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Abramson Cancer CenterNCI CANCERLIT® Search: Testicular Cancer - April 2002
National Cancer Institute®
Last Modified: April 1, 2002
Table of Contents
1
UI - 11213121
AU - Gietema JA; Meinardi MT; van der Graaf WT; Sleijfer DT
TI -
Syndrome X in testicular-cancer survivors.
SO - Lancet 2001 Jan 20;357(9251):228-9
2
UI - 11480434
AU - Fukui M
TI -
Testicular cancer and syndrome X.
SO - Lancet 2001 Jul 21;358(9277):242
3
UI - 11851625
AU - Miano R; Lee L; Mannion EM; Rustin GJ; Christmas TJ
TI -
Mixed germ cell tumour arising from abdominal testicular tissue after
apparent orchidectomy.
SO - BJU Int 2001 Dec;88(9):980-1
AD - Department of Urology, Charing Cross Hospital, London, UK.
4
UI - 11782038
AU - Steyerberg EW; Vergouwe Y; Keizer HJ; Habbema JD; ReHiT Study Group
TI -
Residual mass histology in testicular cancer: development and validation
of a clinical prediction rule.
SO - Stat Med 2001 Dec 30;20(24):3847-59
AD - Center for Clinical Decision Sciences, Department of Public Health,
Erasmus Medical Center Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The
Netherlands. steyerberg@mgz.fgg.eur.nl
After chemotherapy for metastatic non-seminomatous testicular cancer,
surgical resection is a generally accepted treatment to remove remnants
of the initial metastases, since residual tumour may still be present
(mature teratoma or viable cancer cells). In this paper, we review the
development and external validation of a logistic regression model to
predict the absence of residual tumour. Three sources of information
were used. A quantitative review identified six relevant predictors from
19 published studies (996 resections). Second, a development data set
included individual data of 544 patients from six centres. This data set
was used to assess the predictive relationships of five continuous
predictors, which resulted in dichotomization for two, and a log, square
root, and linear transformation for three other predictors. The multiple
logistic regression coefficients were reduced with a shrinkage factor
(0.95) to improve calibration, based on a bootstrapping procedure.
Third, a validation data set included 172 more recently treated
patients. The model showed adequate calibration and good discrimination
in the development and in the validation sample (areas under the ROC
curve 0.83 and 0.82). This study illustrates that a careful modelling
strategy may result in an adequate predictive model. Further study of
model validity may stimulate application in clinical practice. Copyright
2001 John Wiley Sons, Ltd.
5
UI - 11857565
AU - Canto P; Soderlund D; Ramon G; Nishimura E; Mendez JP
TI -
Mutational analysis of the luteinizing hormone receptor gene in two
individuals with Leydig cell tumors.
SO - Am J Med Genet 2002 Mar 1;108(2):148-52
AD - Research Unit in Developmental Biology, Hospital de Pediatria, Centro
Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico,
D.F., Mexico.
Inactivating mutations of the luteinizing hormone receptor (LHR) gene in
males induce Leydig cell agenesis or hypoplasia, while activating
mutations cause testotoxicosis. Recently, it was demonstrated that a
somatic heterozygous activating mutation of the LHR gene (Asp578His),
limited to the tumor, was the cause of Leydig cell adenomas in three
unrelated patients. We describe the molecular study of two unrelated
boys with gonadotropin-independent hypersecretion of testosterone due to
Leydig cell adenomas. Genomic DNA was extracted from the tumor, the
adjacent normal testis tissue, and blood leukocytes. Both individuals
exhibited an heterozygous missense mutation, limited only to the tumor,
consisting of a guanine (G) to cytosine (C) substitution at codon 578
(GAT to CAT), turning aspartic acid into histidine. The presence of the
same mutation in different ethnic groups demonstrates the existence of a
mutational hot spot in the LHR gene. Indeed, this mutation occurs at the
conserved aspartic acid residue at amino acid 578, where a substitution
by glycine is the most common mutation observed in testotoxicosis and
where a substitution by tyrosine has been linked to a more severe
clinical phenotype where diffuse Leydig cell hyperplasia is found. Our
results confirm the fact that somatic activating mutations of
gonadotropin receptors are involved in gonadal tumorigenesis. Copyright
2002 Wiley-Liss, Inc.
6
UI - 11905918
AU - Dixon FJ; Moore RA
TI -
Testicular tumors. A clinicopathological study. 1953.
SO - J Urol 2002 Feb;167(2 Pt 2):896-918; discussion 919
7
UI - 11905919
AU - Cooper JF; Leadbetter WF; Chute R
TI -
The thoracoabdominal approach for retroperitoneal gland dissection: its
application to testis tumors. 1950.
SO - J Urol 2002 Feb;167(2 Pt 2):920-6; discussion 927
8
UI - 11905920
AU - Einhorn LH; Donohue J
TI -
Cis-diamminedichloroplatinum, vinblastine, and bleomycin combination
chemotherapy in disseminated testicular cancer. 1997.
SO - J Urol 2002 Feb;167(2 Pt 2):928-32; discussion 933
9
UI - 11905921
AU - Perlin E; Engeler JE Jr; Edson M; Karp D; McIntire KR; Waldmann TA
TI -
The value of serial measurement of both human chorionic gonadotropin and
alpha-fetoprotein for monitoring germinal cell tumors. 1976.
SO - J Urol 2002 Feb;167(2 Pt 2):934-7; discussion 938
10
UI - 11889161
AU - Richter-Unruh A; Wessels HT; Menken U; Bergmann M; Schmittmann-Ohters K;
TI -
Schaper J; Tappeser S; Hauffa BP
Male LH-independent sexual precocity in a 3.5-year-old boy caused by a
somatic activating mutation of the LH receptor in a Leydig cell tumor.
SO - J Clin Endocrinol Metab 2002 Mar;87(3):1052-6
AD - Department of Hematology/Oncology and Endocrinology, University
Children's Hospital, 45122 Essen, Germany.
annette.richter-unruh@uni-essen.de
We describe the clinical features of severe sexual precocity in a
3.5-yr-old boy. Hormonal evaluation showed LH-independent T
hypersecretion. Initial examination of the adrenals and testes revealed
no evidence of congenital adrenal hyperplasia, hCG- or
androgen-secreting tumors, or McCune-Albright syndrome. In the coding
sequence of the LH receptor gene no activating mutation was found.
Spironolactone (5.7 mg/kg x d) and testolactone (40 mg/kg x d) were
unsuccessful in suppressing the elevated concentration of T. To further
determine the origin of the elevated serum T, a selective venous
sampling procedure was planned. However before the sampling procedure,
high resolution ultrasound examination showed a small tumor in the left
testis, which was removed. Histology proved the tumor to be a Leydig
cell adenoma. Sequencing of the tumor LH receptor gene revealed a
heterozygous mutation in exon 11 encoding a replacement of aspartic acid
at position 578 with histidine, which has been shown to be a
constitutively activating mutation. These findings indicate that in male
patients with gonadotropin-independent sexual precocity, the presence of
small testicular Leydig cell tumors harboring a somatic mutation of the
LH receptor gene should be considered.
11
UI - 11762823
AU - Karapetis CS; Strickland AH; Yip D; van der Walt JD; Harper PG
TI -
PET and PLAP in suspected testicular cancer relapse: beware sarcoidosis.
SO - Ann Oncol 2001 Oct;12(10):1485-8
AD - Department of Medical Oncology, Guy's Hospital, London, UK.
A 31-year-old man previously treated with chemotherapy for metastatic
testicular cancer presented with new mediastinal lymphadenopathy and
peripheral lung opacities. Serum tumour markers were not elevated and a
PET (positron emission tomography) scan revealed increased FDG
(fluoro-deoxyglucose) uptake in the lungs and mediastinum consistent
with testis cancer relapse. A biopsy of a mediastinal lymph node was
performed and the pathology was that of sarcoidosis.
Immunohistochemistry however was positive for PLAP (placental alkaline
phosphatase) and negative for EMA (epithelial membrane antigen). This
immunohistochemical profile raised concerns that the observed pathology
represented a sarcoid reaction to micro-metastatic testicular cancer
relapse. We performed immunohistochemical pathology analysis on four
known cases of sarcoidosis and found the same
immunohistochemical-staining pattern. This case highlights the problem
of specificity when interpreting the significance of PET scans and
immunohistochemical analysis in this situation. Sarcoidosis, a condition
that has been associated with testicular cancer, should always be
considered in the differential diagnosis.
12
UI - 11920527
AU - Hendry WF; Norman AR; Dearnaley DP; Fisher C; Nicholls J; Huddart RA;
TI -
Horwich A
Metastatic nonseminomatous germ cell tumors of the testis: results of
elective and salvage surgery for patients with residual retroperitoneal
masses.
SO - Cancer 2002 Mar 15;94(6):1668-76
AD - Academic Department of Urology, The Royal Marsden National Health
Service Trust and Institute of Cancer Research, Sutton, Surrey, United
Kingdom.
BACKGROUND: A mass may persist in the para-aortic region after patients
undergo chemotherapy for metastatic, nonseminomatous germ cell tumor of
the testis (NSGCT). Retroperitoneal lymphadenectomy removes the mass,
which may contain residual active malignancy, and allows histologic
assessment of the effectiveness of the chemotherapy. Whereas some have
favored early, elective removal of such masses, others have chosen to
observe them, reserving salvage surgery for patients who experience
disease recurrence. A retrospective analysis was undertaken to define
the outcome in these two groups of patients. METHODS: After receiving
chemotherapy for metastatic NSGCT, 442 men underwent lymphadenectomy for
residual masses (measuring > or = 1 cm in greatest dimension) between
1976 and 1999, inclusive. Three hundred thirty men underwent elective
surgery within 3 months of the completion of chemotherapy, and 112 men
underwent salvage surgery after receiving reinduction chemotherapy for
tumor recurrence. RESULTS: The residual mass was removed completely in
87% and 72% of patients in the elective and salvage lymphadenectomy
groups, respectively; was removed with difficulty and possibly
incompletely in 9% and 21% of patients, respectively; and was definitely
removed incompletely in 4% and 7% of patients, respectively. The
operative mortality rate was 0.9% in the elective surgery group and 1.8%
in the salvage surgery group. There was malignant teratoma,
undifferentiated in 8.5% of patients in the elective surgery group and
in 49% of patients in the salvage surgery group (P < 0.001).
Differentiated teratoma and necrosis/fibrosis were present in 66.0% and
25.4% of patients in the elective surgery group, respectively, and in
38.4% and 12.5% of patients in the salvage surgery group, respectively.
The authors were unable to produce a clinically useful model to predict
the presence of necrosis/fibrosis only in either group. The 5-year
recurrence free and overall survival rates were 83% and 89%,
respectively, in the elective surgery group and 62% and 56%,
respectively, in the salvage surgery group. For the salvage surgery
group, the completeness of surgical excision and the presence of
undifferentiated teratoma were of overriding importance for overall
survival. A variety of other patient-related, tumor-related, and
surgery-related factors also were significant in the final model for the
elective surgery group. CONCLUSIONS: The current results demonstrate the
low level of morbidity that can be obtained, even in the salvage surgery
group, and the importance of complete surgical resection in this
setting. Because it is not possible to predict with sufficient accuracy
which patients will have favorable pathology (necrosis/fibrosis), the
authors continue to recommend elective surgery for all suitable men with
residual masses after they receive first-line chemotherapy. Copyright
2002 American Cancer Society.
13
UI - 11848466
AU - Chang A; Yousef GM; Jung K; Rajpert-De Meyts E; Diamandis EP
TI -
Identification and molecular characterization of five novel kallikrein
gene 13 (KLK13; KLK-L4) splice variants: differential expression in the
human testis and testicular cancer.
SO - Anticancer Res 2001 Sep-Oct;21(5):3147-52
AD - Department of Pathology and Laboratoty Medicine, Mount Sinai Hospital,
Toronto, Ontario, Canada.
The kallikrein gene family is comprised of genes that have either
established or potential applications in prostate and breast cancer
diagnostics. New members of the human kallikrein gene family have been
recently identified. By using the positional candidate gene approach, we
were able to clone a novel human serine protease gene that maps to
chromosome 19q13.3-q13.4, the location of the kallikrein gene family. We
named this gene KLK-L4 (now also known as KLK13). Here, we describe the
identification of five new KLK-L4 splice variants which are not
expressed in any other tissue except the human testis. We have further
established that these splice variants can be detected in normal testis
but not in the adjacent matched testicular tumors. In addition,
differential expression of the KLK-L4 gene was found in various
histological types of testicular cancer. Our results suggest that the
KLK-L4 gene is expressed in normal and cancerous testicular tissue;
however, its five variants are all expressed in normal tissue but not in
testicular tumors. The physiological relevance of these variants and the
implications of their differential expression between cancerous and
normal tissues are currently unknown.
14
UI - 11842380
AU - Wang BY; Rabinowitz DS; Granato RC Sr; Unger PD
TI -
Gonadal tumor with granulosa cell tumor features in an adult testis.
SO - Ann Diagn Pathol 2002 Feb;6(1):56-60
AD - Lilian and Henry M. Stratton-Hans Popper Department of Pathology, The
Mount Sinai School of Medicine, The Mount Sinai Medical Center, New
York, NY 10029, USA.
Granulosa cell tumor is almost exclusively an ovarian tumor. Rare cases
of granulosa cell tumor have been reported involving the testes. We
report a testicular gonadal stromal tumor with granulosa cell
differentiation in a 54-year-old white man. The tumor was discovered by
an ultrasound evaluation for left hydrocele. The patient was clinically
asymptomatic. On frozen section, the initial impression was a malignant
lymphoma. Final histology on the orchiectomy specimen showed a gonadal
stromal tumor with granulosa cell features. Immunohistochemical studies
excluded malignant lymphoma and germ cell tumors, consistent with a
stromal tumor. This case report illustrates the challenges for the
pathologist in making an accurate diagnosis in unusual testicular
tumors. Copyright 2002 by W.B. Saunders Company
15
UI - 11733909
AU - Ciftci AO; Bingol-Kologlu M; Senocak ME; Tanyel FC; Buyukpamukcu M;
TI -
Buyukpamukcu N
Testicular tumors in children.
SO - J Pediatr Surg 2001 Dec;36(12):1796-801
AD - Departments of Pediatric Surgery and Pediatric Oncology, Hacettepe
University Medical Faculty, Ankara, Turkey.
PURPOSE: The aim of this study was to present an updated picture of
surgical management of pediatric testicular tumors based on our 30
years' experience, which consisted of one of the largest noncollected
series treated in a single medical center. METHODS: Records of children
who were treated for testicular tumor in our unit from 1970 to 1999,
inclusive, were reviewed retrospectively. Information recorded for each
patient included age, sex, past medical history, clinical
characteristics, diagnostic procedures, treatment methods,
histopathologic findings, and outcome. RESULTS: Fifty-one patients with
a mean age of 3.8 +/- 0.5 years were treated for testicular tumors. Of
these, 35 (69%) had germ cell testis tumor (GCT) and 16 (31%) had
non-germ cell testis tumor (NGCT). Endodermal sinus tumor and
paratesticular rhabdomyosarcoma were the dominant histologic subtypes in
each group, respectively. The most common mode of presentation was
painless scrotal mass. At initial presentation, retroperitoneal (n = 5),
both retroperitoneal and lung (n = 2), and retroperitoneal and liver (n
= 3) metastases were recorded in 10 (19%) patients. Initial operative
procedures were radical inguinal orchiectomy (RIO) (n = 29), scrotal
orchiectomy (SO; n = 9), bilateral RIO (n = 2), both RIO and unilateral
retroperitoneal lymph node (RPLN) excision (n = 6), testis-sparing
enucleation of the tumor (n = 5). SOs were performed elsewhere, and
these patients underwent high ligation (n = 4) and both high ligation
plus RPLN excision (n = 5) in our unit. Histopathologically, spermatic
cord invasion and RPLN involvement were present in 10 patients. Scrotal
recurrences were encountered in 2 patients who had scrotal orchiectomy
initially. Retroperitoneal recurrences were noted in a patient
presenting with stage I embryonal carcinoma and in 2 patients presenting
with group IV paratesticular rhabdomyosarcoma. The mean follow-up period
was 89 +/- 10 months. Four patients with stage IV embryonal carcinoma (n
= 2) and group IV paratesticular rhabdomyosarcoma (n = 2) died of
progression of the disease. All remaining patients were alive and
disease free at their last outpatient appointment. No significant
difference was noted with regard to 5-year survival rates between (1)
malignant GCT and paratesticular rhabdomyosarcoma patients (91% v 80%)
and (2) patients treated by RIO (88%), SO plus high ligation (87%), and
RIO plus RPLN excision (80%). Five-year survival rates were 100% for
stage I, II, III patients and 33.3% for stage IV and group IV patients
presenting with malignant testicular tumors (P <.05). CONCLUSIONS:
Childhood testicular tumors deserve special attention from the
therapeutic point of the view. A solid scrotal mass should be considered
malignant until proved otherwise. Any suspicion of the testicular tumor
warrants an inguinal approach to prevent scrotal violation by the tumor.
Current trends emphasize that testis-sparing surgery should be performed
for benign lesions such as teratoma, leydig cell tumor, and epidermoid
cyst based on frozen biopsy findings. Literature findings and our
experience suggest that RIO is the accurate treatment for stage I
malignant GCT and group I and IIa paratesticular rhabdomyosarcoma. RPLN
excision is not of benefit either as a staging or therapeutic procedure
in stage I and group I and IIa diseases of these tumors. RPLN excision
should be reserved for (1) malignant GCT patients who have persistent
elevation of alpha-fetoprotein after orchiectomy in the presence of
normal total body CT scan, and for patients presenting with stage II and
III disease with definitive abnormality on CT scans, and (2) group IIb,
IIc, and III paratesticular rhabdomyosarcoma patients with radiologic
evidence of retroperitoneal involvement on CT scans. High ligation
should be done as a complementary procedure after SO to increase the
survival rates. J Pediatr Surg 36:1796-1801. Copyright 2001 by W.B.
Saunders Company.
16
UI - 11733935
AU - Trobs RB; Korholz D; Bennek J
TI -
Outcome of paratesticular involvement in infants with neuroblastoma.
SO - J Pediatr Surg 2001 Dec;36(12):E23
AD - Department of Pediatric Surgery, University of Leipzig, Germany.
The authors report on 3 infants suffering from disseminated
neuroblastoma (NB) involving the testes or paratesticular structures.
INSS stage 4 in 2 cases, and "biological" INSS stage 4S were considered,
respectively. One patient with a stage 4 NB died of tumor progression;
one patient is under therapy. The patient with NB 4S was cured with
preservation of both testes after antineoplastic chemotherapy and
reduction of the retroperitoneal primary. J Pediatr Surg 36:E23.
Copyright 2001 by W.B. Saunders Company.
17
UI - 11410198
AU - Levi F; La Vecchia C; Boyle P; Lucchini F; Negri E
TI -
Western and eastern European trends in testicular cancer mortality.
SO - Lancet 2001 Jun 9;357(9271):1853-4
Testicular cancer is curable if treated appropriately. We used national
mortality data to compare specific death rates from the disorder in
western and eastern Europe, the USA, and Japan. Testicular cancer
mortality rates have fallen by about 70% in the USA and western Europe
since the 1970s. In eastern Europe, however, death rates from testicular
cancer have been declining only since the late 1980s, and at a much
slower rate than that recorded elsewhere (about 20%). Consequently, many
avoidable deaths, mainly in young adults, are still occurring in eastern
Europe. Available effective treatment strategies for testicular cancer
must be implemented in these countries.
18
UI - 11896102
AU - Petersen PM; Giwercman A; Daugaard G; Rorth M; Petersen JH; Skakkeaek
TI -
NE; Hansen SW; von der Maase H
Effect of graded testicular doses of radiotherapy in patients treated
for carcinoma-in-situ in the testis.
SO - J Clin Oncol 2002 Mar 15;20(6):1537-43
AD - Department of Growth & Reproduction, Finsencenter, Copenhagen University
Hospital, Rigshospitalet, Copenhagen. pmp@post11.tele.dk
PURPOSE: To determine the effect of radiotherapy in doses 14 to 20 Gy on
eradication of carcinoma-in-situ (CIS) testis and on the Leydig cell
function. PATIENTS AND METHODS: Forty-eight patients presented with
unilateral testicular germ cell cancer and CIS of the contralateral
testis. The CIS-bearing testis was treated with daily irradiation doses
of 2 Gy, 5 days a week, to a cumulative dose of 20 Gy (21 patients), 18
Gy (three patients), 16 Gy (10 patients), and 14 Gy (14 patients).
RESULTS: All patients treated at dose levels 20 Gy to 16 Gy achieved
histologically verified complete remission without signs of recurrence
of CIS after an observation period of more than 5 years. One of 14
patients treated at dose level 14 Gy had a relapse of CIS 20 months
after irradiation. Leydig cell function was examined before and
regularly after radiotherapy in 44 of 48 patients. The levels of
testosterone were lower after radiotherapy than before. Testosterone
showed a stable decrease for more than 5 years after treatment (3.6% per
year) without dose dependency. The levels of luteinizing hormone and
follicle-stimulating hormone were increased after radiotherapy. The need
of androgen substitution therapy was similar at all dose levels.
CONCLUSION: Testicular irradiation is a safe treatment at dose level 20
Gy (10 x 2 Gy). Decrease of dose to 14 Gy (7 x 2 Gy) might lead to risk
of relapse of CIS. Impairment of hormone production without clinically
significant dose dependency is seen in the dose range 14 to 20 Gy.
19
UI - 11896104
AU - Kersemaekers AM; Mayer F; Molier M; van Weeren PC; Oosterhuis JW;
TI -
Bokemeyer C; Looijenga LH
Role of P53 and MDM2 in treatment response of human germ cell tumors.
SO - J Clin Oncol 2002 Mar 15;20(6):1551-61
AD - Department of Pathology/Laboratory for Experimental Patho-Oncology,
University Hospital Rotterdam/Daniel, Josephine Nefkens Institute,
Erasmus University Rotterdam, Rotterdam, The Netherlands.
PURPOSE: Testicular germ cell tumors (TGCTs) of adolescents and adults
are very sensitive to systemic treatment. The exquisite chemosensitivity
of these cancers has been attributed to a high level of wild-type P53.
MATERIALS AND METHODS: To clarify the role of P53 in treatment
sensitivity and resistance of TGCTs, we performed immunohistochemistry
and Western blotting analysis on a series of 39 fresh-frozen primary
TGCTs before therapy (unselected series). In a series of formalin-fixed
paraffin-embedded TGCTs of patients with fully documented clinical
course, including treatment-sensitive (n = 17) and -resistant (n = 18)
tumors, P53 status was assessed by immunohistochemistry and mutation
analysis. In addition, the involvement of MDM2, a P53 antagonist, was
investigated by immunohistochemistry, reverse transcriptase polymerase
chain reaction, and in situ hybridization. RESULTS: Immunohistochemistry
demonstrated absence of staining for P53 in 36%, 41%, and 17% of the
unselected, responding, and nonresponding TGCTs, respectively. Of the
positive TGCTs, most tumors, ie, 49%, 41%, and 33%, showed 1% to 10%
positive nuclei. This overall low level of P53 was confirmed by Western
blotting. Mutation analysis revealed only one silent P53 mutation in one
of the responding patients. All embryonal carcinomas were homogeneously
positive for MDM2, encoded by the full length mRNA, while a
heterogeneous pattern was found for the other histologic components.
Amplification of MDM2 was detected in one out of 12 embryonal
carcinomas. CONCLUSION: Although our results are in line with previous
findings of the presence of wild-type P53 in TGCTs, they show that a
high level of P53 does not relate directly to treatment sensitivity of
these tumors, and inactivation of P53 is not a common event in the
development of cisplatin resistance.
20
UI - 11570405
AU - Oliver RT
TI -
Trends in testicular cancer.
SO - Lancet 2001 Sep 8;358(9284):841
21
UI - 11832607
AU - Kaushik R; Attri AK; Kaur L; Nada R
TI -
Leiomyoma of the vas deferens.
SO - J Postgrad Med 2001 Apr-Jun;47(2):133-4
AD - Department of Surgery, Government Medical College and Hospital,
Chandigarh, India. robinkaushik@yahoo.com
22
UI - 9605748
AU - Avizienyte E; Roth S; Loukola A; Hemminki A; Lothe RA; Stenwig AE; Fossa
TI -
SD; Salovaara R; Aaltonen LA
Somatic mutations in LKB1 are rare in sporadic colorectal and testicular
tumors.
SO - Cancer Res 1998 May 15;58(10):2087-90
AD - Department of Medical Genetics, Haartman Institute, University of
Helsinki, Finland.
Germ-line mutations in a serine/threonine kinase gene, LKB1, were
recently shown to underlie Peutz-Jeghers syndrome (PJS), a hereditary
disorder that predisposes to benign and malignant tumors of multiple
organ systems. Most mutations that have been described thus far
dramatically change the predicted protein and are likely to be of an
inactivating nature. This observation and a previous observation that
the LKB1 locus is often deleted in PJS polyps suggest that the gene may
function as a tumor suppressor. We examined whether somatic mutations in
this gene are present in sporadic carcinomas of the colon and testis,
tumors that are characteristic of PJS. First, 20 randomly selected
colorectal and 28 testicular tumors were analyzed by single-strand
conformation polymorphism analysis. No mutations in LKB1 were found in
colorectal tumors. One testicular tumor displayed a heterozygous
missense type variant, in which glycine 163 was changed to aspartic
acid. This change was absent in the DNA of normal tissue. To better
focus our efforts, we tested 75 additional colon carcinomas for loss of
heterozygosity at 19p, where LKB1 is localized. Of 75 samples analyzed,
50 were informative with a closely linked marker, D19S886, and 13 (26%)
of these displayed loss of heterozygosity. The 13 tumors were
scrutinized for LKB1 mutations by genomic sequencing. This analysis
revealed no changes. Together, these findings suggest that somatic
mutations of LKB1 are not frequent in colorectal and testicular cancer.
23
UI - 9887330
AU - Ylikorkala A; Avizienyte E; Tomlinson IP; Tiainen M; Roth S; Loukola A;
TI -
Hemminki A; Johansson M; Sistonen P; Markie D; Neale K; Phillips R;
Zauber P; Twama T; Sampson J; Jarvinen H; Makela TP; Aaltonen LA
Mutations and impaired function of LKB1 in familial and non-familial
Peutz-Jeghers syndrome and a sporadic testicular cancer.
SO - Hum Mol Genet 1999 Jan;8(1):45-51
AD - Hartman Institute and Biocentrum Helsinki and Department of Medical
Genetics, Haartman Institute, PO Box 21, University of Helsinki, 00014
Helsinki, Finland.
Germline mutations in LKB1 have been reported to underlie familial
Peutz-Jeghers syndrome (PJS) with intestinal hamartomatous polyps and an
elevated risk of various neoplasms. To investigate the prevalence of
LKB1 germline mutations in PJS more generally, we studied samples from
33 unrelated PJS patients including eight non-familial sporadic
patients, 20 familial patients and five patients with unknown family
history. Nineteen germline mutations were identified, 12 (60%) in
familial and four (50%) in sporadic cases. LKB1 mutations were not
detected in 14 (42%) patients, indicating that the existence of
additional minor PJS loci cannot be excluded. LKB1 is predicted to
encode a serine/threonine kinase. To demonstrate the putative Lkb1
kinase function and to study the consequences of LKB1 mutations in PJS
and sporadic tumors, we have analyzed the kinase activity of wild-type
and mutant Lkb1 proteins. Interestingly, while most of the small
deletions or missense mutations resulted in loss-of-function alleles,
one missense mutation (G163D) previously identified in a sporadic
testicular tumor demonstrated severely impaired but detectable kinase
activity.
24
UI - 11921289
AU - Schneider DT; Schuster AE; Fritsch MK; Calaminus G; Gobel U; Harms D;
TI -
Lauer S; Olson T; Perlman EJ
Genetic analysis of mediastinal nonseminomatous germ cell tumors in
children and adolescents.
SO - Genes Chromosomes Cancer 2002 May;34(1):115-25
AD - Division of Pediatric Pathology, Department of Pathology, Johns Hopkins
Medical Institutions, Baltimore, Maryland 21287, USA.
Primary mediastinal germ cell tumors (M-GCTs) represent a heterogeneous
group of tumors that varies with regard to age at presentation,
histologic differentiation, and outcome. We retrospectively analyzed
archival tissue samples of mediastinal mature and immature teratomas (n
= 15) and malignant nonseminomatous M-GCTs (n = 20) with comparative
genomic hybridization (CGH). The aim of this study was to define
distinct genetic subgroups of M-GCT among the pediatric cohort that may
differ in their clinical behavior and prognosis. All pure teratomas
showed normal CGH profiles. Malignant M-GCTs in infants and children < 8
years old most frequently showed a gain of 1q, 3, and 20q and a loss of
1p, 4q, and 6q. Gain of 12p and sex chromosomal abnormalities were not
observed in this age group. In contrast, the gain of 12p was the most
common aberration in M-GCTs that arose in children > or = 8 years old.
Additional recurrent changes included the loss of chromosome 13 and the
gain of chromosome 21. All ten adolescents with malignant M-GCT were
male, and five showed a gain of the X chromosome. In two of these five
patients, Klinefelter syndrome was confirmed by cytogenetic analysis or
by fluorescence in situ hybridization (FISH). In conclusion, CGH
analysis of M-GCTs defines distinct genetic subgroups. Mediastinal
teratomas show no genetic gains or losses. Malignant M-GCTs in children
< 8 years old show the same pattern of gains and losses identified in
sacrococcygeal and testicular GCTs at this age, and they lack
sex-chromosomal abnormalities. Malignant M-GCTs in children > or = 8
years old show the same genetic profile previously reported in gonadal
GCTs at this age. In addition, approximately 50% demonstrate a gain of
the X chromosome, consistent with Klinefelter syndrome. Cooperative
group studies reveal a significantly better prognosis of malignant M-GCT
arising in infants compared to that in adolescents, suggesting that
these genetic differences are associated with differences in clinical
behavior. Copyright 2002 Wiley-Liss, Inc.
25
UI - 11883131
AU - Bajaj P; Agarwal K; Niveditha SR; Pathania OP
TI -
Leiomyosarcoma arising from tunica vaginalis testis: a case report.
SO - Indian J Pathol Microbiol 2001 Apr;44(2):145-6
AD - Department of Pathology, Lady Hardinge Medical College, New Delhi.
Benign and malignant soft tissue tumors of the paratesticular region
i.e. those arising from the testicular tunics, epididymis and spermatic
cord are uncommon. Of these, leiomyosarcoma arising from the tunica
vaginalis is extremely rare. On extensive computerised search, a single
case has been reported till date in the literature. We hereby report one
such case because of its rarity.
26
UI - 11881732
AU - Hekimgil M; Altay B; Yakut B D; Soydan S; Ozyurt C; Killi R
TI -
Leydig cell tumor of the testis: comparison of histopathological and
immunohistochemical features of three azoospermic cases and one
malignant case.
SO - Pathol Int 2001 Oct;51(10):792-6
AD - Department of Pathology, Ege University Faculty of Medicine, Izmir,
Turkey. hekimgil@alpha.med.ege.edu.tr
Leydig cell tumors of the testis are rare, mostly presenting as a
testicular mass or as endocrinological symptoms. Here, three patients
who were admitted for investigation of primary infertility and one
patient presenting with a testicular mass are reported. The histological
features were reviewed and an immunohistochemical study was done using a
panel of antibodies against cytokeratin, vimentin, inhibin A, S-100,
Ki-67, follicle-stimulating hormone, luteinizing hormone, prolactin,
p53, bcl-2, and c-erbB2. The latter case (lost during follow up of
metastatic disease) demonstrated massive tumor necrosis, extension
through the tunica albuginea, and a high mitotic activity and MIB-1
score. Only this malignant case was bcl-2 positive. Of the two oncogenic
markers studied, none of the cases were positive for c-erb2, while p53
was positive in more than 50% of cells in the malignant case and in one
case of infertility with a large tumor, hemorrhage, focal necrosis and
atypical cytological features. We recommend the evaluation of infertile
men for Leydig cell tumors, and we believe that a panel of antibodies,
including Ki-67, p53 and bcl-2, used for immunohistochemical analysis
could be of diagnostic value in the identification of malignant and
borderline cases of Leydig cell tumor.
27
UI - 11904381
AU - Einhorn LH
TI -
Curing metastatic testicular cancer.
SO - Proc Natl Acad Sci U S A 2002 Apr 2;99(7):4592-5
AD - Indiana University Medical Center, 535 Barnhill Drive, RT 473,
Indianapolis, IN 46202-5289, USA. leinhorn@uipui.edu
Our initial studies with cisplatin + vinblastine + bleomycin began 27
years ago in 1974, changing the cure rate for disseminated disease from
5 to 60%. Subsequently, through random prospective clinical trials, we
have modified the treatment regimen to reduce both the duration and
dosages of the chemotherapy drugs. Cisplatin + etoposide was first used
at Indiana University as salvage chemotherapy in 1978, representing the
first time that a solid tumor had been cured with second-line
chemotherapy. We next did a clinical trial comparing bleomycin +
etoposide + cisplatin (BEP) to cisplatin + vinblastine + bleomycin. The
BEP regimen was proven to have less toxicity and a higher cure rate and
therefore, since 1984, has been standard chemotherapy. More recent
studies have evaluated the use of lesser chemotherapy to maintain the
same cure rate for patients with good-prognosis disease. Standard
therapy for these patients is either three courses of BEP or four
courses of EP, and over 90% of these patients will be cured of their
disease. Patients who are not cured with their initial BEP chemotherapy
are usually treated with salvage chemotherapy. Approximately 50% of
these testicular cancer patients will subsequently be cured with salvage
chemotherapy with tandem transplant of high-dose chemotherapy with
peripheral stem cell rescue. Testicular cancer has become a model for a
curable neoplasm. In the early 1970s, metastatic testicular cancer was
associated with only 5% survival. Today, with modern chemotherapy and
surgery techniques, 80% of patients will survive their disease.
28
UI - 11900499
AU - Vaughn DJ; Gignac GA; Meadows AT
TI -
Long-term medical care of testicular cancer survivors.
SO - Ann Intern Med 2002 Mar 19;136(6):463-70
AD - University of Pennsylvania School of Medicine, The Leonard and Madlyn
Abramson Family Cancer Research Institute at the University of
Pennsylvania Cancer Center, 16 Penn Tower, 3400 Spruce Street,
Philadelphia, PA 19104, USA.
Testicular cancer is the most common solid tumor diagnosed in men 20 to
35 years of age. Because of highly effective treatments that may include
surgery, chemotherapy, and radiation therapy, most patients become
long-term survivors. Health-related issues that confront testicular
cancer survivors include the late medical effects of chemotherapy, the
late relapse of disease, the development of second cancers, the effect
of the disease and treatment on fertility, and the psychosocial
consequences. This case-based discussion focuses on the primary care
physician's evaluation and management of a long-term survivor of
testicular cancer who was previously treated with surgery and
chemotherapy.
29
UI - 11968735
AU - Iida K; Tsutsumi M; Ishikawa S
TI -
[Metachronous primary malignant lymphoma of the bilateral tests: a case
report]
SO - Hinyokika Kiyo 2002 Feb;48(2):93-5
AD - Department of Urology, Hitachi General Hospital.
We report a case of metachronous malignant lymphoma of the bilateral
testes. A 62-year-old man presented with a mass in the right scrotal
contents. Physical examination revealed a solid painless mass in the
right scrotal contents measuring 4 cm in diameter. He underwent right
high orchiectomy. The histological examination confirmed non-Hodgkin's
lymphoma of diffuse, large-sized cells of the B cell type. Computed
tomography of the abdomen revealed paracaval lymphandenopathy at stage
IIE according to Ann Arbor classification. Chemotherapy was initiated
with cyclophosphamide, adriamycin and vincristine. Eleven months after
the initial operation, the patient complained of left scrotal swelling,
and subsequently underwent left high orchiectomy. The histological
examination revealed the same pathology as observed in the right one
scrotal contents. He was free from recurrence at 15 months after the
second operation.
30
UI - 11718451
AU - Baou N; Bouras M; Droz JP; Dutrieux-Berger N; Bouvier R; Benahmed M;
TI -
Krantic S
Somatostatin receptor expression profile as a potential criterion for
discrimination between seminoma and non-seminoma testicular tumors.
SO - Cancer Detect Prev 2001;25(5):446-53
AD - INSERM 407, Faculte de Medecine Lyon Sud, Oullins, France.
The expression of five (sst1-sst5) somatostatin (SRIF) receptor mRNAs
was compared between normal and tumoral testicular samples diagnosed as
either seminoma or non-seminoma. Reverse transcriptase-polymerase chain
reaction (RT-PCR) analysis indicated that all testicular tissues studied
(total of 24) contained sst5 receptor transcripts, whereas the sst2 was
absent in all of them. In contrast to the normal tissue samples, both
types of tumors (total of 12) did not contain sst4 transcripts. sst3
mRNA was expressed in normal and non-seminoma samples, but not in
seminomas. sst1 transcripts were not found in normal and seminoma
tissues. However, all studied non-seminomas contained this mRNA. Our
data thus points to a specific pattern of SRIF receptor mRNA expression
in each type of the samples analyzed. Moreover, they further indicate
that the presence of sst1 and sst3 transcripts might be used as an
additional criterion to distinguish between seminoma and nonseminoma
tumors.
31
UI - 11956262
AU - Kollmannsberger C; Rick O; Derigs HG; Schleucher N; Schoffski P; Beyer
TI -
J; Schoch R; Sayer HG; Gerl A; Kuczyk M; Spott C; Kanz L; Bokemeyer C
Activity of oxaliplatin in patients with relapsed or
cisplatin-refractory germ cell cancer: a study of the German Testicular
Cancer Study Group.
SO - J Clin Oncol 2002 Apr 15;20(8):2031-7
AD - Department of Hematology/Oncology, University of Tuebingen Medical
Center, Tuebingen, Germany.
PURPOSE: To investigate the efficacy and toxicity of oxaliplatin, a
diaminocyclohaxane platinum derivative with incomplete cross-resistance
to cisplatin in patients with relapsed or cisplatin-refractory germ cell
cancer. PATIENTS AND METHODS: Thirty-two patients with nonseminomatous
cisplatin-refractory germ cell cancer or relapsed disease after
high-dose chemotherapy (HDCT) plus autologous stem-cell support were
treated with single-agent oxaliplatin 60 mg/m(2) on days 1, 8, and 15
repeated every 4 weeks (group 1; n = 16) or oxaliplatin 130 mg/m(2)
given on days 1 and 15 of a 4-week cycle (group 2; n = 16). Patients
were pretreated with a median of seven (range, three to 13)
cisplatin-containing treatment cycles; 78% had received
carboplatin/etoposide-based HDCT before oxaliplatin therapy.
Twenty-seven patients (84%) were considered refractory (n = 20; 63%) or
absolutely refractory (n = 7; 22%) to cisplatin therapy. RESULTS:
Overall, four patients achieved a partial remission (13%; 95% confidence
interval, 1% to 24%). Two additional patients achieved disease
stabilization. All responses were observed in cisplatin-refractory
patients, including three who had not responded to previous HDCT.
Patients received a median two cycles of oxaliplatin with a median
cumulative dose of 350 mg/m(2). Hematologic toxicity was generally mild,
with five patients developing grade 3/4 thrombocytopenia. Nonhematologic
side effects consisted mainly of nausea/vomiting. One patient developed
grade 3 neurotoxicity. CONCLUSION: Considering the particularly
unfavorable prognostic characteristics of this patient population
compared with patients from previous trials for new drugs in germ cell
cancer, eg, paclitaxel and gemcitabine, a 13% overall response rate and
a 19% response rate in the group treated with oxaliplatin 130 mg/m(2)
seems to be of interest. Oxaliplatin may be a palliative treatment
option for this patient population, and evaluation in combination
regimens is warranted.
32
UI - 11956460
AU - Hansen KS; Sheley RC
TI -
Aortoenteric fistula in advanced germ cell tumor: a rare lethal
complication.
SO - J Urol 2002 May;167(5):2131
AD - Department of Oncology and Interventional Radiology, Legacy Good
Samaritan Hospital, Portland, Oregon, USA.
33
UI - 11763316
AU - Albanese JM; Reuter VE; Bosl GJ; Houldsworth J; Chaganti RS
TI -
Expression of ID genes in differentiated elements of human male germ
cell tumors.
SO - Diagn Mol Pathol 2001 Dec;10(4):248-54
AD - Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York,
New York 10021, USA.
The ID genes are members of a family of genes that encode
helix-loop-helix (HLH)-containing proteins. The Id proteins, unlike
other HLH proteins, lack an adjacent DNA binding domain and hence act as
dominant negative regulators of HLH transcription factors that have been
implicated in control of cellular differentiation. Although the role of
Id genes in murine development has been documented, their roles in human
embryogenesis remain unknown. In this study, human male germ cell tumors
(GCTs) were used as a model for examining the expression of the ID genes
in various histologies that are reflective of different temporal phases
of human development. In seminomas, little or no expression of IDI, ID2,
and ID3 was detected, consistent with the uncommitted germ cell-like
phenotype of this tumor histology. Likewise, GCTs with histologies
reflective of extraembryonic and embryonic patterns of differentiation
exhibited patterns of expression of the three ID genes often similar to
those noted during murine development. It was also evident, as revealed
by ID expression patterns, that despite the overall aberrant spatial
differentiation patterns displayed by these tumors, some tissue-tissue
interactions reminiscent of those observed during normal embryogenesis
are retained. Thus, adult male GCTs offer a unique system in which the
role of genes such as the IDs can be studied in human embryogenesis.
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