By Jonathan S. Berek MD MMS, Neville F. Hacker AM MD
- Concise, entire insurance guarantees your entry to present wisdom of normal rules, in addition to clinical and surgical operation for the whole diversity of gynecologic cancers: cervical, breast, ovarian, vulvar and vaginal, and uterine.
- Evidence-based, templated chapters pace you on to the data you need.
- Extensively revised, separate chapters at the newest recommendations in laparoscopy and robotics maintain you as much as date.
- Expert authorship, together with the services of various foreign members, retains you on the vanguard 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 better navigation
- A strong seek instrument that attracts effects from content material within the publication, your notes, or even the web
- Cross-linked pages, references, and extra for simple navigation
- Highlighting software for less complicated reference of key content material through the text
- Ability to take and proportion notes with associates and colleagues
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Extra info for Berek and Hacker’s Gynecologic Oncology
About two-thirds of hereditary ovarian cancers are caused by BRCA1 mutations and one-third by BRCA2 mutations. Hereditary cases account for about 10% of all invasive epithelial ovarian cancers and 20% of high-grade serous cases. 5% to about 15–25% in BRCA2 carriers and 25–40% in BRCA1 carriers (140–145). BRCA1 and BRCA2 mutations are rare and carried by fewer than 1 in 500 individuals in most populations (144–146). Most BRCA1–2 mutations involve deletions or insertions encoding truncated protein products that are clearly dysfunctional.
Loss of the other copy of the TP53 gene is not required. Most TP53 missense mutations are transitions rather than transversions or microdeletions (194), which suggests that they occur spontaneously, rather than as a result of exogenous carcinogens. Most high-grade serous ovarian cancers that do not overexpress p53 protein have TP53 mutations that result in truncated protein products (192,195). These are usually accompanied by loss of the other copy of the gene, consistent with the classic two-hit model of tumor suppressor gene inactivation.
From a translational perspective, patient-specific tumor microenvironmental characteristics may influence the response to antiangiogenic therapy (40). Therapeutic strategies to target angiogenesis include VEGF-A neutralizing antibodies (Bevacizumab) and multikinase inhibitors that target the VEGF-receptors along with other kinases. Bevacizumab is widely used in the treatment of metastatic colorectal cancer, advanced nonsmall cell lung cancer, glioblastoma, and metastatic renal cell carcinoma. Sorafenib and pazopanib are two examples of multikinase inhibitors that are approved for the treatment of metastatic renal cell carcinoma.