1/87. Clinical value of protein-bound fucose in patients with carcinoma and other diseases.Protein-bound fucose content in sera from normal persons and patients with various malignant and non-malignant diseases was measured and statistically analyzed. Normal serum gave a mean value of 6.84 /- 0.13 mg/100 ml, and rarely exceeded 9 mg/100 ml. Although no significant difference was found between sexes, there was a tendency of fucose content to decrease in older persons. It was noted that more than 90% of cancer-bearing patients have significantly higher level than critical value (9 mg/100 ml), while only 8.7% of patients with benign tumor showed positive result. These results were not limited to special organs but in common to all cases studied. The elevation of serum fucose content in malignant tumor was well correlated with its stages of progression, though the levels were less significant in early and in rather locally restricted breast and thyroid cancer. Serial postoperative follow-up study showed that the levels in serum fucose content was a useful parameter for judging the effectiveness of therapy and the prognosis of the patient. The fucose content in malignant tumor tissue and metastasized lymph node appeared to be significantly elevated than that in normal tissue. The practical usage and limitation of the fucose value in various diseases, together with a possible source of serum fucose were discussed.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
2/87. A translocation breakpoint at chromosome band 12q13 associated with B-cell chronic lymphocytic leukemia.Low-grade B-cell lymphoproliferative disorders are frequently associated with an extra copy of chromosome 12. This well-documented acquired anomaly is one of the most specific numerical chromosome alterations to occur in human hematological malignancies. We have cytogenetically characterized bone marrow and peripheral blood cells from a patient with B-cell chronic lymphocytic leukemia (CLL) having a unique acquired translocation involving chromosomes 6 and 12, t(6;12) (p21.3;q13), which implicates band 12q13 as the site of the gene(s) important in this lymphoproliferative B-cell disorder. aneuploidy, in the form of trisomy of chromosome 12, is not a requirement for neoplastic transformation in B-cell CLL, but gene rearrangement (present case) or nondisjunctional acquisition of additional copies of defective genes on chromosome 12 at band q13 may be involved in the genesis or progression of this disorder.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
3/87. High grade, synchronous colon cancers after renal transplantation: were immunosuppressive drugs to blame?Recipients of renal transplants are known to have an increased incidence of cancer, which is believed to be related to the use of immunosuppressive drugs used to prevent rejection. Although the risks of lymphoma and Kaposi's sarcoma are clearly increased in this setting, the association with colon cancer is controversial. We report a 44-yr-old woman, 20 yr post-renal transplant, and with no family history of colorectal cancer or polyps, who was found to have synchronous, poorly differentiated colon cancers associated with extensive abdominal lymph node, bone marrow, and bone (skull) metastasis. The long term immunosuppressive drugs that she had received may have been an important factor in her tumor development and/or progression. Our case and literature review suggest a possible mild, increased risk of colon cancer development in patients after renal transplantation.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
4/87. Epstein-Barr virus-positive primary gastrointestinal Hodgkin's disease: association with inflammatory bowel disease and immunosuppression.Inflammatory bowel disease (IBD) is associated with an increased risk of lymphoma, which is usually extraintestinal but sometimes may involve the diseased bowel itself. Most lymphomas described in this setting are of non-Hodgkin's type, but rare cases of Hodgkin's disease (HD) have been reported. We describe the clinicopathologic and molecular features of four patients with primary gastrointestinal HD. Three patients had preexistent Crohn's disease (CD), for which two of them had received immunosuppressive therapy. The fourth patient had a longstanding history of diverticulitis and myasthenia gravis and was receiving immunosuppressive therapy for the latter. Multifocal involvement of the bowel by HD was noted in all four cases. disease was staged as IVA in one patient, IIIB in one patient, and IE in one patient, and the fourth patient died in the postoperative period before further workup. Two patients received chemotherapy, one of whom was dead at 9 months, whereas the other has no evidence of disease at 25 months' follow-up. The patient with IE disease did not receive any therapy because only a few microscopic foci of disease were present and is also without any evidence of disease at 17 months. The Reed-Sternberg (RS) cells in all four cases expressed CD30, CD15, EBER-1, and LMP-1; two of four were focally CD20-positive. VJ-polymerase chain reaction for immunoglobulin heavy chain (IgH) rearrangement showed a polyclonal pattern in all four cases. In two cases, laser capture microdissection was used to isolate individual RS and Hodgkin's cells, which contained rearranged immunoglobulin genes, confirming a B-cell genotype. Whereas one case showed a dominant clonal band present in all isolates, cells from the patient with stage IE disease clearly showed a polyclonal population of RS cells. Our findings indicate that HD arising in the setting of IBD or chronic inflammation is the result of an Epstein-Barr virus-driven lymphoproliferation, analogous to that found in other immunodeficient states. Disordered immunoregulation inherent to CD and immunosuppressive therapy for the latter may contribute to its development. The finding of polyclonal RS cells in a patient with early stage disease and apparent cure by surgical resection versus monoclonal RS cells in the patient with disseminated disease suggests that HD in the setting of immunodeficiency also may show molecular progression, in a manner similar to that occurring in conventional B-cell lymphoproliferative disorders arising in the same setting.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
5/87. lymphoscintigraphy, sentinel lymph node biopsy, and Mohs micrographic surgery in the treatment of Merkel cell carcinoma.BACKGROUND: Merkel cell carcinoma (MCC) is an aggressive cutaneous malignancy with a high incidence of occult nodal metastases. MCC is believed to be similar in natural history to thick or ulcerated melanomas in its propensity for locoregional recurrence and early lymph node metastasis. Studies have shown that nodal status is statistically correlated to survival in MCC. Radiolocalization and superselective lymph node biopsy is a recent technique that has been proven to be of great value in evaluating the status of occult lymph node disease in malignant melanoma and breast cancer patients. OBJECTIVE: In previously untreated patients, an orderly progression of metastases is observed for both cutaneous carcinomas and malignant melanomas and is anticipated for MCC. methods/RESULTS. We present two patients with MCC of the head and neck who underwent simultaneous Mohs micrographic surgery and sentinel lymph node biopsy with intraoperative radiolocalization. CONCLUSION: sentinel lymph node biopsy and intraoperative lymphoscintigraphy may prove to be a useful technique in evaluating occult nodal involvement and in limiting the potentially unnecessary morbidity of more comprehensive lymph node dissections in MCC patients who do not yet have metastatic involvement.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
6/87. Oral etoposide for Merkel cell carcinoma in patients previously treated with intravenous etoposide.We describe three patients with advanced Merkel cell carcinoma who were treated with etoposide given orally for recurrent regional lymph node involvement 18 to 30 months after exposure to etoposide given intravenously. etoposide given orally (100 mg/day) was given for 10 to 14 consecutive days and repeated every 21 to 28 days for a median of three courses (range: two to four). Toxicity was minimal and mainly hematologic. Two patients showed a complete response and one a partial response, all of very rapid onset. All three patients are alive 6, 9, and 42 months from the start of oral treatment. Two remain progression free, and one had a recurrence 1 month after completion of chemotherapy. We suggest that orally administered etoposide, a topoisomerase II inhibitor, has a strong antitumor effect in advanced Merkel cell carcinoma, even in patients previously treated parenterally with the same drug. This action may be explained by the greater dependence of the drug's efficacy on the duration of administration rather than the dose intensity.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
7/87. Cytogenetic heterogeneity and clonal evolution in synchronous bilateral breast carcinomas and their lymph node metastases from a male patient without any detectable BRCA2 germline mutation.Two synchronous bilateral breast carcinomas and their matched lymph node metastases from a 70-year-old man were cytogenetically analyzed. All four tumors were near-diploid, and except for the primary tumor from the right breast, had a 45,X,-Y clone in common. The loss of the y chromosome was, however, common to all four tumors, whereas metaphase cells from peripheral blood lymphocytes showed a normal 46, XY chromosome complement. The primary tumor from the right breast was monoclonal, with loss of the y chromosome and gain of 1q, whereas its metastasis had two related clones: the 45,X,-Y clone, and the other a more complex version of the clone in the primary tumor, with inv(3), -14, and del(16)(q13) as additional changes. The primary tumor from the left breast was polyclonal with three unrelated clones: 45,X,-Y/45,XY,-18/47,XY, 20, two of which were present in its metastasis. dna flow cytometric studies showed diploidy for both primary tumors. No mutation in the BRCA2 gene was found on analysis of dna from peripheral blood lymphocytes. The present findings show that del(16)(q13) is a recurrent finding among male breast carcinomas and that some of the primary cytogenetic abnormalities, as well as the pattern of chromosomal changes during the progression of sporadic breast carcinoma in the male, are similar to those in the female. In addition, the loss of the y chromosome in the tumors but not in peripheral blood lymphocytes, suggests a possible role for this abnormality in the pathogenesis of male breast carcinoma.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
8/87. Soft tissue sarcomas after radiation treatment for breast cancer. Three case studies and review of literature.AIMS: By means of 3 cases with infield soft tissue carcinomas after radiotherapy for breast cancer, symptoms and therapy are described. Consequences for treatment planning and patient's information before radiotherapy for breast cancer are discussed. patients: Three of 1,025 patients with breast cancer irradiated from 1984 to 1997 suffered from infield secondary soft tissue sarcomas. The latency periods were 61, 49 and 59 months. Two patients had been treated with breast-conserving therapy (computerized planning, 50 Gy to reference point, 5 times 2 Gy/week, 5-MV photons), 1 patient received a local boost dose of 15 Gy (10-MeV electrons), patient 3 radiotherapy of the thoracic wall and regional lymph nodes after mastectomy using 12-MeV electrons (thoracic wall) and 5-MV photons (lymph node areas) to 50 Gy, 5 times 2 Gy/week. No adjuvant chemotherapy was given. All sarcomas were very extensive, all patients died from local progression and/or distant failure after 17, 13 and 12 months. RESULTS: The incidence of spontaneous sarcomas of the breast is about 0.06%, after operation and radiotherapy 0.09 to 0.45%. No correlations to radiotherapy technique and no risk factors were found. radiation dose could play a role, but there are very sparse data about this. CONCLUSIONS: Secondary soft tissue sarcomas are very rare, but familiar complications of radiotherapy. Only early diagnosis leads to a chance for cure. Because of unclear correlations to the treatment parameters and rareness of this event, in our opinion no regular information to the patient receiving radiotherapy for breast cancer is mandatory.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
9/87. Bladder cancer genotype stability during clinical progression.genomic instability is manifested by the accumulation of large numbers of mutations. The rate at which mutations accumulate has been difficult to estimate because serial comparisons are required. For further insight into how quickly mutations accumulate during clinical progression, cell lines sequentially isolated 6 or 11 months apart from two patients with metastatic bladder cancer were compared for loss of heterozygosity (LOH). The genomes were scanned at approximately 200 polymorphic microsatellite loci to increase the resolution and sensitivity for losses. The cell lines from both patients had evidence of genomic instability, with aneuploidy, chromosomal instability, and fractional allelic losses of 0.15 and 0. 48, respectively. However, additional changes were relatively infrequent, with more than 90% identity between the initial and recurrent cell lines. Allelic losses were not randomly scattered, but clustered on specific chromosomes. Therefore, the numbers of loci with further LOH during the clinical progression of some bladder cancers are small relative to the total number of loci with LOH, suggesting that most allelic losses accumulate before clinical presentation.- - - - - - - - - - ranking = 6keywords = progression (Clic here for more details about this article) |
10/87. Metastatic carcinoma of penis complicated by hypercalcemia.A fifty-three-year-old man with epidermoid carcinoma of the penis metastatic to the right inguinal lymph nodes and adjacent areas was found to have persistent hypercalcemia. Associated with this biochemical abnormality was an elevated parathormone activity in the absence of any bony metastases. Other than a transient response to furosemide-inducded diuresis he was refractory to treatment with oral inorganic phosphates and mithramycin. Ablation of the primary tumor did not affect his hypercalcemia. However, when therapy using external irradiation and parenteral bleomycin was directed to the metastases, his serum calcium stabilized and became normal and remained so until further progression of his humor. We postulate that the penile cancer metastases were elaborating parathyroid hormone-like substances responsible for the hypercalcemia and suppression of normal parathyroid activity.- - - - - - - - - - ranking = 1keywords = progression (Clic here for more details about this article) |
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