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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2915_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Library of Congress Cataloging-in-Publication Data
- •Contents
- •Preface
- •5. Diagnostic and Evaluation
- •6. Pathology
- •7. Staging
- •8. Routes of Spread
- •9. Prognostic Factors
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk factors
- •3. Anatomy
- •4. Clinical Features
- •10. Treatment
- •11. Treatment Technique
- •Conclusion
- •Abstract
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnostic and Evaluation
- •6. Pathology
- •7. Routes of Spread
- •8. Staging
- •9. Prognostic factors
- •10. Treatment
- •11. Radiotherapy Techniques
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Routes of Spread
- •8. Prognostic Factors
- •9. Treatment
- •10. Radiotherapy Technique
- •Conclusion
- •Section - II. Head and Neck Cancer
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Routes of Spread
- •8. Staging
- •9. Prognostic Factors
- •10. Treatment by Site
- •11. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Routes of Spread
- •8. Staging
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Routes of Spread
- •8. Staging
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Techniques
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Staging
- •8. Routes of Spread
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Techniques
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Pathology
- •6. Diagnostic and Evaluation
- •7. Staging
- •8. Routes of Spread
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Pathology
- •6. Diagnostic and Evaluation
- •7. Staging
- •8. Routes of Spread
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Technique
- •Conclusion
- •Section - III. Genitourinary Cancer
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Anatomy
- •3. Risk Factors
- •4. Pathology
- •5. Diagnosis and Evaluation
- •6. Staging
- •7. Routes of Spread
- •8. Prognostic Factors
- •9. Treatment
- •10. Radiotherapy Technique
- •Conclusion
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Routes of Spread and Recurrence
- •8. Staging
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Pathology
- •7. Staging
- •8. Routes of Spread
- •9. Prognostic Factors
- •10. Treatment
- •11. Radiotherapy Techniques
- •Conclusion
- •Section - IV. Hematology Cancer
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Pathology
- •6. Diagnostic and Evaluation
- •7. Staging
- •8. Prognostic Factors
- •9. Treatment
- •10. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Anatomy
- •4. Clinical Features
- •5. Pathology
- •6. Diagnostic and Evaluation
- •7. Staging
- •8. Prognostic Factors
- •9. Treatment
- •10. Radiotherapy Techniques
- •Conclusion
- •Introduction
- •1. Epidemiology
- •2. Risk Factors
- •3. Clinical Features
- •4. Diagnostic and Evaluation
- •5. Staging
- •6. Prognostic Factors
- •7. Treatment
- •8. Radiotherapy Techniques
- •Conclusion
- •Section - V. Palliative Radiotherapy
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Pathology
- •3. Clinical Features
- •4. Diagnosis and Evaluation
- •5. Prognostic Factors
- •6. Treatment
- •7. Radiotherapy Technique
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Anatomy
- •3. Clinical Features
- •4. Pathology
- •5. Diagnosis and Evaluation
- •6. Prognostic Factors
- •7. Treatment
- •8. Radiotherapy Techniques
- •Conclusion
- •Abstract
- •Introduction
- •1. Epidemiology
- •2. Anatomy
- •3. Pathology
- •4. Clinical Features
- •5. Diagnosis and Evaluation
- •6. Prognostic Factors
- •7. Radiotherapy Techniques
- •Conclusion
- •Index

Bladder Cancer
181
normal bladder function and minimizing side effects. One such advance, intensity-modulated
radiation therapy, allows the dose to the primary bladder tumor and pelvic lymph nodes to be
escalated because of its tight conformation to the target volume (figure-5), with the
expectation of improved tumor control with equal or lesser toxicity to normal tissues. The
narrow planning target margins and steep dose gradients emphasize the importance of daily
online imaging to ensure accurate treatment delivery.
Figure 5. Comparision between the isodose lines distribution of IMRT and 3DCRT evidencing a dose
reduction in the normal tissue around the target.
Conclusion
• Bladder cancer is a relatively common genitourinary tumors and early detection and
investigation is extremely important.
• Nonmuscle invasive bladder cancer can be stratified into low, intermediate and high
risk categories and patients require endoscopic resection followed by adjuvant
intravesical treatment and careful surveillance.
• Muscle invasive tumor needs of extirpative surgery in patients with good
performance status, and for these patients, there is a role for neoadjuvant chemotherapy.
• Multimodal treatment with transuretheral resection and chemoradiation is an
alternative for patients who refuse surgery or want preserve the organ.
• After surgery patients with extravesical disease (pT3 or above) and/or lymph node
metastasis may benefit from adjuvant chemotherapy.


Testicular Cancer
Primary testicular tumors are the most common solid malignant tumor in
younger men with less than 35 years in United States.
There are several risk factors associated with developing of testicular neoplasia.
However, criptorchdism is the most importante factor.
Testicular tumors typically present as a nodule or painless swelling of one
testicle, which may be noted incidentally by the patient.
The evaluation of a testicular mass begins with an ultrasonographic exam.
Testicular ultrasonography is a sensitive and specific test that can differentiate
between a testicular neoplasm and nonmalignant processes such as hydrocele,
testicular torsion, spermatocele, varicocele, and epididymitis.
Geminative cell tumors (GCT) account for about 95 % of testicular tumors.
Among the GCTs pure seminomas account for approximately 50 % of all
testicular GCTs.
Chapter 12
Abstract
orchiectomy to establish the histologic diagnosis and definitive treatment.
Active surveillance, adjuvant limited field radiation therapy (RT), or a short
course of adjuvant single agente carboplatin can be offered after orchiectomy for
seminoma clinical stage I.
Low-dose RT to the paraaortic lymph nodes and superior ipsilateral pelvis (20
Gy) followed by a small boost to the involved nodal áreas (25 Gy) is
recommended for patients with stage IIA/IIB seminoma.
Cisplatin-based polychemotherapy is an option for patients in whom RT is not
feasible or for patients with bulky stage IIB/IIC seminoma.
Introduction
Primary testicular tumors are the most common solid malignant tumor in younger men
with less than 35 years in United States. Approximately 9,000 new cases have been diagnosed
in United States every year, and only about 350 to 400 deaths have occurred annually. In the

Gustavo Arruda Viani
184
past, testicular cancer was usually treated with large fields of radiotherapy, higher doses and
the salvage treatment was based on polychemotherapy. But recent advances in treatment,
including the use of lower doses associated with smaller fields of radiotherapy and
carboplatin based chemotherapy, have considerably reduced the late adverse effects while
keeping the high rates of cure. In this chapter we discuss the role of radiotherapy in the
management of seminomas. Due to the non-seminomatous testicular cancers are less sensitive
to radiation, radiotherapy plays a limited role in its treatment. Consequently, detailed
discussion on the treatment of nonseminomatous testicular cancer is beyond the scope of this
chapter.
1. Epidemiology
• In the USA in 2010, 8,480 new cases of testicular cancer was diagnosed, and ~350
patients died from the disease.
• Testicular cancer is more commonly diagnosed in Caucasians with a bimodal
distribution.
• The major peak occurs between ages 15 and 35 years, owing almost exclusively to
tumors of germ cell origin, which account for approximately 95% of all testicular
cancer.
• Embryonal carcinoma represents the predominant histopathologic diagnosis up to the
age of 35 years, after which seminoma is more common up to the age of 75 years.
• The incidence of testicular cancer varies markedly based on geographic distribution.
• Testicular cancer appears to be increasing among young white males in the
Scandinavian countries, the United Kingdom, and the United States. The trend may
be attenuating in some countries, such as Denmark, and there appears to be large
geographic differences in the changing incidences.
Reference
Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012. CA Cancer J Clin. 2012;62(1):10.
2. Risk Factors
There are several risk factors associated with developing of testicular neoplasia. All of
these risk factors predispose to the development of carcinoma in situ and invasive testicular
cancer (table-1)

Testicular Cancer
185
Cryptorchidism
Patients with cryptorchidism are 10 to 40 time more likely to develop
testicular carcinoma than are those with normally descended testes.
The risk for developing cancer in a testis is 1 in 80 if retained in the inguinal
canal and 1 in 20 if retained in the abdomen.
Surgical placement of an undescended testis into the scrotum before 6 years
of age reduces the risk for cancer.
Testicular feminization
syndromes
It increases the risk for cancer in the retained gonad by 40-fold. Tumors in
these patients are often bilateral.
Contralateral testicular
cancer
A small percentage of men with testicular cancer will have a second testicular
cancer, and the incidence of bilateral tumors at presentation is between 1 and
5 %.
Family medical history:
Familial history increases fourfold in a male with a father who had a germ
cell tumors (GCT), and nine fold with an affected brother
Other risk factors
The magnitude of other suggested risk factors, such as a history of orchitis,
testicular trauma, or irradiation, is not known.
References
Fosså SD, Chen J, Schonfeld SJ, McGlynn KA, McMaster ML, Gail MH, Travis LB. Risk of
contralateral testicular cancer: a population-based study of 29,515 U.S. men. J Natl
Cancer Inst. 2005;97(14):1056.
Batata MA, Chu FC, Hilaris BS, Whitmore WF, Golbey RB. Testicular cancer in crypt-
orchids. Cancer. 1982;49(5):1023.
Harland SJ. Conundrum of the hereditary component of testicular cancer. Lancet.
2000;356(9240):1455.
Table 1. Risk factors for testicular cancer
3. Anatomy
The scrotum includes the testicles, epididymis and part of the spermatic cord. The tunica
dartos layer sticks to the scrotal skin, and consists of superficial and deep layers of superficial
fascia. It contains smooth muscle fibers called the dartos muscle. This muscle is an important
factor in the temperature regulation of the testes. This layer contains little fat tissue but is rich
in elastic leaves (figure-1).
Figure 1. Testicular anatomy.

Gustavo Arruda Viani
186
Symptoms
Mass and pain
Painful enlargement of the testis occurs in 30% to 50% of
patients and may be the result of bleeding or infarction in the
tumor.
Acute pain in a patient with a cryptorchid testis suggests the
possibility of torsion of a testicular cancer.
Acute
epididymitis
Nearly 25% of patients with mixed teratoma and embryonal cell
tumor present with findings indistinguishable from acute
epididymitis.
Gynecomastia
Due to high levels of serum hCG is rarely a presenting sign.
Infertility
It is the primary symptom in about 3% of patients.
Back pain
Due retroperitoneal node metastases is a presenting feature in
10% of patients
Physical
exam
Scrotum
A testicular mass is nearly always present. The testis should be
palpated using bimanual technique; the finding of irregularity,
induration, or nodularity is indication for further evaluation.
Lymph nodes
Patients must be carefully examined for lymphadenopathy,
particularly in the supraclavicular region.
Scrotal contamination, such as following testicular biopsy,
vasectomy, or herniorrhaphy, alters the normal lymphatic
drainage; as a result, ipsilateral inguinal nodes may become
involved.
Breasts
Gynecomastia is associated with tumors that secrete high levels
of hCG.
4. Clinical Features
Testicular tumors typically present as a nodule or painless swelling of one testicle, which
may be noted incidentally by the patient. The other most common symptoms are described in
table-2.
Table 2. Symptoms and findings of physical examination from testicular cancer
Reference
Bosl GJ, Motzer RJ. Testicular germ-cell cancer. N Engl J Med. 1997;337(4):242.
5. Diagnosis and Evaluation
• The evaluation of a testicular mass begins with an ultrasonographic exam (figure-2).
Testicular ultrasonography is a sensitive and specific test that can differentiate
between a testicular neoplasm and nonmalignant processes such as hydrocele,
testicular torsion, spermatocele, varicocele, and epididymitis.
• The presence of heterogeneous masses or hypoechoic on ultrasonographic
examination should prompt a thorough subsequent orchiectomy.

Testicular Cancer
187
Figure 2. Ultrasonographic Images of the Right Testis. A transverse image through the right testicle
(Panel A) shows a complex intratesticular mass with a cystic component (arrowhead) and a solid
component (arrow). Gross Features of the Testicular Tumor.
• Similarly, a negative ultrasonogram fairly reliably establishes the absence of
intrascrotal GCT. Both testes should be examined, since 2% to 4% of patients will
harbor bilateral lesions. There is no role for trans-scrotal biopsy in the diagnosis of
testicular tumors.
• Orchiectomy is the definitive procedure for both pathologic diagnosis and local
control of the primary tumor and in some cases may be a curative procedure.
Furthermore, important predictive factors can be identified with routine histologic
techniques that are crucial to risk assessment strategies used in the clinical
management of these patients.
• The first step after the histologic confirmation of a GCT is to determine the extent of
the disease (staging) so that appropriate therapy can be undertaken. An assessment of
risk of metastases (in the case of local disease) or response to systemic therapy (in
the case of advanced disease), utilizing the results of histopathologic, biochemical,
and radiographic evaluations, should be an integral element of the staging process.
• Chest computed tomography (CT) scan can detect occult posterior mediastinal or
pulmonary parenchymal metastases. This is not usually a necessary test if the PA and
lateral chest x-rays are abnormal.
• Abdominal and pelvic CT scans assist assessment of retroperitoneal or rarely pelvic
adenopathy. Fluorodeoxyglucose-positron emission tomography (FDG–PET) has no
benefit over computed tomography (CT) alone except restaging for residual masses
(figure-3).
References
Benson CB. The role of ultrasound in diagnosis and staging of testicular cancer. Semin Urol.
1988;6(3):189.
Richie JP, Garnick MB, Finberg H. Computerized tomography: how accurate for abdominal
staging of testis tumors? J Urol. 1982;127(4):715.

Gustavo Arruda Viani
188
Marker
Description
HCG
hCG is markedly elevated with pure choriocarcinoma and also elevated in embryonal cell
carcinoma and may be mildly elevated in patients with pure seminoma. The blood halflife of hCG is 18 to 24 hours.
hCG may also be found in patients with a variety of other tumors, including melanoma,
large cell lung cancer, breast, ovary, or pancreatic cancer.
The presence of hCG after orchiectomy constitutes proof that the patient has residual
cancer and requires further treatment. The absence of hCG, however, does not exclude the
presence of active cancer, particularly in previously treated patients.
Seminoma: 10% hCG elevated/Choricarcinoma: 100% hCG elevated/Embryonal
carcinomas / teratomas: 65% hCG elevated
AFP
AFP is produced by yolk sac elements and is most commonly associated with embryonal
carcinomas and yolk sac tumors. Elevated levels of AFP are never found in patients with
pure seminoma or pure choriocarcinoma. The blood half-life of AFP is 5 days, but may be
much longer after successful chemotherapy.
Seminoma: 0% AFP elevated
Choricarcinoma: 0% AFP elevated
Embryonal carcinomas / teratomas: 65% AFP elevated
Huddart RA, O'Doherty MJ, Padhani A, Rustin GJ, Mead GM, Joffe JK, Vasey P, Harland
SJ, Logue J, Daugaard G, Hain SF, Kirk SJ, MacKewn JE, Stenning SP. NCRI Testis
Tumour Clinical Study Group. 18fluorodeoxyglucose positron emission tomography in
the prediction of relapse in patients with high-risk, clinical stage I nonseminomatous
germ cell tumors: preliminary report of MRC Trial TE22--the NCRI Testis Tumour
Clinical Study Group. J Clin Oncol. 2007;25(21):3090.
Figure 3. CT scan and PET scan of alymph nodal metastatic testicular cancer.
5.1. Tumor Markers
Tumor markers are sensitive indicators of testicular cancer. Serum hCG and α-AFP are
essential markers for these tumors. One or both of these serum markers are present in more
than 90% of patients with metastatic nonseminomatous germ cell cancer of the testis. The
incidence rates of these markers according to tumor histology are shown in table-3.
Table 3. Tumor markers for testicula cancer

Testicular Cancer
189
Seminoma
Seminoma with syncytiotrophoblastic cells
Spermatocytic seminoma
Spermatocytic seminoma with sarcoma
Nonseminomatous germ cell tumors
Embryonal carcinoma
Teratoma
Trophoblastic tumors (choriocarcinoma)
Yolk sac tumor (endodermal sinus tumor)
Mixed germ cell tumors
Sex cord-stromal tumors
Sertoli cell tumor
Leydig cell tumor
Granulosa cell tumor
Mixed types (eg, Sertoli-Leydig cell tumor)
Reference
Gilligan TD, Seidenfeld J, Basch EM, Einhorn LH, Fancher T, Smith DC, Stephenson AJ,
Vaughn DJ, Cosby R, Hayes DF, American Society of Clinical Oncology. American
Society of Clinical Oncology Clinical Practice Guideline on uses of serum tumor markers
in adult males with germ cell tumors. J Clin Oncol. 2010;28(20):3388.
6. Pathology
Geminative cell tumors (GCT) account for about 95 % of testicular tumors. Among the
GCTs pure seminomas account for approximately 50 % of all testicular GCTs, and a
seminomatous component is present in approximately 20 % of mixed GCTs (table-4).
Table 4. Pathological distribution of testicular tumors with details of different
histological subtypes
Reference
Krag Jacobsen G, Barlebo H, Olsen J, Schultz HP, Starklint H, Søgaard H, Vaeth M.
Testicular germ cell tumours in Denmark 1976-1980. Pathology of 1058 consecutive
cases. Acta Radiol Oncol. 1984;23(4):239.
The modified Royal Marsden Hospital staging system is often used in the clinical
practice for staging seminoma tumors (Table-5).
7. Staging

Gustavo Arruda Viani
190
Stage
Description
I
Tumor confined to the testis
II
IIA
IIB
IIC
IID
Infradiaphragmatic nodal involvement
Greatest dimension of involved nodes < 2 cm
Greatest dimension of involved nodes ≥2 cm but < 5 cm
Greatest dimension of involved nodes 5 cm or more but < 10 cm
Greatest dimension of involved nodes ≥10 cm
III
Supraclavicular or mediastinal involvement
IV
Extranodal metastases
Table 5. Royal marsden staging system
Reference
Thomas G, Jones W, VanOosterom A et al. Consensus statement on the investigation and
management of testicular seminoma 1989. Prog Clin Biol Res. 1990; 357:285–294
8. Routes of Spread
• Lymphatic spread is the predominant routes of dissemination of seminoma, while
nonseminoma favors hematogenous spread.
• The right testis: drainage is along the inferior vena cava first into the inter-aortocaval
region, then to the pre-aortic and para-aortic lymph nodes, with possible cross-over
within the retroperitoneum (figure-4).
• The left testis: drainage is first into the nodes of preaortic and para-aortic lymph
nodes around the left renal hilum and then to the inter-aortocaval nodes mostly
without cross-over.
• Nodal spread to iliac chain is a rare event (~3%)
• Inguinal node spread is also an infrequent event < 5% without lymphatic disruption
by prior surgery
Figure 4. Lymphatic drainage for testicular cancer.
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