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Gynae Path 2 Flashcards

1
Q

What’s the distinction between high and low grade gynae cancers?

A

Surgical operation may differ​:
Omentectomy​
Lymphadenectomy​

​Adjuvant therapy may differ​

​Prognosis: ​
Recurrence free survival
grade 1, 95% ​
grade 2, 82% ​grade 3, 68%

Overall survival​
grade 1, 89%
grade 2, 84%
grade 3, 63%

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2
Q

What is a Stage I Tumour confined to the corpus uteri​?

A

IA No or less than half myometrial invasion​

IB Invasion equal to or more than half of the myometrium

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3
Q

What is a stage 2 tumour?

A

Stage II Tumour invades cervical stroma

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4
Q

What is a Stage III Local and/or regional spread of the tumour?

A

IIIA Tumour invades the serosa of the corpus uteri and/or adnexa​

IIIB Vaginal and/or parametrial involvement​

IIIC Metastases to pelvic and/or para-aortic lymph nodes​

IIIC1 Positive pelvic nodes​

IIIC2 Positive para-aortic lymph nodes with or without positive pelvic lymph nodes

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5
Q

What is a Stage IV Tumour invades bladder and/or bowel mucosa, and/or distant metastases?

A

IVA Tumour invasion of bladder and/or bowel mucosa​

IVB Distant metastases, including intra-abdominal metastases and/or inguinal lymph nodes

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6
Q

What is the TCGA classification?

A

Group 1: EEC with mutations in POLE (Polymerase E- ultramutated) ​

​Group 2: EEC with MSI (hypermutated)​

​Group 3: EEC with low copy number alterations​

Group 4: (serous-like) tumours show TP53 mutations

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7
Q

What are POLE mutant tumours?

A

​These tumours often appear to be high-grade. ​

In the absence of the knowledge of their POLE gene mutation status, they would be mistakenly included into a category of tumours with bad prognosis. ​

POLE gene mutation confers a quite better prognosis. ​

So, the identification of this mutated subgroup is essential for better personalised treatment and prognosis analysis.

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8
Q

A fundamental cellular mechanism for preventing DNA alteration that are created largely during DNA replication

A

A fundamental cellular mechanism for preventing DNA alteration that are created largely during DNA replication

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9
Q

What is the Mismatch repair system?

A

Mutations or silencing by hypermethylation of one of the DNA mismatch repair genes results in MSI​

​

Microsatellite instability (MSI): Alterations in the length of short, repetitive DNA sequences called microsatellites.​

​

This results in an increase of the rate of mutations contributing to tumorigenesis, again with a high mutation burden.​

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10
Q

What shows strong nuclear expression in tumour cells of endometrioid carcinoma.​?

A

HMLH1 (A), PMS2 (B), MSH2 (C) and MH6 (D) show strong nuclear expression in tumour cells of endometrioid carcinoma.

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11
Q

What are hypersensitive to the immune checkpoint inhibitor, anti-PD-1, monotherapy?

A

EECs exhibiting POLE mutations and MSI are hypersensitive to the immune checkpoint inhibitor, anti-PD-1, monotherapy because,​

these tumours are characterised by a high mutation load which produces more neo-antigens. ​

they have a higher number of tumour infiltrating lymphocytes.

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12
Q

What are Gp 4 tumours?

A

​Composed mostly of SCs, but also include some EEC; many grade 3 but also some grades 1 and 2

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13
Q

What are the 4 patterns of p53 staining?

A

There are 4 main patterns of p53 staining:​

Normal/wild-type​

Complete absence​

Overexpression​

Cytoplasmic

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14
Q

What are leiomyomas?

A

Smooth muscle tumour of myometrium​

Commonest uterine tumour​

20% of women >35yrs​

Lay term is fibroid​

Usually multiple​

May be intramural, submucosal or ​

subserosal
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15
Q

What are leiosarcomas?

A

Malignant counterpart of leiomyoma - rare​

Usually solitary​

Usually postmenopausal​

Local invasion and blood stream spread​

5yr survival 20-30%

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16
Q

What are endometrial stromal sarcomas?

A

Low grade, high grade and other ​Tumour types

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17
Q

What is endometriosis?

A

Presence of endometrial glands and stroma outside the uterus​

​

Common – 10% of premenopausal women​

​

Origin:​

Metaplasia of pelvic peritoneum​

Implantation of endometrium, retrograde menstruation​

​

Ectopic endometrial tissue is functional and bleeds at time of menstruation > pain, scarring and infertility​

​

Can develop hyperplasia and malignancy

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18
Q

What are the types of ovarian cysts?

A

Non neoplastic cysts:​

Follicular and luteal cysts ​

Polycystic ovarian disease: ​

3-6% of reproductive age women​

patients have persistent anovulation​

obesity and hirsutism / virilism​

​

Endometrioitc cyst

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19
Q

What is the classification of ovarian tumours?

A

Primary tumours​

​

Epithelial tumours​

​

Sex cord-stromal tumours​

​

Germ cell tumours​

​

Miscellaneous tumours​

​

Secondary tumours

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20
Q

What is the Incidence and age of onset of epithelial tumours?

A

make up 65% of all ovarian tumours & 95% of malignant ovarian tumours​

​

50% found in 45-65 age group

21
Q

What is the Incidence and age of onset of germ cell tumours?

A

have bimodal distribution; one peak 15-21 year olds and one peak at 65-69

22
Q

What is the Incidence and age of onset of sex cord stromal tumours?

A

most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group

23
Q

What is the WHO classification of serous, mucinous and endometroid tumours?

A

Serous tumours​

Benign: cystadenoma and adenofibroma​

Borderline ​

Malignant:​

Low-grade serous carcinoma​

High-grade serous carcinoma​

​

Mucinous tumours​

Benign: cystadenoma and adenofibroma​

Borderline​

Malignant​

Mucinous carcinoma​

​

Endometrioid tumours​

Benign: Endometriotic cyst, cystadenoma and adenofibroma​

Borderline ​

Malignant​

Endometrioid carcinoma

24
Q

What is the WHO classification of clear cell, Brenner and seromucinous tumours?

A

Clear cell tumours​

Benign: cystadenoma and adenofibroma ​

Borderline​

Malignant​

Clear cell carcinoma​

​

​

Brenner tumours​

Benign​

Borderline​

Malignant​

Malignant Brenner tumour​

​

Seromucinous tumours​

Benign: cystadenoma and adenofibroma​

Borderline​

Malignant​

Seroumucinous carcinoma

25
What are the benign epithelial tumours?
​Serous Cystadenomas​ Cystadenofibromas​ Mucinous cystadenomas​ Brenner tumour
26
What are benign epithelial tumours?
Tumours whose biologic behaviour cannot be predicted on histologic grounds ​ ​ Tumours that have very low but definite metastatic potential​ ​ Morphologically similar tumours may behave differently ​ ​ To date, there are no reliable histological or molecular predictive markers for the behaviour of these tumours
27
What is the epidemiology of malignant epithelial tumours?
Worldwide is the 6th most common cancer in women​ ​ 2nd commonest female cancer causing death in women​ Difficult to diagnosis at an early stage​ Develops resistance to therapeutic agents
28
What are the RFs of malignant epithelial tumours?
Nulliparity, infertility, early menarche, late menopause.​ ​ Genetic predisposition: Family history of ovarian and breast cancers
29
Describe hereditary ovarian cancer
Up to 10% of epithelial ovarian cancer cases are familial​ ​ ​ 3 familial syndromes: All are transmitted in an autosomal dominant fashion​ familial breast-ovarian cancer syndrome​ site-specific ovarian cancer​ cancer family syndrome (Lynch type II)​ ​ Familial breast-ovarian cancer and site-specific ovarian cancer syndromes​ Associated with mutations of the BRCA1 and BRCA2; account for 90% of familial ovarian cancers​ ​ Hereditary ovarian cancer occurs at a younger age than sporadic​ ​ Carriers have 15 fold increase risk of ovarian carcinoma to non-carriers ​ ​ > 90% cancers are of serous: ovarian, peritoneal, fallopian tube.
30
What is Lynch syndrome?
HNPCC is responsible for 3% of ovarian carcinomas​ ​ Ovarian cancers associated are mainly of the endometrioid and clear cell types​ ​
31
What has Molecular analysis has shown?
Molecular analysis has shown that different patterns of genetic aberrations underlie the development of the different histologic subtypes. ``` PTEN beta catenin KRAS TP53/ Rb PIK3CA BRAF ```
32
Describe High Grade Serous Carcinoma​
Most common type of malignant tumours (80%)​ ​ Aggressive​ ​ Alteration in P53, in virtually all​ ​ BRCA1 or BRCA2 abnormalities (germline and somatic mutations; BRCA1 promoter methylation) ​ These genes encode proteins that play important roles in DNA repair (homologous recombination).
33
What is the Significance of Homologous Recombination Deficiency Testing​?
Identification of hereditary cases.​ Current data suggests that BRCA2 mutations confer an overall survival advantage compared with either being BRCA-negative or having a BRCA1 mutation in high-grade serous ovarian cancer. ​ BRCA mutation status has a major influence on response to chemotherapy. ​ Patients can benefit from targeted therapy by PARP inhibitors.
34
What are low grade serous carcinomas?
Distinct pathogenesis from high grade serous carcinoma.​ ​ Low grade, relatively indolent, arise de novo or from borderline ovarian tumours. ​ ​ Mutations in KRAS, BRAF. ​ ​ No association with BRCA mutations.
35
What are mucinous tumours?
Morphological features similar to mucinous tumours of the gastrointestinal tract.​ KRAS mutations.
36
What are secondary ovarian tumours?
​Metastatic colorectal carcinoma: ​ Ovaries, an anatomic site prone to involvement by metastatic colorectal adenocarcinoma.​ 4-10% of CRC go to ovary.​ Ovarian lesions are identified prior to the primary tumor in 14-32% of cases.​ ​ Krukenberg tumours: ​ Bilateral metastases composed of mucin producing signet ring cells.​ Most often of gastric origin or breast.
37
What are endometrial carcinomas?
10-20% associated with endometriosis, but most others thought to be derived from surface epithelium​ ​ Co-existence with endometrioid carcinoma in uterus common
38
Which mutations are associated with endometrial carcinomas?
CTNNB1 (38%-50%) ​ PTEN (15-20%)​ KRAS and BRAF (4%-36%)​ MSI (8-38%)​ PIK3Ca in (20%)​ P53 >60% and usually in high Endometriosis is a precursor
39
What is associated with Clear cell carcinoma?
Strong association with endometriosis​ ​ Molecular changes:​ MSI (6-21%)​ PTEN (6%)​ P53 (8.3%)​ BRAF (6.3%)​ PIK3Ca (20-25%)​ B-catenin (3%)
40
What are the sex cord stromal tumours?
Pure stromal tumours: ​ e.g. Fibroma, Thecoma, microcystic stromal tumour​ Pure sex cord cells: ​ e.g. Adult type and juvenile granulosa cell tumour​ Mixed sex cord-stromal tumours:​ e.g. Sertoli Leydig cell tumour Fibroblasts: Fibromas: ​benign, no endocrine production​ Granulosa cells: Granulosa cell tumor variable behaviour, may produce estrogen​ Thecal cells: Thecoma:​ benign, may secrete oestrogen, or rarely androgens​ ​ Sertoli-Leydig cells: Sertoli-Leydig cell tumor​ variable behaviour, may be androgenic
41
What are the Molecular Changes in Sex Cord-Stromal Tumours​?
Adult type granulosa cell tumour (GCT):​ 97% of adult GCT show somatic mutation of the Forkhead transcription factor FOXL2, is a master transcription factor that regulates cell proliferation and apoptosis.​ ​ Microcystic stromal tumour:​ FOXL2 mutation can be done in AGCT to confirm the diagnosis in cases where the diagnosis is in question.​ Mutation in CTNNB1
42
What is Peutz Jeghers syndrome?
Peutz Jeghers syndrome:​ Germline mutations of STK11 ​ ​ Sex cord stromal tumour with annular tubules​ ​ Cases occurring in PJS usually show indolent behaviour.​
43
What is DICER1 syndrome?
DICER1 Syndrome​ Germline mutation in DICER1, a gene encoding an RNAse III endoribonuclease.​ ​ Familial multinodular goitre with sertoli / leydig cell tumour, and tumour susceptibility includes pleuropulonry blastoma in childhood.​ ​ Found in up to 60% of seroli-Leydig cell tumours.
44
What are germ cell tumours in?
20% of ovarian tumours​ 95% benign​ predominantly occur in first or second decade
45
What are dermoid tumours?
Benign ​ Solid or cystic ​ May show many lines of differentiation but all mature adult type tissues​ Teeth and hair very common
46
What are immature teratomas?
Indicates presence of embryonic elements​ Neural tissue particularly conspicuous​ A malignant neoplasm that grows rapidly, penetrates the capsule and forms adhesions to the surrounding structures​ Spreads in the peritoneal cavity by implantation​ Metastasis to lymph nodes, lung, liver and other organs​ Three tier grading system according to amount of primitive elements
47
What are Mature cystic teratoma with malignant transformation​?
​ Malignant transformation is rare occurring in 2% of cases, usually in post menopausal women​ ​ Most frequently squamous cell carcinoma​ ​ Also carcinoid, thyroid carcinoma, basal cell carcinoma, malignant melanoma, intestinal adenocarcinoma, leiomyosarcoma, chondrosarcoma and angiosarcoma
48
What are Prognostic Factors in ovarian malignancies?
Stage of Disease​ Tumour type​ Tumor grade​ Size of residual disease ​ Tumor response to therapy

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