GROUP 7 PRESENTATION

Module: Reproductive Health

TASK: ENDOMETRIAL CANCER

 GROUP MEMBERS
222000742 DUSENGEYEZU MUHIRE EMMANUEL
222000716 DUSHIMIYIMANA ERIEL
222000939 IRADUHA UWIMANA MARIE FAUSTINA
222000882 ISHIMWE MOISE
222000958 MIGABO THEOPHILE
222001054 NIYITANGA ALINE
222000807 NIYOMIZERO PACIFIQUE
222000743 TUYISENGE ERIC
222000578 UWINEZA FLORA
 ENDOMETRIAL CANCER
INTRODUCTION

The term cancer means a disease in which abnormal cells in the body
grow out of control.
Endometrial cancer is a type of cancer that begins in the lining of the
uterus where the cells in the endometrium (the inner lining of the uterus)
start to grow out of control. It is one of the most common cancers
affecting the female reproductive organs. Understanding its
pathophysiology, types, causes, symptoms, diagnosis, staging,
management, and prevention strategies is crucial for effective treatment
and patient outcomes.
 PARTHOPHYSIOLOGY
Hormonal imbalance, particularly involving estrogen and progesterone,
plays a central role in the development of endometrial cancer. The
endometrium is highly responsive to these hormones, and an imbalance
between them, especially unopposed estrogen, can lead to abnormal
cellular proliferation and eventually cancer.

Actually, Estrogen stimulates the growth and thickening of the

endometrium during the first half of the menstrual cycle (proliferative
phase). It promotes the proliferation of endometrial cells, preparing the
uterus for potential pregnancy.
Under normal conditions, this estrogenic stimulation is balanced by
progesterone, which is secreted during the second half of the menstrual
cycle (secretory phase) after ovulation. Progesterone counteracts the
proliferative effects of estrogen by promoting differentiation and
stabilization of the endometrial lining, making it ready for implantation
or, if pregnancy does not occur, leading to its shedding (menstruation).
Unopposed estrogen effects
•Prolonged exposure to estrogen (Hyperestrogenism) without the
counterbalancing effect of progesterone can lead to endometrial
hyperplasia and, eventually, cancer.
•When estrogen is not balanced by sufficient levels of progesterone (a
condition referred to as unopposed estrogen), it continuously stimulates
the endometrium, causing hyperplasia (excessive proliferation of cells).
•This prolonged exposure to high levels of estrogen without progesterone
leads to increased cell division, which raises the risk of genetic mutations.
Over time, this can result in the development of abnormal cells and
eventually cancerous cells.
•Inflammation: Chronic inflammation contribute to the carcinogenic
process by weaken tissue barrier function and expose the stem cell
compartment to environmental carcinogens or to bring stem cells to a
closer to carcinogens factors such as free ions of metals.

• Genetic mutation can lead to cancer because they cause changes in the
DNA of cells, which disrupt normal cell functions, particularly those
involved in growth and division.
 TYPES OF ENDOMETRIAL CANCER
• Type 1 Endometrial Cancers:

• Includes endometrioid carcinoma and mucinous carcinoma

1. Endometrioid carcinoma is the most common type of

endometrial cancer, arising from the lining of the uterus (the
endometrium). It is classified as a Type I endometrial cancer,
which means it is typically hormone-sensitive (often driven
by excess estrogen) and usually has a better prognosis
compared to other types of endometrial cancer.
Characteristics: This type is generally estrogen-driven, with
histological features that resemble normal endometrial tissue. It tends to
have a better prognosis compared to other types of uterine cancers,
especially if detected early.

[Link] Carcinoma
Origin: can arise in various organs, but it is most commonly associated
with the ovaries and the colon. It can also occur in the pancreas and
breast.

Characteristics: it is characterized by secretion of mucus like as a signs.

• These categories of tumors are influenced by excessive estrogen
stimulation, tamoxifen use, obesity, polycystic ovary syndrome,
and other factors
• Commonly occurs in postmenopausal women with high estrogen
levels, often due to conditions like obesity, diabetes, tamoxifen use
or polycystic ovary syndrome and Nulliparity.

• The presence of endometrial intraepithelial neoplasm (EIN) or

atypical endometrioid hyperplasia is a significant risk factor
TYPE 2 ENDOMETRIAL CANCERS
Includes serous carcinoma, clear cell carcinoma, carcinosarcoma, and
undifferentiated carcinoma.
1. Serous Carcinoma
Origin: Serous carcinoma is the most common type of epithelial
ovarian cancer and can also occur in the endometrium.
Characteristics: It often presents as high-grade serous carcinoma,
which is aggressive and usually diagnosed at an advanced stage.

2. Clear Cell Carcinoma

Origin: Primarily associated with the ovaries, it can also arise in the
endometrium. It is linked to endometriosis.
Characteristics: This type is distinguished by clear cytoplasm in tumor
cells and has a different molecular profile than serous carcinoma. It may
also show resistance to certain chemotherapy agents.

3. Small Cell Carcinoma

Origin: A rare and aggressive type that can arise in the ovaries or
endometrium.
Characteristics: This carcinoma has small, round cells and often
behaves aggressively, similar to small cell lung cancer. It is typically
diagnosed at an advanced stage.
4. Undifferentiated Carcinoma
Origin: Can arise in various tissues, including the endometrium and
ovaries.
Characteristics: As the name suggests, these tumors lack distinct cellular
differentiation and may not resemble any specific cell type. This can
make diagnosis challenging.

• These are high-grade tumors that are aggressive in nature.

• In most cases at the time of diagnosis, the tumors are found to be in

advanced (metastatic) stages

• Unopposed estrogen exposure is less of a risk factor, when compared to

type 1 cancers
RISK FACTORS FOR
ENDOMENTRIAL CANCER
Several factors increase the risk of developing endometrial cancer:
 Obesity: Excess body fat increases estrogen [Link] tissue,
become the primary sources of circulating estrogen in postmenopausal
women.
adipose tissue is a source of mesenchymal stem cells, which can be
recruited to support tumor growth and progression.
 estrogen metabolites further contribute to DNA damage and genetic
instability
Hormonal Factors: Irregular menstrual cycles, early menarche, late
menopause, andhormone replacement therapy can affect risk.
 Irregular periods often indicate an imbalance in estrogen and
progesterone levels. Excess estrogen, without sufficient progesterone,
can lead to a thickened endometrial lining, increasing the risk of
abnormal cell growth and cancer.
Genetic Syndromes: like Lynch syndrome , Individuals with Lynch
syndrome have a mutation in one of the mismatch repair (MMR) genes,
which impairs the body's ability to correct DNA replication errors,
leading to an increased likelihood of tumor development
Women with Lynch syndrome have a lifetime risk of endometrial cancer
that can be as high as 40-60%, significantly higher than the general
population.
Endometrial cancer associated with Lynch syndrome often occurs at a
younger age than typical cases, usually before age 50.
Diabetes: Associated with obesity and hyperinsulinemia.
Insulin resistance, common in type 2 diabetes, can lead to increased
levels of insulin and insulin-like growth factors, which may promote the
growth of endometrial cells.
Diabetes is often associated with obesity, a significant risk factor for
endometrial cancer.
Chronic inflammation associated with diabetes may contribute to
cancer development, including endometrial cancer.
Age: Risk increases with age, particularly in women over 50.
The majority of endometrial cancer cases occur in postmenopausal
women, typically between ages 50 and 70. The risk increases as women
age.
after menopause, the ovaries produce less estrogen, but many women
have higher estrogen levels due to factors like obesity or hormone
replacement therapy. Prolonged exposure to estrogen without the
balancing effect of progesterone can increase cancer risk.
 SIGNS AND SYMPTOMS OF ENDOMETRIAL
CANCER.
Abnormal Vaginal Bleeding: This can include heavy bleeding, bleeding
between periods, or bleeding after menopause.

Pelvic Pain: Persistent pain in the pelvic area that doesn't seem to be related
to other conditions.

Unexplained Weight Loss: Losing weight without trying can be a warning

sign.
Changes in Menstrual Cycle: Irregular or unusually heavy menstrual
periods.
Discharge: Unusual vaginal discharge, especially if it is watery, pink, or
has a foul odor.

Pain During Intercourse: Discomfort or pain during sexual activity.

Urinary Symptoms: Frequent urination or difficulty urinating may

occur if the cancer affects surrounding structures.
 STAGES OF ENDOMETRIAL CANCER
Endometrial cancer is staged using the FIGO (International Federation
of Gynecology and Obstetrics) system, which classifies the cancer based
on its extent of spread:
Stage I: localised
IA: Cancer is confined to the endometrium (the lining of the uterus) and
has not invaded the muscle layer.
IB: Cancer has invaded the myometrium (the muscle layer of the uterus)
but remains within the uterus.
Stage II: local invasion
Cancer has spread to the cervix but is still confined to the uterus.
Stage III: region spread
IIIA: Cancer has spread to the outer layer of the uterus and/or the
fallopian tubes and/or ovaries.
IIIB: Cancer has spread to the vagina or pelvic sidewall.
IIIC: Cancer has spread to regional lymph nodes.
Stage IV: Distant metastasis
IVA: Cancer has spread to nearby organs, such as the bladder or rectum.
IVB: Distant metastasis has occurred, meaning cancer has spread to
distant organs, such as the lungs or liver.
 DIAGNOSIS

• Physical examination and a complete medical history

• Cystoscopy: During cystoscopy, a physician inserts a narrow tube called
cystoscope, to look directly into the bladder to see if cancer from
endometrium has spread to the bladder.
• MRI and Computerized tomography scan of the abdomen and pelvic
region may be used to assess spread.
• Transvaginal Ultrasound: To evaluate the thickness of the endometrium.
• Endometrial Biopsy: The gold standard for diagnosis, involving sampling
of endometrial tissue.
• Hysteroscopy as a medical procedure that allows a doctor to examine the
inside of the uterus (womb) using a thin, lighted tube called a
hysteroscope.
 MANAGEMENT
Management of endometrial cancer as other cancers depends on staging,
The following treatment can be done respectively

• Hysterectomy: In this procedure, the uterus and cervix are removed.

• Radical hysterectomy: The uterus, cervix, the upper part of the vagina and tissues,

next to the uterus are removed.

• Hysterectomy (abdominal) with salpingo-oophorectomy: It is a surgical

procedure involving the removal of the uterus, and of the fallopian tube and ovary

(salpingo-oophorectomy)
Pelvic exenteration: The uterus, tissues surrounding the uterus, cervix,
pelvic lymph nodes, and the upper part of the vagina, are removed. In
addition, depending on the tumor spread, the remainder of the vagina,
the bladder, rectum, and a part of the colon, may also be removed.
Recovery from this surgery may take a long period of time.

• Chemotherapy for Endometrial Cancer: Chemotherapy is a

treatment that uses drugs to kill cancer cells. In this treatment,

combinations of two or more chemotherapy drugs are usually used.

• Radiation therapy for Endometrial Cancer: Radiation therapy

attempts to destroy cancer cells by aiming high-energy beams at the

cancer cells

• Hormone therapy: Hormonal therapy is a medical treatment used for

women with advanced Endometrial Cancer that has metastasized

beyond the uterus.

• Palliative care can be done if all management ways failed

 COMPLICATIONS
Emotional distress
The cancer can metastasize (spread) to the fallopian tube, ovary, cervix,
bone, liver, lung, and brain and other organs
Perforation in the uterus, which may occur during a diagnostic
Sexual dysfunction
At the end stage painful situation occur
Recurrence of the cancer following incomplete surgical removal
PREVENTION OF ENDOMETRIAL CANCER

Physical activity: reduced physical activity and diet high in fats can
read to obesity and additional related risk factors, such as increased
estrogen level that re risk factors for endometrial cancer.
Pregnancy and breastfeeding: During pregnancy and while
breastfeeding, the estrogen levels are lowered. Being pregnant
and/or breastfeeding may lower a woman’s risk for
Endometrial Cancer.
Combination of oral contraceptives: Taking a combination
of
oral contraceptives, such as estrogen and progestin, decrease
the risk for Endometrial Cancer.
Regular Check-ups: Monitoring hormonal health and early
detection strategies are
essential, especially for high-risk individuals.
REFERENCES

• American College of Obstetricians and Gynecologists. Practice Bulletin No. 149:

Endometrial cancer. Obstetrics & Gynecology. 2015;
doi:10.1097/[Link]. Reaffirmed 2021.

• Greten FR, Grivennikov SI. Inflammation and Cancer: Triggers, Mechanisms, and
Consequences. Immunity. 2019 Jul 16;51(1):27-41. doi:
10.1016/[Link].2019.06.025. PMID: 31315034; PMCID: PMC6831096.
• Sorosky, J.I., 2012. Endometrial cancer. Obstetrics & Gynecology, 120(2 Part 1),
pp.383-397.
• Uterine cancer. [Link].
[Link] Accessed March 7,
2023.
THANK YOU FOR ATTENTION!!!!!!!