C. W. Burger

Sentinel node detection in cervical cancer

Background For superficial tumors such as melanoma, breast, and vulvar cancer, sentinel node detection prevents unnecessary extensive lymph node dissections. Sentinel node detection has not yet proved feasible in tumors, such as cervical cancer, that drain to deep pelvic lymph nodes. Technique We injected technetium-99m colloidal albumin around the tumor allowing preoperative lymphscintigraphy and intraoperative gamma probe detection of sentinel nodes. For visual detection, blue dye was injected at the start of surgery. Experience In six of 10 eligible women who had Wertheim-Meigs operations for cervical cancer stage Ib, one or more sentinel nodes could be detected by scintigraphy. Intraoperative gamma probe detection was successful in eight of ten women, whereas visual detection found sentinel nodes in only four. They were found as far as the common iliac level. One woman had positive lymph nodes, of which one was a sentinel node. Conclusion Identification of sentinel nodes using radio-nuclide is possible in women with cervical cancer and potentially identifies women in whom lymph node dissection can be avoided.

Ovulation induction with pulsatile luteinizing releasing hormone in women with clomiphene citrate-resistant polycystic ovary-like disease: clinical results*†

Eighty-four treatment units were given to 11 women with clomiphene citrate-resistant polycystic ovarian disease (PCOD). PCOD was defined as oligomenorrhea elevated luteinizing hormone (LH), normal follicle-stimulating hormone (FSH), and preference-elevated androgens. Luteinizing-releasing hormone (LRH) was administered intravenously via a portable infusion pump. Doses varied between 5 and 40 micrograms/pulse given at 60-, 90-, or 120-minute intervals. In 11 women, 85 treatment units (TUs) were completed, of which 74 were ovulatory, showing no specific advantage of any particular pulse dose or pulse interval. Five pregnancies occurred in three women. Two women did not ovulate during 52 and 284 consecutive days of therapy, respectively. Oligomenorrheic patients with PCOD can be made more regular by means of LRH, not necessarily leading to a regular menstrual cycle. In general, LRH is sufficient for luteal support. No signs of hyperstimulation were observed, although two patients incidently developed unilocular cysts with a maximum diameter of 8 cm. Ovulation induction with LRH in PCOD is possible, although the disease itself does not change during therapy. This may be further evidence that altered hypothalamic LRH secretion is more the result, rather than the cause, of the phenomenon of PCOD.

Cytogenetics of a malignant ovarian germ-cell tumor

Cytogenetic investigation of a malignant ovarian tumor diagnosed as a mixed germ‐cell tumor, composed of extensive choriocarcinoma and foci of yolk‐sac tumor, revealed a highly abnormal chromosomal pattern. We found a chromosome number in the hypertriploid/hypotetraploid range, and several clonal structural abnormalities, including 2 copies of an isochromosome 12p. We showed that the chromosomal pattern of this ovarian tumor is very similar to that of testicular germ‐cell tumors. This finding, together with reported cytogenetic data of malignant ovarian germ‐cell tumors, supports the hypothesis that ovarian and testicular germ‐cell tumors are strongly related entities that may have a similar origin and pathogenetic pathway. Int. J. Cancer 77:217–218, 1998.© 1998 Wiley‐Liss, Inc.

Hormone replacement therapy and breast cancer morbidity, mortality and recurrence☆

The effects of short-term and long-term HRT (in its various forms, unopposed oestrogens, sequentially combined HRT and continuous combined HRT) on the female breast are reviewed. The question is addressed whether HRT will increase the risk of breast cancer as well as the risk of dying from breast cancer in healthy women, and whether or not women who already run an increased risk on the basis of a positive family history, use of DES during pregnancy or because of the presence of premalignant epithelial abnormalities in the breast, increase their risk for breast cancer further. The risks of HRT and the options for HRT in patients who have a history of breast cancer are discussed and alternative treatment modalities for climacteric complaints (e.g. clonidine, paced-respiration) or for preventive HRT (e.g. tamoxifen, tibolone) are reviewed.

LHRH agonist treatment of breast cancer and gynecological malignancies : a review

Since 1982 LHRH agonists have been used as a treatment modality in patients with disseminated breast cancer and gynecologic malignancies, based on the assumption of steroid dependence of these cancers. They have been successfully used in the treatment of premenopausal women with breast cancer; response rates reported are 31-63%. Less optimistic results have been reported in postmenopausal breast cancer patients as well as in the treatment of women suffering from ovarian cancer. Response rates for treatment of postmenopausal breast- and ovarian cancer patients appear to be up to 22% and 29%, respectively. Studies using LHRH agonists to treat endometrial and cervical intra-epithelial neoplasia are still rare and, until now, no data about the efficacy of LHRH agonists in treating these malignancies have been reported. This paper reviews clinically important studies of LHRH agonists, including a rationale for the use of LHRH agonists in breast cancer and gynecological cancer treatment. In view of the changed endocrine state in postmenopausal women on the one hand and alterations in endocrine metabolism in breast cancer tissue on the other hand, it is concluded that it might be more effective to use a combination of LHRH agonists and other endocrine modalities to treat disseminated breast cancer and gynecological malignancies.

Ovulation induction with pulsatile luteinizing hormone-releasing hormone in women with clomiphene citrate-resistant polycystic ovary-like disease: endocrine results *

The pituitary and gonadal response to pulsatile luteinizing hormone-releasing hormone (LH-RH) administration during the first and consecutive second treatment unit (TU) was studied in nine women with clomiphene citrate-resistant polycystic ovary-like disease (PCOD). The control group consisted of eight eumenorrheic women. Luteinizing hormone levels, LH amplitudes, and total urinary excretion/24 hours did not differ between ovulatory and anovulatory TUs, but were significantly higher compared with the control group. Follicle-stimulating hormone (FSH) in PCOD did not differ from normal cycles. Androgen values in the anovulatory TUs were significantly higher compared with the ovulatory TUs (P = 0.001). We conclude that LH-RH therapy may result in ovulation; however, it does not redress the intrinsic abnormality in PCOD and FSH, and androgen levels do not seem to be critical in ovulation induction.

Pituitary response during pulsatile luteinizing hormone-releasing hormone ovulation - induction in patients with clomiphene citrate-resistant polycystic ovary-like disease

The pituitary response to pulsatile luteinizing hormone-releasing hormone (LRH) was studied in 6 women with clomiphene-resistant polycystic ovary-like disease (PCOD). PCOD was defined as oligomenorrhea, elevated luteinizing hormone (LH), normal follicle-stimulating hormone (FSH), and, in general, elevated androgens. LRH was administered in a pulsatile way, chronically, with a pulse dose of 20 micrograms and a pulse interval of 60, 90 and 120 minutes. Blood was drawn every 10 minutes for 6 hours, at the start of therapy (pulse study 1) and 9-15 days after the start of therapy (pulse study 2). Five patients ovulated within 10 days of therapy, which meant that pulse study 2 was performed during the luteal phase. One patient remained anovulatory. The follicular and luteal response during LRH therapy was comparable to that of normal cycles, although the pituitary response was enhanced in PCOD at the start of therapy, which might be related to the state in which the ovary finds itself with respect to follicular development. Desensitization for LH to LRH occurred only incidentally during pulse study 1. Desensitization for FSH to LRH already developed during pulse study 1 and continued to existed during therapy. The 60, 90 and 120 minute LRH pulse interval regimes resulted in LH nadir intervals with wide ranges, although the medians were 60, 90 and 120 minutes respectively.