Verbal Disclosure. Endometrial Cancer: Epidemiology

Size: px

Start display at page:

Download "Verbal Disclosure. Endometrial Cancer: Epidemiology"

Blanche Waters
5 years ago
Views:

Gynecologic Malignancies: What is the latest? MISTY WHITE WHNP GYNECOLOGIC ONCOLOGY UT MD ANDERSON CANCER CENTER Verbal Disclosure q I have nothing to disclose.

1 Gynecologic Malignancies: What is the latest? MISTY WHITE WHNP GYNECOLOGIC ONCOLOGY UT MD ANDERSON CANCER CENTER Verbal Disclosure q I have nothing to disclose. Outline q Endometrial Cancer Incidence Presentation and diagnosis Treatment and Practice Updates, Recent Advancements q Cervical Cancer and HPV Incidence Presentation and Diagnosis Treatment and Practice Updates, Recent Advancements q Ovarian Cancer Incidence Presentation and Diagnosis Treatment and Practice Updates, Recent Advancements Endometrial Cancer: Epidemiology q Most common type of cancer in the female reproductive system q Estimated New Cases ,250 q Estimated Deaths in ,350 q Percent surviving 5 years 81.1% ( ) Endometrial Cancer: Epidemiology q 90 % of cases are Sporadic q 5 % heredity: Lynch Syndrome % lifetime risk of endometrial cancer Onset years prior to sporadic cases 50 % of women with Lynch Syndrome : Endometrial cancer is sentinel cancer Types of Endometrial Cancer q Type I Tumors Account for 80 % of endometrial carcinomas Endometrioid histology, grade 1 or grade 2 Favorable prognosis Estrogen responsive May be preceded by intraepithelial neoplasm, complex atypical endometrial hyperplasia q Type II Tumors - Account for 10-20% of endometrial carcinomas Include grade 3 endometrioid tumors, as well as non- Endometrioid tumors (serous, clear cell, mucinous, squamous, transitional cell, undifferentiated) Types of Endometrial Cancer q Uterine Sarcoma Account for 3-9% of uterine malignancies Arise from myometrium or connective tissue elements, supporting structures of uterus and leiomyomas Present early, but are aggressive Rarely cancerous fibroids occur, less than 1 in 1000 Who Should Be Screened? All patients with post menopausal bleeding Post menopausal women with a pyometra Asymptomatic women with endometrial cells on a pap smear, particularly reported as atypical Perimenopausal patients with intermenstrual bleeding or increasingly heavy periods Perimenopausal patients with abnormal uterine bleeding, particularly if there is a history of anovulation Type 1 Precursor Lesions Risk of Cancer Developing Simple Hyperplasia 1% Complex Hyperplasia 3% Simple Hyperplasia with Atypia 9% Complex Hyperplasia with Atypia 30% EIN (endometrial intraepithelial neoplasia) 40-50% 1

Clinical Features Type 1 and Type 2 Type 1 (85% ) Type 2 (15%) Risk Factor Unapposed Estrogen Age Precursor Lesion Atypical Hyperplasia EIC (endometrial intraepithelial carcinoma) Race White>African

Differentiated Poorly Differentiated Histology Endoemtrioid Serous, Clear Cell, G3 Endometrioid, Carcinosarcoma Risk Factors for Type 1 Factor Risk Obesity > 30 lbs overweight 3 Obesity > 50 lbs

5 FIGO Staging Stage Extent of Disease 5 Year Survival I Limited to body of uterus ~85% Ia No myometrial invasion or <50% of myometrial invasion Ib >50% myometrial invasion II Limited to body of

2 Clinical Features Type 1 and Type 2 Type 1 (85% ) Type 2 (15%) Risk Factor Unapposed Estrogen Age Precursor Lesion Atypical Hyperplasia EIC (endometrial intraepithelial carcinoma) Race White>African American>Hispanic> Asian White = African American Differentiation Well to Mod. Differentiated Poorly Differentiated Histology Endoemtrioid Serous, Clear Cell, G3 Endometrioid, Carcinosarcoma Risk Factors for Type 1 Factor Risk Obesity > 30 lbs overweight 3 Obesity > 50 lbs overweight 10 Nulliparity 2 Late Menopause 2.4 Unopposed Estrogen 9.5 Atypical Hyperplasia > 30 Tamoxifen Use 7.5 FIGO Staging Stage Extent of Disease 5 Year Survival I Limited to body of uterus ~85% Ia No myometrial invasion or <50% of myometrial invasion Ib >50% myometrial invasion II Limited to body of uterus and cervix ~75% III Extension to uterine serosa, peritoneal cavity, and/or ~45% lymph nodes IIIa Extension to uterine serosa, adnexae or peritoneal cavity (positive peritoneal washings/ascites) IIIb Extension to vagina or parametrium IIIc1 Pelvic lymph node involvement IIIc2 Para- aortic lymph node involvement Prognosis Favorable Not Favorable 40% endometrial cancer deaths IV Extension to adjacent organs or beyond true pelvis ~25% IVa Extension to adjacent organs e.g. bladder, bowel IVb Distant metastases or positive inguinal lymph nodes Staging Prognostic Factors Type 1 q Minimal Invasive Approach TLH, BSO, IOLNM, Limited lymphadenectomy Robotic / Traditional laparoscopy q FIGO Stage q Histologic Cell Types q Grade q Sentinel Lymph Node Mapping and Biopsy q Myometrial invasion q LVSI Landmark Studies on Adjuvant Treatment of Early Stage Endometrial Cancer Summary of Treatment for Type I Endometrial Cancers Type II Endometrial Cancers No Treatment Brachytherapy EBRT EBRT + Chemo Chemo q More aggressive tumor biology Stage IA G1-2 LVSI - Stage IA G3 Stage IA or B Grades 1-2, LVSI + Stage II G1-2 LVSI - Stage IB G3 Stage IIIA, IIIB Stage II G3, or G1-2 and IIIC LVSI+ Stage IV q Stage is the strongest prognostic factor q 60-70% have extrauterine disease at time of diagnosis q No randomized trials due to small numbers q Most of the data extrapolated from trials including both Type I and Type 2 patients 2

Summary of Treatment for Type II Endometrial Cancers Stage IA IB II IIIA IIIB IIIC 1 and IIIC 2 Treatment Options Brachytherapy followed by chemotherapy (Consider observation if no residual disease

EBRT followed by chemotherapy Recent advancements q Conservative treatment of patients with CAH or early grade endometrial cancer with an levonorgestrel-releasing intrauterine device Forty-six

3 Summary of Treatment for Type II Endometrial Cancers Stage IA IB II IIIA IIIB IIIC 1 and IIIC 2 Treatment Options Brachytherapy followed by chemotherapy (Consider observation if no residual disease in hysterectomy specimen) Brachytherapy or EBRT followed by chemotherapy Brachytherapy or EBRT followed by chemotherapy Brachytherapy or EBRT followed by chemotherapy EBRT followed by chemotherapy EBRT followed by chemotherapy Recent advancements q Conservative treatment of patients with CAH or early grade endometrial cancer with an levonorgestrel-releasing intrauterine device Forty-six patients diagnosed with complex atypical hyperplasia or early grade endometrial cancer were treated with the LNG-IUD. Overall response rate was 75% (95% CI = 57-89) at 6 months; 80% (95% CI = 52-96) in complex atypical hyperplasia, 67% (95% CI = 30-93) in grade 1 endometrial cancer, and 75% (CI = 35-97) in grade 2 endometrial cancer q Phase II study of the levonorgestrel intrauterine device alone or in combination with the mtor inhibitor, everolimus, for the treatment of complex atypical hyperplasia and stage IA Grade endometrial cancer Cervical Cancer Hot topics q HPV and HPV Vaccination q Recent study reveals higher rates of recurrence in laparoscopic radical hysterectomy surgical cases q Clinical trials / Immunotherapy IV Chemotherapy Cervical Cancer Risk Factors q Age: The risk of cervical cancer increases with age. It is found most often in women over the age of 40. However, younger women often have precancerous lesions that require treatment to prevent cancer. q Smoking: Cigarette smoke contains chemicals that damage the body's cells. It increases the risk of precancerous changes in the cervix, especially in women with HPV. q Sexual behavior: Certain types of sexual activity may increase the risk of getting HPV infection. These include: 1) Multiple sexual partners, 2) high-risk male partners, 3) first intercourse at an early age and 4) not using condoms during sex. Cervical Cancer Risk Factors q Lack of regular Pap tests q Having a sexually transmitted disease (STD), including chlamydia q Diethylstilbestrol (DES) exposure before birth: This drug was used between 1940 and 1971 to help women not have miscarriages. Women whose mothers took DES during pregnancy have a high risk of vaginal and cervical cancers. q HIV infection q Weakened immune system: Having an organ transplant or taking steroids raise your risk q Being overweight or not eating a healthy diet Cervical Cancer Epidemiology qcervical cancer is the most common HPV associated cancer among women q Estimated new cases in ,240 q Estimated deaths in ,170 q In 2015, there were an estimated 257,524 women living with cervical cancer in the United States. q Percent surviving in 5 years HPV ~40 Types HPV Types and Disease Associations Mucosal sites of infection Cutaneous sites of infection ~ 80 Types q HPV Human Papilloma Virus Almost ALL will be infected with at least 1 type of HPV at some point Most will never know they have been infected Can occur with any intimate sexual contact High risk (oncogenic) HPV 16, 18, 45,56 and Intermediate risk 31,33,35,39,51,52,55,58,59,66,68 Low risk (non-oncogenic) HPV 6, 11 most common Intercourse is NOT necessary infection 26,42,44,54,70,73 q Each year 42,700 new cases of cancer are found in parts of the body where HPV is often found. HPV causes about 33,700 of these cancers q 79 million Americans currently infected HPV most common in teens 14 million new infections a year in the US Cervical Cancer Anogenital Cancers Oropharyngeal Cancer Cancer Precursors Low Grade Cervical Disease Genital Warts Laryngeal Papillomas Low Grade Cervical Disease Common Hand and Foot Warts 3

Age 21-29 Pap test every three years Age 30-64 Pap test and HPV test every five years Over Age 65 recommends against screening if not high risk Hysterectomy- recommends against screening if no

4 Cervical Dysplasia / Pre-Cancer q 1.4 Million new cases od low-grade cervical dysplasia q 330,000 new cases of high-grade cervical dysplasia Pap and HPV Testing q MD Anderson recommends the following screening exams for cervical cancer Age Pap test every three years Age Pap test and HPV test every five years Over Age 65 recommends against screening if not high risk Hysterectomy- recommends against screening if no history of high grade precancerous lesion or cervical cancer HPV Prophylactic Vaccines q Recombinant L1 capsid proteins that form virus-like particles (VLP) q Non-infectious and non-oncogenic q Produce higher levels of neutralizing antibody than natural infection About the HPV Vaccine There are three HPV vaccines approved by the U.S. Food and Drug Administration. q Cervarix (HPV 2) and Gardasil (HPV 4) protect against the most common HPV types and against cervical, anal, vulvar, vaginal, penile and oropharyngeal cancers. Only Gardasil protects against the HPV types most likely to cause genital warts. These vaccines prevent about 70% of cervical cancers. q Gardasil 9 (HPV 9), protects against nine types of HPV, including five that other vaccines don t cover. It also will prevent about 90% of cervical cancers. Dosing Schedule Dose Age range/ health condition Schedule 2 dose Males and females prior to 15 th birthday. Early as age 9. 0, 6-12 months If 1 st & 2 nd dose administered <5 months apart, a 3 rd dose is required. FDA indication Cervarix Gardasil 4 Gardasil 9 Bivalent (HPV 16,18) Quadrivalent (HPV 6,11,16,18) 9-valent (HPV types 16, 18, 31, 33, 45, 52, and 58) Cervical Cancer Vulvar, Vaginal Cancer Anal Cancer q Gardisil-9 is effective for females age 9-26 and males age Newly approved by females up to age 45.MD Anderson recommends that girls and boys receive the vaccine around age 11 to 12. The vaccine is given at this age so boys and girls have time to develop an immune response. q HPV vaccines are given in two shots over six months. Your child must get both shots for maximum protection from cancer. 3 dose Males and females on or after 15 th birthday. Immunocompromised HIV infection, cancer, autoimmune disease. As late as age 26. 0, 2, 6 months CIN, AIS VIN, VAIN AIN Genital Warts Males Age 9-26 Female Age 9-26 Males Age 9-45 Females Age 9-45 (only through 25) FDA Approves Expanded use of Gardasil 9 for individuals age HPV Vaccination Safety HPV Vaccination Safety q 3,200 women 27 through 45 years of age, followed for 3.5 years qgardasil was 88% effective in the prevention of a combined endpoint of persistent infection, genital warts, vulvar and vaginal precancerous lesions, cervical precancerous lesions, and cervical cancer related to HPV types covered by the vaccine qacip (Advisory Committee on Immunization Practices) Recommendations and Vote q 100 Million Doses in US q 286 Million Doses World Wide qcochrane Review (26 studies involving 73,428 adolescent girls and women) All trials evaluated vaccine safety over 0.5 to 7 years Ten trials (3.5-8 years) evaluated protection against precancer High-certainty evidence that HPV vaccines protect against cervical precancer in adolescent girls and women who are vaccinated between 15 and 26 qsafety & efficacy has been reviewed and confirmed: World Health Organization Global Advisory Committee on Vaccine Safety Food and Drug Administration (FDA) European Medicines Agency (EMA) International Federation of Gynecology & Obstetrics (FIGO) qauthorities in individual countries such as Lancet Dec 20;384(9961): British Journal of Cancer (2011) 105, The protection is lower when part of the population is already infected with HPV The vaccines do not increase the risk of serious adverse events, miscarriage, or pregnancy termination Cochrane Database of Systematic Reviews 2018, Issue 5. Art. No.: CD Medicines & Healthcare Products Regulatory Agency of the UK [MHRA] Therapeutic Goods Administration of Australia Centers for Disease Control, USA q No evidence for neurological /autoimmune diseases qno deaths directly attributed to HPV vaccine 4

5 HPV Vaccination Safety VAERS No new safety concerns identified in post-licensure vaccine safety surveillance among any recipients 7.9% serious side effects=headache, N/V, fatigue, dizziness, syncope, generalized weakness Syncope a frequently reported adverse event following immunization among adolescents 15-minute observation period is encouraged Cervical Cancer Clinical Staging q History and Physical careful exam of FULL genital tract q Biopsy of lesion + / - colposcopy q Imaging - PET CT, Skull to mid thigh, CT Chest/ Abdomen / Pelvis, MRI Pelvis Cervical Cancer Staging FIGO q Stage I Carcinoma confined to cervix IA microscopic, deepest invasion less than or = 5mm, largest extension 7mm IA1 stromal invasion of less than or = 3mm with deepest extension of less than or = 7mm IA2 stromal invasion of greater than 3mm and not greater than 5mm, extension not greater than 7mm IB clinically visible lesions limited to the cervix uteri or preclinical cancers greater than 1A IB1 clinically visible lesion less than or = 4cm IB2 clinically visible lesion greater than 4cm in greatest dimension Cervical Cancer Staging FIGO q Stage II cervical carcinoma invades beyond the uterus but not to the pelvic wall or to the lower third of the vagina IIA Without parametrial invasion IIA1 Clinically visible lesion less than or = 4cm greatest dimension IIA2 Clinically visible lesion greater than 4cm greatest dimension IIB With obvious parametrial invasion q Stage III The tumor extends to the pelvic wall and / or involves lower third of vagina and/or causes hydronephrosis or non functioning kidney IIIA Tumor involves lower third of the vagina, with no extension to the pelvic wall IIIB Extension to the pelvic wall and/ or hydronephrosis, non functioning kidney Cervical Cancer Staging FIGO q Stage IV The carcinoma has extended beyond the true pelvis or has involved (biopsy proven) the mucosa of the bladder or rectum. IVA Spread of growth to adjacent organs IVB Spread to distant organs Cervical Cancer Treatment qia Microinvasive Cone biopsy Simple hysterectomy q IA2 Pelvic lymphadenectomy plus cone biopsy, or radical trachelectomy Modified radical hysterectomy, pelvic lymphadenectomy If medically unfit, intracavitary radiation may be used q IB1 IIA1 Radical hysterectomy, pelvic lymphadenectomy Allows for more targeted adjuvant radiation Primary radiation in this population is reserved for medically unfit Cervical Cancer Treatment qib2 Primary chemoradiation q IIB to IVA External beam radiation therapy followed by brachytherapy Extended field radiation therapy Concurrent chemotherapy Minimally Invasive versus Abdominal Radical Hysterectomy for Cervical Cancer q 319 patients assigned to minimally invasive surgery, 312 to open surgery q In this trial, minimally invasive radical hysterectomy was associated with lower rates of disease-free survival and overall survival than open abdominal radical hysterectomy among women with early-stage cervical cancer. (Funded by the University of Texas M.D. Anderson Cancer Center and Medtronic; LACC ClinicalTrials.gov number, NCT ) q Minimally invasive surgery was associated with a lower rate of disease free survival than open surgery (3-year rate, 91.2% vs. 97.1%) q Minimally invasive surgery was associate with and a higher rate of locoregional recurrence (3- year rate of locoregional recurrence free survival, 94.3% vs. 98.3%) 5

Immunotherapy Trials q (Recruiting) DNA Plasmid-encoding Interleukin-12/HPV DNA Plasmids Vaccine INO-3112 and Durvalumab in treating participants with recurrent or metastatic HPV associated cancers q

gov Surgical Trials q (recruiting) Conservative surgery for women with low risk, early stage cervical cancer: Conservative surgery involves the removal of the pelvic lymph nodes (pelvic

6 Immunotherapy Trials q (Recruiting) DNA Plasmid-encoding Interleukin-12/HPV DNA Plasmids Vaccine INO-3112 and Durvalumab in treating participants with recurrent or metastatic HPV associated cancers q (Not yet recruiting) FT500 as a monotherapy and in combination with immune checkpoint inhibitors in subjects with advanced solid tumors q Clinicaltrials.gov Surgical Trials q (recruiting) Conservative surgery for women with low risk, early stage cervical cancer: Conservative surgery involves the removal of the pelvic lymph nodes (pelvic lymphadenectomy) and/or lymphatic mapping with sentinel lymph node biopsy. The cervix and parametrium are left intact. Ovarian Cancer Epidemiology qestimated new cases in ,240 q Estimated deaths in ,070 q Percent surviving in 5 years 47.4% q Peak incidence 63 years Ovarian Cancer Pathology q 90% Epithelial Cell Serous (75-80%), majority high grade Endometrioid resemble endometrial cell Mucinous resemble endocervical cells Clear Cell Risk Factors q Age q Obesity q Late pregnancy, or Nulliparity q Infertility q Late menopause q Family History q Geography BRCA 1 and BRCA 2 q Inherited germline mutations predispose women to breast and ovarian cancer q Hereditary cases only account for about 10% of all invasive epithelial ovarian cancers, and 20% of high grade serous cases q Lifetime risk of ovarian cancer increases from 1.5% to 25-40% in BRCA 1 carriers q Lifetime risk of ovarian cancer increases from 1.5% to 15-25% in BRCA 2 carriers Presentation and Clinical Features q General abdominal discomfort or pain (gas, indigestion, pressure, swelling, bloating, cramps) q Bloating and/or a feeling of fullness, even after a light meal q Nausea, diarrhea, constipation or frequent urination q Unexplained weight loss or gain q Loss of appetite q Abnormal vaginal bleeding q Unusual fatigue q Back pain q Pain during sex q Menstrual changes Ovarian Cancer Staging q Stage I Tumor confined to ovaries or fallopian tubes q Stage II Tumor involves one or both ovaries with pelvic extension below pelvic brim qstage III Tumor involves one or both ovaries with histological confirmation of spread to the peritoneum outside the pelvis and or metastasis to retroperitoneal lymph nodes qstage IV Distant metastasis, excluding peritoneal metastasis 6

Ovarian Cancer Treatment q MOST ovarian malignancies are managed with a combination of two treatment modalities Surgery cytoreduciton, optimal tumor debulking Chemotherapy q Optimal Cytoreduction is

at 5 years q What if we cant get it all? Would the patient benefit from neoadjuvant chemo then an interval debulking?

tumor evaluation q A validated composite scoring system is utilized to determine ability to resect to no gross residual disease. Patients with scores < 8 proceed with primary cytoreductive surgery.

7 Ovarian Cancer Treatment q MOST ovarian malignancies are managed with a combination of two treatment modalities Surgery cytoreduciton, optimal tumor debulking Chemotherapy q Optimal Cytoreduction is key optimal is <1-2 cm residual disease Major prognostic indicator of survival Prolonged progression free survival 60% of patients that were in the optimally debulked category will be free of disease at 5 years q What if we cant get it all? Would the patient benefit from neoadjuvant chemo then an interval debulking? Enter the Anderson Algorithm Anderson Algorithm q At our center, all patients presenting with presumed advanced-stage (Stage III or IV) ovarian cancer are considered for a two-surgeon laparoscopic tumor evaluation q A validated composite scoring system is utilized to determine ability to resect to no gross residual disease. Patients with scores < 8 proceed with primary cytoreductive surgery. q Patients with scores 8 receive NACT with subsequent interval tumor reductive surgery. q Fresh frozen tumor samples are obtained from the following pre-specified sites: 1) ovary (or suspected primary); (2) omentum; (3) & (4) from two additional metastatic sites at the time of primary assessment (diagnostic laparoscopy and/or primary cytoreductive surgery). The Anderson Algorithm for laparoscopic disease assessment of patients with advanced ovarian cancer. PIV = predictive index value. TRS = tumor reductive surgery. NACT = neoadjuvant chemotherapy. QI = quality improvement Adjuvant Therapies for Ovarian Cancer q Platinum/ Taxane Gold standard is Carboplatin / Paclitaxel (Taxol) Plus or minus Bevacizumab, anti angiogenesis, anti Veg-F Platinum sensitive Platinum refractory Dose Dense vs every three weeks q IP (intraperitoneal) chemotherapy 2006 Initial studies showed increased overall PFS with optimally debulked stage III ovarian cancer (49 vs 41 months) Also demonstrated catheter related complications and increased toxicity In the GOG 172 study testing IV Cisplatin/ Taxol vs IP Cisplatin/ Taxol: Only 42 % of patients in study received all 6 cycles Remains contentious Adjuvant Therapies for Ovarian Cancer q Radiation Generally reserved single site recurrence Palliative q Secondary Cytoreduction for recurrence When ALL disease can be resected q Chemotherapy for recurrence Based on time since last treatment Still platinum sensitive? Performance status, baseline neuropathy at recurrence What s New in Ovarian Cancer Treatment q Moon Shots Program Untreated high-grade serous ovarian cancer (HGSOC) Optimizing up front HGSOC treatment, Anderson Algorithm Recurrent HGSOC 80% will recur Novel drugs Targeted therapy Low-grade serous ovarian cancer Improve Outcomes Low Grade tumor database- uncovering the biology of these rare tumors PARP Inhibitors q In recent years, PARP inhibitors have emerged as a new therapy for a few advanced cancers for which there have been limited treatment options. qthe PARP inhibitors olaparib, niraparib and rucaparib are approved by the FDA for patients with BRCA-related and non-brca related advanced ovarian cancer in the advanced and maintenance settings q These drugs essentially block DNA repair pathways in cancer cells, without the DNA repair, the cells cannot divide and spread q Somatic BRCA Mutations q Homologous Recombination Deficiency Olaparib Lynparza q On Aug. 17, 2017, the U.S. Food and Drug Administration granted regular approval to olaparib tablets (Lynparza, AstraZeneca) for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer, who are in a complete or partial response to platinum-based chemotherapy. q SOLO 2 Trial, Study 19 q 300mg orally twice daily q Weekly labs, until stable Rucaparib- Rubraca q On April 6, 2018, the Food and Drug Administration approved rucaparib (Rubraca, Clovis Oncology Inc.), a poly ADP-ribose polymerase (PARP) inhibitor, for the maintenance treatment of recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in a complete or partial response to platinum-based chemotherapy q ARIEL3 Study q 600mg (two 300mg tablets) orally twice daily q Weekly labs until stable 7

complete or partial response to platinum-based chemotherapy.

8 Niraparib- Zejula q On March 27, 2017, the U.S. Food and Drug Administration approved niraparib (ZEJULA, Tesaro, Inc.), a poly ADP-ribose polymerase (PARP) inhibitor, for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in complete or partial response to platinum-based chemotherapy. q NOVA Study q 300mg orally once daily q Weekly labs until stable Immunotherapy in Ovarian Cancer q This all started in treatment of melanoma and spreading to other cancers Manipulates the immune system to better recognize and kill cancer cells qimmune Checkpoint Inhibitors Durvalumab Nivolumab Pembrolizumab q Immune Checkpoint Inhibitors Today there is more HOPE than ever! Questions? 8

Staging and Treatment Update for Gynecologic Malignancies

Staging and Treatment Update for Gynecologic Malignancies Bunja Rungruang, MD Medical College of Georgia No disclosures 4 th most common new cases of cancer in women 5 th and 6 th leading cancer deaths