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Biomedical subjects

R von Knobloch

Publications and source records attributed to R von Knobloch.

8 recordsLinked to original sources
PubMed2001

Current status of cytotoxic chemotherapy in hormone refractory prostate cancer.

Adenocarcinoma of the prostate is the most prevalent neoplastic disease in men and continues to be a major cause of morbidity and mortality. Death from prostate cancer is associated with objective and biochemical progression following hormonal manipulations often described as hormone refractory prostate cancer (HRPCA). Therapy for HRPCA is primarily palliative and therapeutic efficacy has to be balanced against potential treatment-related side effects. Therapeutic efficacy may be assessed by evaluating the percentage of patients obtaining a PSA decline of > 50%, evaluating the response of bidimensionally measurable disease or by improvements in quality of life assessments. The most effective cytotoxic therapies at the present time seem to be combinations of estramustine phosphate with taxanes and etoposide. Regimes employing ketoconazole with estramustine, vinblastine or bisphosphonates seem to be worthy of further evaluation. Mitoxantrone has an impressive palliative effect in patients, particularly when combined with hydrocortisone. Oral chemotherapeutic regimens with a combination of estramustine phosphate, cyclophosphamide and prednisone appear to offer a less toxic alternative. For the future we need prospective randomized clinical phase-III studies, prognosticators identifying patients as being at high or low risk who might benefit from different therapeutic approaches and generally binding eligibility and response guidelines in order to be able to compare trials of different therapeutic approaches.

Anthracyclines↗
PubMed2000

Allelic changes at multiple regions of chromosome 5 are associated with progression of urinary bladder cancer.

This study has analysed 65 urothelial carcinomas for allelic imbalance at 22 loci of chromosome 5 and has determined three regions of interest. A commonly duplicated region was mapped to chromosome 5p between loci D5S1473 and D5S819, one region of deletion to chromosome 5q22-23 between loci D5S2055 and D5S659, and another to chromosome 5q33-34 between loci D5S1456 and D5S1465. An allelic imbalance was detected in 54% of the cases. Only 10% of grade 1 tumours showed allelic changes at chromosome 5, whereas 60% and 63% of grade 2 and grade 3 cancers, respectively, had alterations of chromosome 5. The frequency of chromosome 5 changes increased from 24% in pTa tumours up to 72% in pT3-4 tumours. Of particular interest, ten out of 12 urothelial carcinomas showing metastatic growth in regional lymph nodes at the time of cystectomy had alterations at chromosome 5. No specific region, but genetic changes in general were associated with the grading and staging of bladder cancers.

Alleles↗
PubMed2000

Management of contralateral adrenal metastasis from renal cell carcinoma: possibility of inferior vena cava tumour thrombus.

OBJECTIVE: The contralateral adrenal gland is a rare metastatic site in renal cell carcinoma (RCC). We describe our experiences with this metastasis in a cohort of 610 radical nephrectomy patients analysed. To our knowledge this study is the first to demonstrate an inferior vena cava tumour thrombus from metachronous contralateral adrenal metastasis. PATIENTS AND METHODS: After radical nephrectomy for RCC, 610 patients treated at our institution from 1985-99 were retrospectively investigated for the incidence of contralateral adrenal metastasis, additional clinical findings, treatment modalities and survival after treatment for contralateral adrenal gland metastasis. RESULTS: The incidence of contralateral adrenal metastasis was 1.1% (7/610 patients), while the incidence of ipsilateral metastasis was 3.4% (21/610). In 3 of 7 cases the contralateral adrenal metastasis occurred simultaneously with primary RCC in the kidney. The contralateral adrenal gland was affected by distant tumour spread metachronously in 4 of 7 cases (3/4 bilateral adrenal involvement, 1/4 unilateral disease). In 1 case a metachronous contralateral adrenal metastasis caused vena cava tumour thrombus by propagation via the suprarenal venous route. After a mean follow-up of 20 months (range 1-54 months), 4 of 6 patients showed no evidence of disease after contralateral adrenalectomy. CONCLUSIONS: The probability of contralateral adrenal metastasis from RCC is 1.1%. Adrenalectomy in these cases offers a good chance of cure. In 71% of cases contralateral adrenal metastasis occurs in conjunction with ipsilateral disease, which provides a strong argument for routine ipsilateral adrenalectomy during radical nephrectomy. Care must be taken in preoperative diagnostics, as metachronous adrenal metastasis is capable of causing vena cava tumour thrombus.

Adrenal Gland Neoplasms↗
PubMed1999

Microsatellite analysis reveals deletion of a large region at chromosome 8p in conventional renal cell carcinoma.

Loss of heterozygosity (LOH) at chromosome 8p is associated with the progression of conventional (non-papillary) renal cell carcinomas (RCC). To determine the tumor suppressor gene locus, we carried out a deletion mapping of chromosome 8p at 10 microsatellite loci in 96 RCCs. LOH occurred in 32% of the tumors. The smallest overlapping region of deletion at chromosome 8p11.2-p23.1 corresponds to approximately 34-cM genetic distance. No small interstitial deletion was seen.

Carcinoma, Renal Cell↗
PubMed1999

Radical nephrectomy for renal cell carcinoma: Is adrenalectomy necessary?

OBJECTIVES: The role of simultaneous adrenalectomy in combination with radical nephrectomy in the treatment for renal cell carcinoma (RCC) remains controversial. With nephron-sparing surgery being commonly applied, the indication for adrenalectomy has to be critically assessed. PATIENTS AND METHODS: In a retrospective analysis the outcome of 589 patients, who underwent ipsilateral adrenalectomy along with radical nephrectomy in the treatment for RCC between 1985 and 1997 at our institution, was evaluated. The mean follow-up time was 34 months (range 1-95). RESULTS: Histologically an ipsilateral adrenal metastasis was found in 19/589 patients (3.2%). 16/19 patients had >/= T3, 3/19 had T1 tumours. The average size of the primary tumours with adrenal metastasis was 7.8 cm (range 2.3-13) in diameter with no preferential primary tumour site within the kidney (6/19 upper, 4/19 middle and 9/19 lower third). Only 4/19 patients had suspect adrenal findings in preoperative diagnostics (ultrasound, CT scan). 6/19 (31.5%) patients with adrenal metastasis are alive without evidence of disease at a mean of 41 months (range 11-95) after surgery for RCC. CONCLUSIONS: The probability of adrenal metastasis correlates with primary tumour stage, but not with its location within the kidney. The preoperative diagnostics are not reliable concerning small adrenal metastases. We thus still recommend simultaneous adrenalectomy in those cases where radical nephrectomy in patients with RCC is indicated.

Adrenal Gland Neoplasms↗
PubMed1998

Duplication and overexpression of the mutant allele of the MET proto-oncogene in multiple hereditary papillary renal cell tumours.

Previous karyotyping showed a combined trisomy of chromosome 7 and 17 in sporadic and hereditary papillary renal cell tumours (RCT). A recent molecular analysis revealed a mutation in the MET tyrosine kinase (chromosome 7q31) in the germline of four out of seven families with hereditary papillary RCT (HPRCT). We have analysed germline cells as well as multiple tumours obtained from HPRCT families and sporadic cases for alteration of the MET tyrosine kinase and for allelic duplication at chromosome 7 and 17. We have detected a germ line mutation in the MET tyrosine kinase in one of the two families with HPRCTs and also found the same mutation in the germ line of one patient with clinically recognized multiple, bilateral papillary RCTs but without family history. The mutant MET allele is consequently duplicated and overexpressed in tumour cells indicating that duplication of the mutant MET allele is necessary before cells enter the tumorigenic pathway. The lack of germline mutation in two members of another HPRT family and duplication of the same parental allele of chromosome 7 in multiple tumours suggests that a germ line event other than mutation of MET tyrosine kinase is involved in the development of these tumours. Duplication of different alleles of chromosome 7 in sporadic and of chromosome 17 in both types of tumours excludes a germline mutation at these chromosomal sites.

Adenoma↗