age at the time of repair. Trisomy 21 patients are fifty times more likely to get testicular cancer.
Common inherited testicular cancer has been linked to recessive mutation inheritance. The HLA class II allele DRB1*0410 was associated with this connection in a Japanese population. It appeared to be linked to a homozygous allele of the GSTP1 gene, and the proliferation of (CAG)n repeats in a UK investigation.
The Testicular Cancer Society states: “The rate of survival is in excess of ninety-five percent. The survival probability is ninety-nine percent if identified early and the cancer is contained to the testicle.
The survival rate is ninety-six percent if cancer has spread to local lymph nodes, and maybe there is distant metastasis, the survival percentage is approximate 70%.”
https://www.ncbi.nlm.nih.gov/books/NBK448137/
https://www.ncbi.nlm.nih.gov/books/NBK563159/
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