By Jonathan S. Berek MD MMS, Neville F. Hacker AM MD
- Concise, accomplished insurance guarantees your entry to present wisdom of common rules, in addition to scientific and surgery for the total diversity of gynecologic cancers: cervical, breast, ovarian, vulvar and vaginal, and uterine.
- Evidence-based, templated chapters velocity you on to the knowledge you need.
- Extensively revised, separate chapters at the most modern thoughts in laparoscopy and robotics retain you as much as date.
- Expert authorship, together with the services of various overseas individuals, retains you on the leading edge of your box and is helping you organize for board exams.
- New illustrations and drawings, in addition to pathology slides and clinically-relevant diagrams, assist you visualize key concepts.
- Complete content material with superior navigation
- A robust seek instrument that draws effects from content material within the publication, your notes, or even the web
- Cross-linked pages, references, and extra for simple navigation
- Highlighting device for simpler reference of key content material during the text
- Ability to take and proportion notes with acquaintances and colleagues
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Get the evidence-based, sensible suggestions you must offer state of the art care to ladies with gynecologic cancers. From prognosis via scientific and surgical administration, Berek and Hacker's Gynecologic Oncology, sixth variation offers beneficial wisdom and services on each element of gynecologic malignancies.
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Additional info for Berek and Hacker’s Gynecologic Oncology
In addition, the TCGA study found a high frequency of mutations in the PIK3R1 gene that encodes a PIK3 regulatory subunit. Both inactivation of PTEN or unrestrained PIK3 can lead to activation of AKT, which in turn leads to upregulation of the mammalian target of rapamycin (mTOR), a key regulator of apoptosis and cellular growth. Clinical trials with the mTOR inhibitors, temsirolimus, everolimus, and ridaforolimus, have shown promising single agent activity in the treatment of type I endometrial cancer (125–128).
Sporadic Endometrial Cancer Several approaches have been undertaken to evaluate the spectrum of genetic changes involved in the pathogenesis of sporadic endometrial cancers. Cytogenetic studies have described gross chromosomal alterations in endometrial cancers, including changes in the number of copies of specific chromosomes (84). Comparative genomic hybridization (CGH) studies have demonstrated areas of chromosomal loss and gain in both endometrial cancers and atypical hyperplasias (85,86). The most common sites of chromosomal gain are 1q, 8q, 10p, and 10q (87–89).
B b Germline APC mutations are responsible for the adenomatous polyposis coli syndrome and somatic mutations are common in sporadic colon cancers, but APC mutations have not been described in endometrial cancers (51,129). The APC gene may be inactivated in some endometrial cancers because of promoter methylation. It has been shown that missense mutations in exon 3 of -catenin lead to the same end result—namely, abrogation of the ability of APC to induce -catenin degradation—which results in abnormal transcriptional activity.