Genitourinary Tract Tumours
case studies
Radek Lakomy, MD, PhD
Alexandr Poprach, MD, PhD
Ivo Kocak, MD, PhD
Genitourinary Tract Tumours
• Tumours of the kidney
• Tumours of the urinary bladder
• Tumours of the prostate
• Tumours of the testis
• Tumours of the penis
Age distribution of the genitourinary tract tumours
%ofcasesperagegroup
C60 – penis – incidence – male
age distribution of the patient population
C62 – testis – incidence – male
age distribution of the patient population
%ofcasesperagegroup
Sample size: N = 11910 http://www.svod.cz Data source: UZIS CR
%ofcasesperagegroup
C61 – prostate – incidence – male
age distribution of the patient population
Sample size: N = 106410 http://www.svod.cz Data source: UZIS CR Sample size: N = 106410 http://www.svod.cz Data source: UZIS CR
Tumours of the kidney
Epidemiology and aetiology
• Sporadic forms
– Smoking, polycyclic aromatic
carbohydrates, heavy metals,
polycystic kidney, obesity, DM,
hypertension
 50-80 % von Hippel-Lindau tumour
suppressor gene mutation
• Hereditary forms (2-3%)
– von Hippel-Lindau disease
 VHL suppressor gene mutation (3p)
– Hereditary papillary renal cell
carcinoma
 MET proto-oncogene mutation (7q)
– Hereditary leiomyomatosis and
renal cell carcinoma
 FH (fumarate-hydratase) gene
mutation
 Birt-Hogg-Dubé syndrome
 FLCN – folliculin protein gene
mutation (17p)
C64 – kidney other than renal pelvis
development in time
No.ofcasesper100000people
Sample size: N (inc.) = 69280 N (mor.) = 33620 http://www.svod.cz
C64 – C66 – kidney, renal pelvis and…
Comparison of incidence in CZ and other countries, ASR – global standard
Tumours of the kidney – histological types
• Benign tumours
– oncocytoma, adenoma,
angiomyolipoma
• Malignant tumours
(2% of all adult malignancies)
– Adenocarcinoma (90%)
clear cell carcinoma (75 %)
papillary Ca (10-15%)
chromophobe Ca (5%)
– Sarcoma
– Lymphoma
– Foetal renal tumours –
nephroblastoma (Wilms
tumour) – in children
 Kidney tumours – often
accidental finding on an
ultrasound or CT scan
Localized disease
• Surgical treatment
– Radical nephrectomy
– Partial nephrectomy – preferred (pole tumours, single
kidney, CRI)
• Adjuvant treatment – none
– Radiotherapy, chemotherapy, immunotherapy – failure in
adjuvant setting
– Clinical studies with biological treatment (sunitinib,
sorafenib, pazopanib) – also no effect on OS
Disseminated disease
• Targeted treatment = currently the most effective
systemic treatment
– tyrosine kinase inhibitors (PDGFR alfa a beta, VEGFR 1,2,3), c-kit,
Flt, RET etc.
– angiogenesis and tumour proliferation inhibition
 sunitinib, sorafenib, pazopanib, axitinib
– m-TOR inhibitors
 temsirolimus, everolimus
– monoclonal anti-VEGF antibodies – angiogenesis inhibition,
effective combination with INF alfa
 bevacizumab
• Research: modern immunotherapy with checkpoint
inhibitors
 Anti-CTLA-4 antibody: ipilimumab
 Anti-PD-1 antibodies: nivolumab, pembrolizumab, pidilizumab
 Anti-PD-L1 antibodies: atezolizumab
Case study
• 60 years old patient, male
• FH: father died of kidney ca aged 65, mother died of stomach ca aged 82
• PH: 6/2011 haemorrhoid surgery, hypertension from 2008, otherwise healthy
• Treatments: lisinopril tablets 5mg 1-0-0
• Allergies: 0
• Social history: married, 2 children
• Occupational history: managerial position Tesco United Kingdom, currently unemployed
• Abuses: smokes 20 cig/day/40 years, currently in the process of stopping, black coffee 3/day, alcohol 0
• Symptoms – pain in the right lumbar region in 1/2012
• Ultrasound => right kidney tumour
• Staging
– CT scan of the lungs, abdomen, pelvis in 2/2012 – tumour of the inferior pole of the right
kidney 80 x 66 mm, RCC-like, small metastases in the lungs bilaterally 3 – 20 mm
– Skeletal scintigraphy 6. 2. 2012 Faculty Hospital Motol in Prague – no evident metastases of
the bones
CT before the treatment in 2/2012
Surgical treatment
• 8.2.2012 – laparoscopic radical NE l. dx., perisurgically
extensive tumour of the inferior pole of the
left kidney, Faculty Hospital Motol Prague
• Histology - adenoCa renis, clear cell Ca, pT1, G 2-3
• TNM classification – pT1bNXM1 (pulm.), st. IV
Treatment in MOU
• Outpatient consultation 20.2.2012
• KI 100%, asymptomatic, surgical wound healed,
laboratory investigations normal
• MSKCC – medium prognosis
– 1 criterion: diagnosis < 1 year from treatment initiation
MSKCC scoring system of 2002: valid for TKI and bevacizumab treatment
LDH > 1.5 times upper limit of normal
Haemoglobin < lower limit of normal
Corrected plasma calcium > 2.5 mmol/L
Karnoffsky index ≤ 70 %
Time from diagnosis to systemic treatment initiation < 1 year
1st line treatment
• sunitinib 50 mg/day, D1-28, every 6 weeks
– start day: 24. 2. 2012
• Well tolerated, no myelotoxicity
– Only arthralgia G1, fatigue G1, hand-foot sy. G1 (from 4th
cycle), hair and eyebrows going grey (from 5th cycle),
hypertension corrected with 2-combination
1st line treatment (sunitinib) – rescan after
3 cycles – partial regression of lung meta
1st line treatment (sunitinib) - rescan after 6 cycles progression
of lung meta
(number and size – 1. 11. 2012)
2nd line treatment
• afinitor 10 mg/day, D1-28
– start on 3. 12. 2012, KI 100%, labs normal
• well tolerated, no myelotoxicity, no pulmonary
toxicity, no mucositis
– nausea G1, acneiform exanthema and pruritus G1
(treated with antihistamines - levocetirizine),
higher plasma glucose (7-9 mmol/L)
2nd line treatment (afinitor) – rescan after
3 cycles – partial regression of lung meta with
subsequent long-term stabilization
2nd line treatment (afinitor) – rescan after
19 cycles – progression of lung meta (30.4.2014)
3rd line treatment
• sorafenib 800 mg/day (2-0-2 / 200 mg)
– start on 23. 6. 2014, KI 90%
• relatively well tolerated at the start, just slight
nausea, light exanthema and skin itching G1
(antihistamines)
– from 3rd cycle: exanthema in progression G2 (local
steroids by a dermatologist + levocetirizine), diarrhoea
G1-2, loss of appetite G1, fatigue G2, hand-foot sy. G1
3rd line treatment (sorafenib) – rescan after
2 cycles – sligh size regression of lung meta (SD)
3rd line treatment (sorafenib) – rescan after
8 cycles – progression of lung meta and pleura with
effusion (13.4.2015) – treatment discontinuation
followed by symptomatic treatment
Summary
• Targeted treatment has prolonged survival of mRCC patients
– our patient was treated for just under 38 months (24.2.2012 –
13.4.2015)
• Development of resistance to TKIs and mTOR inhibitors
continues to limit therapy => palliative treatment
• Quality of life – important treatment success factor
• High hopes in modern immunotherapy with checkpoint
inhibitors (long-term disease control)
• Future – new combinations, targeted treatment sequencing
and immunotherapy
Tumours of the urinary bladder
Epidemiology and aetiology
Aetiology
 Smoking, polycyclic aromatic
amines, dietary factors,
medicines, chronic infections
 Genetic predispositions – can
be up to 10%, familial occurrence
in association with the LYNCH II
syndrome as well as exclusive
entities with autosomal dominant
inheritance – genetically
determined higher sensitivity to
some carcinogens
C67 – urinary bladder – vesicae…
development in time
C67 – urinary bladder
Comparison of incidence in CZ and other countries, ASR – global standard
No.ofcasesper100000people
Tumours of the urinary bladder – most frequent
histology types
 urothelial carcinoma: 90%
 epidermoid carcinoma: 6% - 7%
 adenokarcinoma: 1-2%
Localized disease
1. superficial (non-muscle invasive) - Tis, Ta, T1
• Preferred surgical treatment (TURT) + local…intravesical
BCG or CHT mitomycin administration
2. Invasive (muscle invasive) - T2-4a N0
• Newly treatment with neoadjuvant cisplatin-based
chemotherapy, than radical surgery (RACE) and possibly
ambiguous adjuvant chemotherapy
• Rarely other modalities: radiotherapy, primary surgery,
…
Disseminated disease
• metastatic Ca - T4b / N+ / M+…palliative
cisplatin, gemcitabin, taxan, vinfluvin or
doxorubicin-based chemotherapy
Case study - B.J.; 1954
• FH: father + Ca kidneys, mother CRI, brother brain Tu
• Social history: married
• Occupational history: logistics, no contact with chemicals
• Personal history: HLPP, smoker
• Surgeries: 0
• Treatments: fenofibrate (Lipanthyl Supra 160mg 0-0-1)
• allergies: negates
• abuses: quitted smoking 11/2013, 15 c/day - from 18 years of
age, alcohol ad hoc, coffee sometimes
• Subjective: no complaints, accidental finding during prostate
ultrasound
B.J.; 1954
• 11/13 flexible cystoskopy - susp. Tumorouse changes under
the left urethral opening
• Kidney ultrasound 10/2013 no finding, Chest X-Ray normal,
blood count + biochemistry normal
• 11/2013 surgery: TURT
• Description: Bipolar endorectometer Ch 26 introduced into the.bladder: field coloured with pink
urine, rinsing required, 4 tumours identified, some solid with papillary surface, other form a spruce
growth, size 1x1 to 3x3 cm. TUR performed of all identified tumours: 1. above the left ureteral
opening, 2. base – sample 1, 3. meatus of the bladder – sample 7, 4. right wall, 5. base – sample 5,
6. posterior wall, 7. base - sample 6. Careful elcoagulation, three-way catheter F 18 Ch, balloon 10
ml, lavage - light pink liquid.
• After surgery: intravesical MMC administration.
B.J.; 1954
• Histology
• 1) tu above the left urethral opening : high-grade papillary urothelial carcinoma
with sub-epithelial connective tissue invasion
• 2) sample No. 1 base: negative
• 3) tu in the urinary meatus on No. 7: high-grade papillary urothelial carcinoma
with sub-epithelial connective tissue invasion
• 4) tu of the right wall: high-grade papillary urothelial carcinoma with subepithelial
connective tissue invasion
• 5) sample No. 5 base: negative
• 6) tu of the dorsal wall: high-grade papillary urothelial carcinoma with subepithelial
connective tissue invasion
• 7) sample No. 5 base: negative
• CLASSIFICATION: pTNM(7): pT1
• ……reTURT necessary due
to the positive base
Therapeutic classification of urinary bladder CAs:
1. superficial (non-muscle invasive) - Tis,
Ta, T1
2. invasive (muscle invasive) - T2-4a N0
3. metastatic - T4b / N+ / M+
• 01/2014 reTURT… Tis only here (base negative)…
followed by intravesical BCG
• 04/2014…recurrence according to cytology and
cytoscopy….further reTURT
B.J.; 1954
B.J.; 1954
• 04/2014: re-resection of all areas after TURT
• histology:
• 1,2) Medial from the left opening a focus of invasively spreading high-grade
urothelial carcinoma, negative base.
• 3,4) No. 7-9 in the meatus - high-grade urothelial carcinoma with minimal
invasion into the muscle base.
• 5,6) Chronic inflammation and granulation tissue lateral from the right opening, no malignity, including the base.
• 7) Sample of the mucosa of prostatic urethra with chronic inflammation and surface erosions with granulation tissue, no
malignity.
• CLASSIFICATION: pTNM(7): high-grade CARCINOMA, pT2….restaging necessary!!!
Recurence!!
Recurence!!
Therapeutic classification of urinary bladder CAs:
1. superficial (non-muscle invasive) - Tis,
Ta, T1
2. invasive (muscle invasive) - T2-4a N0
3. metastatic - T4b / N+ / M+
B.J.;1954
• Skeletal scintigraphy
(negative), chest X-ray
(negative), labs - normal
• CT of the abdomen and pelvis
• Tu of the bladder
• Pathologically enlarged paraaortic
nodules in the pelvis
and RP.
TNM and stage: at minimum pT2cN3MX - stage IV.
B.J.;1954
• 4 cycles of neoadjuvant chemotherapy cisplatin +
gemcitabine, leading to regression - 80%
• 10.09.2014 - radical cystektomy (def: usual RACE: complete resection of the
bladder, with prostate and seminal vesicles in male and with uterus, adnexa and the frontal wall of the
vagina in female, and including nodules in some cases (according to peri-surgical finding and previous
abdominal and pelvic CT)).
• Histologically: Urinary bladder without an evidence of residual carcinoma following neoadjuvant
therapy. Resection margins including urethra negative for both urethras. A micrometastasis of a higher
grade carcinoma (1 mm) in 1 of 40 lymphatic nodes. Prostate gland with predominance of glandular
atrophy, a focus of chronic inflammation, granulomatous reaction after endoresection. Regular appendix.
• CLASSIFICATION: pTNM(7): ypT0 pN1(nodes[posit./exam.]:
1/40), L0 V0 R0….i.e. significant regression, almost complete
remission….VERY GOOD PROGNOSIS
B.J.; 1954
• 05/2015: However, CT scan: Conclusion: patient after radical cystectomy with ileal ureteral substitution,
progression with pathological lymphadenopathy in the left groin and by the outer iliac ligament, new
enlarged node in posterior mediastinum, the currently observed nodes had previously regressed
B.J.; 1954
Therapeutic classification of urinary bladder CAs:
1. superficial (non-muscle invasive) - Tis,
Ta, T1
2. invasive (muscle invasive) - T2-4a N0
3. metastatic - T4b / N+ / M+
• Therefore: 3rd metastatic - T4b / N+ / M+…palliative cisplatin,
gemcitabine, taxan, vinfluvin, doxorubicin-based chemotherapy
• a study became available with „check-point inhibitors“: nivolumab – first line
palliative immunotherapy
B.J.; 1954
Tumours of the prostate
Epidemiology a aetiology
Aetiology and risk factors
 Genetic predispositions –
familial 5 %, p53, Bcl-2
 Age – steep rise post 6th decade
 Dietary habits – increased intake
of saturated fatty acids, low intake
of vegetables, obesity
 Professional exposition –
aromatic carbohydrates, heavy
metals
 Ethnic effects – highest in AfroCaribbean,
lowest in Asians
C81 – prostate, male
development in time
C61 – prostate, male
Comparison of incidence in CZ and other countries, ASR – global standard
No.ofcasesper100000people
Localized disease
– RAPE ± pelvic lymphadenectomy (according to nomogram –
Partin, Briganti, MSKCC),
– Curative radiotherapy ± hormone therapy
neoadjuvant/concomitant/adjuvant
– active surveillance or watchful waiting
• Modality selection according to the risk (low, medium, high
– as per the T, PSA and Gleason score), overall health status,
comorbidities, patient attitude towards treatment (age,
sexual activity)
Disseminated disease
• Hormone therapy
• Chemotherapy
• Immunotherapy
• Radioisotopes
• Bisphosphonates, denosumab
Phases of the disease development
Primary hormone-sensitive disease
Androgen deprivation therapy
Hormone-sensitive disease for 2-3 years
Need to establish permanent castration
Development of castration-resistant disease
CRPC systemic treatment modalities
Systemic chemotherapy
Androgen-deprivation therapy
Inclusion of immunotherapy
Supportive treatment of bone metastases
Antiresorptive agents
Radionuclide therapy
Palliative radiotherapy
Bone metastases
Antiresorptive agents:
bisphosphonates
RANKL inhibitor – denosumab
Radionuclide therapy
samarium-153
radium-223
Bone metastases in advanced prostate cancer:
related consequences
SRE are associated with higher morbidity1,2, higher treatment
cost3 and lower quality of life4
Reduced quality of life
Increased
healthcare
costs3
Reduced mobility and
spine compression2
Negative impact on
survival1,2
4
Skeletal events
1. Norgaard, M, et al. J Urol. 2010; 184:162-167. 2. Sathiakumar, N, et al. Pros Canc and Pros Diseases. 2011; 14: 177-183. 3. Lage MJ, et al. Am J Manag Care.
2008;14(5):317-322. 4. Weinfurt KP, et al. Ann Oncol. 2005;16:579-584.
Impact of bone metastases on overall survival
in patients with mCRPC
• Patients with bone disease at the time of diagnosis have significantly poorer
OS than those with lymph node disease
CI = confidence intervala Cox models adjusted according to age at randomization.
Clarke NW, et al. J Clin Oncol. 2013;31(suppl). Abstract 5012.
73%
(95% CI: 67%-78%)
87%
(95% CI: 73%-94%)
57%
(95% CI: 46%-67%)
0
10
20
30
40
50
60
70
80
90
100
Bone Soft tissue Bone + soft tissue
2yearOSrate(%)
Zoledronic
acid
Docetaxel
ADT Zoledronic acid
Sipuleucel-T
ADT
Docetaxel
Cabazitaxel
Denosumab
Abiraterone
pre & post-doc
ADT
Enzalutamide
Radium 223
Zoledronic acid
Sipuleucel-T
ADT
Docetaxel
Cabazitaxel
Denosumab
Abiraterone
Post-doc
<1996
2004
2010
2012
Treatment algorithm
• Patient diagnosed with: Ca prostatae, dg. 1/07, histol.: prostate
adenocarcinoma in both lobes, Gleason 3+3, margin affected,
significant perineural invasion,
pT3a pN0 M0, clin st III, initial PSA 5,6
– patient after RAPE 5/07.
– curative RT of the prostate bed due to positive resection margins
• Patient then observed based on the PSA levels during the hormonesensitive
phase of the disease, bilateral OE performed on
17.9.2010; anti-androgenic treatment involved bicalutamid,
flutamid.
• CRPC (castration-resistant prostate carcinoma) diagnosed in 4.2011
based on PSA elevation and CT scan. Peritoneal excision due to the
atypical finding in the abdominal cavity revealed infiltrations with
prostatic adenocarcinoma structures.
The disease was asymptomatic at the time of CRPC diagnosis
• To address the visceral generalization and the risk of symptom
manifestation, first line palliative CHT with docetaxel was administered
from 18.4.11 to 6.1.12. A total of 13 cycles administered, initial PSA: 82.6.
• Cont. decline in PSA during the docetaxel treatment; docetaxel
discontinued at PSA 0,151. PR on CT also achieved.
• Docetaxel discontinuation led to gradual increase in PSA, asymptomatic
disease, CT in 5/2012 described regression. Patient offered treatment with
abirateron on 24.7.2012.
• Treatment with abirateron very well tolerated no haematol. or
biochemical toxicity. Treatment with abirateron resulted in significant
decline in PSA, with minimal values.
• PSA values:
– 17. 7. 2012: 7.26 – initial value before abirateron initiation
– 12. 11. 2012: 0.192 - nadir in PSA decline
• The treatment aimed to maintain very good health status for as long as
possible. Therefore, treatment continued until clinical progression.
• Clinical progression leading to treatment discontinuation
identified on 19.5.2014 with symptoms corresponding to
disease generalization in the abdominal cavity:
– feeling of full stomach, burning sensation or crumps in the
abdominal wall, no nausea, normal urination, obstipation – used
laxatives, observed enlargement of the abdominal volume,
flatus reduced
• Physical examination of the ascites revealed less palpable
abdominal wall, impaired peristalsis.
• CT on 6.2014:
– Patient after RAPE – no signs of tumour recurrence.
– Ascites – the entire abdominal cavity and pelvis – new.
– Diffuse MTS of the omentum and peritoneum – significant
progression.
• Patient with good biochemical and haematological parameters with PS 2
offered subsequent treatment – re-challenge docetaxel from 6.6.2014,
with initial PSA: 82.7.
• Subsequent treatment led to fast reduction or even elimination of the
abdominal symptomatology, elimination of the ascites according to a
physical examination and re-establishment of PSA decline.
• PSA values:
– 27. 6. 14: 61.3
– 18. 7. 14: 33.5
– 8. 8. 14: 19.9
– 19. 9. 14: 12.0
– 15. 5. 15: 20.3
• 15.5.2015 clinical disease progression occurs after 15 cycles of docetaxel
re-challenge – tense ascites, impaired peristalsis. Anti-tumour treatment
discontinued, the patient referred to palliative care.
Conclusion
Prostate cancer is becoming easier to manage
due to the availability of new data from clinical trials
and availability of further treatment modalities.
Tumours of the testis
Epidemiology a aetiology
One of the most frequent
malignancies in young men aged
20-40 years
Rising incidence – white race,
developed countries (North America
and Europe)
Aetiology – unknown
Risk factors
 Familial occurrence
 Cryptorchidism – increased
temperature, endocrine
disorders, orchidopexy needed
before 1-2 years of age
 Urogenital tract abnormities
 Discussed: inguinal hernias,
orchitis, scrotal trauma
C62 testes, male
development in time
C62 - testes, male
Comparison of incidence in CZ and other countries, ASR – global standard
No.ofcasesper100000people
Testicular tumours – histological types
 Germ cell tumours – germ cells origin – 95% of all testicular
tumours
 Seminomas – classic, anaplastic, spermatocytic
 Nonseminomas - embryonal carcinoma, choriocarcinoma, yolk sac tumour,
teratoma/teratocarcinoma
 Non-germ cell tumours – lymphomas, sarcomas, Leydig and
Sertoli cell tumours
• Surgical treatment – inguinal orchiectomy in all
stages
• Adjuvant treatment
– as per the risk factors – tumour size (> 4cm) and rete testis
invasion in seminomas, angioinvasion in nonseminomas
• Seminomas – surveillance or chemotherapy
(carboplatin monotherapy, 1-2 cycles)
• Nonseminomas – surveillance or chemotherapy
(BEP regimen, 1-2 cycles)
Localised diseas – stage IA,B
Disseminated disease – stage IS, IIA,B,C and
IIIA,B,C (treatment after orchiectomy)
• Stage IS (tumour marker elevation only) and stage II
(retroperitoneal node involvement)
– Seminomas – curative chemotherapy with the BEP regimen (preferred) or
curative radiotherapy in stage IIA,B (cave late toxicity)
• Residuum after therapy with negative PET - surveillance
– Nonseminomas – curative chemotherapy with the BEP regimen
(preferred) or primary RPLND in teratomas
• Residuum after cytostatic treatment over 1cm – retroperitoneal
lymphadenectomy, and followed by chemotherapy if viable tumour
• Stage III (distant metastases)
– Seminomas and nonseminomas – curative chemotherapy with the BEP
regimen, surgery of residual metastases in nonseminomas and according
to PET in seminomas
Case study
• Patient (18 years)
• 11/2006 referred by an urologist due to a resistance in the left
testicle
 FH: negative
 PH: orchidopexy of the left testicle aged 11 years (risk factor)
 Treatments: sine medication, Allergies:0
 Social history: lives with parents
 Occupational history: student
 Abuses: non-smoker, alcohol ocassionally, coffee 0
Initial investigations
 Current disease: 1 year pain in the left testicle and 3 weeks palpable
resistance
 Clinical investigation and + ultrasound of the testis: confirmed tumour of the
testis
 Laboratory: FW 4/7, CRP 16, blood count+diff. and biochemistry normal
 Tumour markers: AFP 17.8 ug/L, HCG 30 360 IU/L, LDH normal
 Chest X-ray – metastases in both lungs, PET – multiple lung, mediastinum,
liver and retroperitoneum metastases
 Surgery: left inguinal orchiectomy
– Histology: mixed germ cell tumour of the testis with predominant
embryocarcinoma, minor choriocarcinoma component, invasion into
seminal ligament, lymphangioinvasion, pT3, C62.9, M 9085/39
 Refused immediate initiation of systemic treatment (Christmas)
Fast disease progression!!!
Acute admission for breathlessness 4 weeks after the surgery
(27.12.2006)
 Chest X-ray: size and numerical progression by more than 100%
 Laboratory: FW 42/79, CRP 168, blood count + diff. normal,
biochemistry – total bilirubin 42, AST 1.11, GMT 3.46, ALP 3.16
 Tumour markers: AFP 128ug/L (17.8), HCG >200 000IU/L (30
360), LDH 34.05 (off norm)
 Clinical: breathlessness at rest, sat. O2 – 88%
Chest X-ray before the surgery and 4 weeks
later
CT of the lungs, abdomen and pelvis at the
treatment initiation
Curative chemotherapy - BEP
TNM classification – pT3N2M1b S3, stage IIIC, poor risk
according to IGCCCG => curative chemotherapy indicated 4x
BEP (bleomycin, etoposide, cisplatin)
 Chemotherapy initiated for vital indication at an ICU
 Hydration, allopurinol, tumour lysis syndrome prevention, Neulasta (G-
CSF)
 A week from treatment initiation (4.1.2007) – generalized epiparoxysm, CT
of the brain – metastasis in the right occipital lobe
 Brain MRI on 9.1.2007 – solitary MTS occipital l.dx. 10x10x18mm =>
stereotactic radiotherapy of a solit. meta of the brain (25Gy) and
continuing curative chemotherapy
Brain MRI on 9.1.2007
Reinvestigation after 4 cycles of chemotherapy
BEP: 28.3.-30.3.2007
 CT of the lungs, abdomen and pelvis: significant regression of
lung, liver and retroperitoneal metastases, elimination of
mediastinal metastases
 Brain MRI: post-radiotherapy scar only
 Tumour markers: AFP - 128…3.6, HCG - >200 000…19.1, LDH –
34.05…3.46
 Clinical: no signs of the disease, no breathlesness
Lung CT before and after 4 cycles of CHT - BEP
CT of the abdomen and pelvis before and after
4 cycles of CHT - BEP
Brain MRI before and after 4 cycles of CHT + SRT
Salvage chemotherapy - VeIP
 Indication – when a patient does not achieve complete remission
on curative 1st line chemotherapy (or surgery)
 Administered a total of 3 cycles (2.4. – 27.5.2007)
 TM after 3rd cycle - AFP 3.7, HCG 3.6, LDH 3.35 – normalization
 4th cycle not administered – deteriorated hearing (cisplatin toxicity)
 Follow up surveillence, repeated follow ups show complete
remission (calcification of necrotic liver metastases)
 Complete remission – continues at present
Thank you for your attention